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1.
Rev. Soc. Bras. Med. Trop ; 54: e0008-22021, 2021. tab, graf
Article in English | LILACS | ID: biblio-1155584

ABSTRACT

Abstract We describe the first report of a patient with chronic mucocutaneous candidiasis associated with disseminated and recurrent paracoccidioidomycosis. The investigation demonstrated that the patient had a mannose receptor deficiency, which would explain the patient's susceptibility to chronic infection by Candida spp. and systemic infection by paracoccidioidomycosis. Mannose receptors are responsible for an important link between macrophages and fungal cells during phagocytosis. Deficiency of this receptor could explain the susceptibility to both fungal species, suggesting the impediment of the phagocytosis of these fungi in our patient.


Subject(s)
Humans , Paracoccidioidomycosis/complications , Paracoccidioidomycosis/diagnosis , Candidiasis, Chronic Mucocutaneous/complications , Candidiasis, Chronic Mucocutaneous/genetics , Receptors, Cell Surface , Lectins, C-Type , Mannose-Binding Lectins
2.
Article in Chinese | WPRIM | ID: wpr-828487

ABSTRACT

OBJECTIVE@#To provide data support for the study of pathogenic mechanism of SARS-CoV-2 at the molecular level, and provide suitable candidate targets for vaccine, antibody and drug research and development through comparative analysis for structural characteristics and epitopes of S protein of SARS-CoV-2 and SARS-CoV.@*METHODS@#Based on the reference sequences of S protein, physical and chemical properties, hydrophobicity, signal peptide, transmembrane region, domain, secondary structure, tertiary structure analysis and antigenic epitopes prediction were carried out. Meanwhile, the tissue expression, related pathways and reactome pathways of angiotensis Ⅰ converting enzyme 2 (ACE2) and C-type lectin domain family 4 member M (CLEC4M) receptors were analyzed.@*RESULTS@#The amino acid sequence of S protein of SARS-CoV-2 and SARS-CoV has a 75.80% consistency. The structural characteristics of the two coronaviruses are highly consistent, but the secondary structure and tertiary structure of SARS-CoV-2 is not as obvious as SARS-CoV. ACE2 and CLEC4M are expressed in alimentary system, heart, kidney, lung and placenta. The main related the pathways of renin-angiotensin system, protein digestion and absorption pathway, and the reactome pathways of metabolism of angiotensinogen to angiotensins, GPCR ligand binding, are related to typical symptoms of coronavirus disease 2019 induced by SARS-CoV-2. Three pairs of highly or completely homologous epitopes of S protein were obtained. The 600-605, 695-703 and 888-896 amino acid residues in SARS-CoV-2 were highly homologous with 586-591, 677-685 and 870-878 amino acid residues in SARS-CoV, respectively.@*CONCLUSIONS@#The similarity of S protein of SARS-CoV-2 and SARS-CoV determines that they have similar infection patterns and clinical manifestations. The candidate epitopes with high reliability can provide reference for virus diagnosis and vaccine development.


Subject(s)
Betacoronavirus , Cell Adhesion Molecules , Coronavirus Infections , Epitopes , Humans , Lectins, C-Type , Ligands , Pandemics , Peptidyl-Dipeptidase A , Pneumonia, Viral , Receptors, Cell Surface , Receptors, Virus , Reproducibility of Results , Spike Glycoprotein, Coronavirus
3.
Article in Chinese | WPRIM | ID: wpr-827996

ABSTRACT

To observe the efficacy of cinnamaldehyde on dextran sulfate sodium(DSS)-induced ulcerative colitis(UC) with Can-dida albicans(Ca) colonization and its effect on dectin-1/TLRs/NF-κB signaling pathway in mice. C57 BL/6 mice were randomly divided into normal group, DSS group, DSS+Ca group, cinnamaldehyde group and mesalazine group. Mice in DSS+Ca group were given Ca(1×10~8 CFU per mouse) through intragastrical administration for 4 consecutive days and then distilled water with 3.0% DSS for 7 consecutive days. In cinnamaldehyde group and mesalazine group, in addition to the induction method of the DSS+Ca group, mice were given 75 mg·kg~(-1) cinnamaldehyde and 200 mg·kg~(-1) mesalazine accompanied with 3.0% DSS for 7 consecutive days, respectively. Mice in normal group and DSS group were correspondingly administered with distilled water. The general conditions of the mice were observed daily, the diseased activity index(DAI) score was calculated, and fungal loads of feces were detected by plate method. The mice were sacrificed on day 12, colon length was measured, colon mucosa damage index(CMDI) score was calculated, and histopathological analysis was carried out by HE staining. Anti-saccharomces cerevisiae antibody(ASCA) and β-1,3-glucan in serum, and TNF-α, IL-1β, IL-6, IL-8, IL-10 in serum and colon tissue were detected by ELISA. The contents of β-1,3-glucan and macrophage infiltration in colon tissues were examined by immunofluorescence staining. The protein expressions of dectin-1, TLR2, TLR4 and NF-κB were detected by Western blot and immunohistochemistry staining. The results showed that cinnamaldehyde could significantly improve the general conditions of UC mice with Ca colonization, decrease DAI and histopathological scores, reduce intestinal mucosal congestion, erosion and colon shortening, decrease Ca load in mouse feces and tissues, down-regulate the contents of ASCA and β-1,3-glucan in serum, reduce the contents of TNF-α, IL-1β, IL-6, IL-8 and increase IL-10 in serum and colon tissues, inhibit macrophages infiltration and down-regulate the protein expression of dectin-1, TLR2, TLR4 and NF-κB in colon tissue. These results suggested that cinnamaldehyde had a therapeutic effect on UC mice with Ca colonization, which might be related to the inhibition of Ca proliferation, the regulation of dectin-1/TLRs/NF-κB signaling pathways and the coordination of the balance between pro-inflammatory and anti-inflammatory factors.


Subject(s)
Acrolein , Animals , Candida albicans , Colitis, Ulcerative , Colon , Dextran Sulfate , Disease Models, Animal , Lectins, C-Type , Mice , NF-kappa B , Signal Transduction
4.
J. venom. anim. toxins incl. trop. dis ; 26: e20190073, 2020. graf, ilus
Article in English | LILACS, VETINDEX | ID: biblio-1135150

ABSTRACT

Neuroblastoma is a pediatric tumor with a mortality rate of 40% in the most aggressive cases. Tumor microenvironment components as immune cells contribute to the tumor progression; thereby, the modulation of immune cells to a pro-inflammatory and antitumoral profile could potentialize the immunotherapy, a suggested approach for high-risk patients. Preview studies showed the antitumoral potential of BJcuL, a C- type lectin isolated from Bothrops jararacussu venom. It was able to induce immunomodulatory responses, promoting the rolling and adhesion of leukocytes and the activation of neutrophils. Methods: SK-N-SH cells were incubated with conditioned media (CM) obtained during the treatment of neutrophils with BJcuL and fMLP, a bacteria-derived peptide highly effective for activating neutrophil functions. Then we evaluated the effect of the same stimulation on the co-cultivation of neutrophils and SK-N-SH cells. Tumor cells were tested for viability, migration, and invasion potential. Results: In the viability assay, only neutrophils treated with BJcuL (24 h) and cultivated with SK-N-SH were cytotoxic. Migration of tumor cells decreased when incubated directly (p < 0.001) or indirectly (p < 0.005) with untreated neutrophils. When invasion potential was evaluated, neutrophils incubated with BJcuL reduced the total number of colonies of SK-N-SH cells following co-cultivation for 24 h (p < 0.005). Treatment with CM resulted in decreased anchorage-free survival following 24 h of treatment (p < 0.001). Conclusion: Data demonstrated that SK-N-SH cells maintain their migratory potential in the face of neutrophil modulation by BJcuL, but their invasive capacity was significantly reduced.(AU)


Subject(s)
Animals , Peptides , Bothrops , Crotalid Venoms/isolation & purification , Lectins, C-Type/isolation & purification , Neuroblastoma , Neutrophils , In Vitro Techniques
5.
Braz. j. med. biol. res ; 53(9): e9693, 2020. tab, graf
Article in English | ColecionaSUS, LILACS, ColecionaSUS | ID: biblio-1132556

ABSTRACT

Ischemic heart disease (IHD) is one of the leading causes of death worldwide. C-type lectin domain family 3 member B (CLEC3B) is a C-type lectin superfamily member and is reported to promote tissue remodeling. The serum levels of CLEC3B are downregulated in patients with cardiovascular disease. However, the molecular mechanisms of CLEC3B in IHD is not well-characterized. Therefore, we overexpressed CLEC3B and silenced CLEC3B in H9c2 rat cardiomyocytes for the first time. We then constructed a model of IHD in vitro through culturing H9c2 cardiomyocytes in serum-free medium under oxygen-deficit conditions. Then, Cell Counting Kit-8 (CCK-8), flow cytometry, qRT-PCR, and western blot assays were performed to investigate cell viability, apoptosis, and expression levels of CLEC3B, phosphatidylinositol 3-kinase (PI3K), phosphorylated PI3K (p-PI3K), protein kinase B (Akt), phosphorylated Akt (p-Akt), and cleaved-caspase 3. We observed that the mRNA expression of CLEC3B was decreased in hypoxic H9c2 cardiomyocytes (P<0.05). Overexpression of CLEC3B increased cell viability (P<0.01), inhibited cell apoptosis (P<0.05), upregulated the levels of p-PI3K/PI3K and p-Akt/Akt (P<0.01 or P<0.05), and downregulated expression of cleaved-caspase 3 (P<0.001) in hypoxic H9c2 cardiomyocytes while silencing of CLEC3B caused the opposite results. Inhibition of the PI3K/Akt pathway reversed the protective effect of CLEC3B on hypoxic H9c2 cardiomyocytes. Our study demonstrated that CLEC3B alleviated the injury of hypoxic H9c2 cardiomyocytes via the PI3K/Akt pathway.


Subject(s)
Humans , Animals , Rats , Apoptosis/physiology , Lectins, C-Type/metabolism , Signal Transduction , Phosphatidylinositol 3-Kinases , Myocytes, Cardiac/physiology , Proto-Oncogene Proteins c-akt/metabolism , Phosphatidylinositol 3-Kinase , Hypoxia
6.
Immune Network ; : e1-2019.
Article in English | WPRIM | ID: wpr-740213

ABSTRACT

Systemic lupus erythematosus (SLE) is the prototypic systemic autoimmune disease characterized by production of autoantibodies to various nuclear antigens and overexpression of genes regulated by IFN-I called IFN signature. Genetic studies on SLE patients and mutational analyses of mouse models demonstrate crucial roles of nucleic acid (NA) sensors in development of SLE. Although NA sensors are involved in induction of anti-microbial immune responses by recognizing microbial NAs, recognition of self NAs by NA sensors induces production of autoantibodies to NAs in B cells and production of IFN-I in plasmacytoid dendritic cells. Among various NA sensors, the endosomal RNA sensor TLR7 plays an essential role in development of SLE at least in mouse models. CD72 is an inhibitory B cell co-receptor containing an immunoreceptor tyrosine-based inhibition motif (ITIM) in the cytoplasmic region and a C-type lectin like-domain (CTLD) in the extracellular region. CD72 is known to regulate development of SLE because CD72 polymorphisms associate with SLE in both human and mice and CD72−/− mice develop relatively severe lupus-like disease. CD72 specifically recognizes the RNA-containing endogenous TLR7 ligand Sm/RNP by its extracellular CTLD, and inhibits B cell responses to Sm/RNP by ITIM-mediated signal inhibition. These findings indicate that CD72 inhibits development of SLE by suppressing TLR7-dependent B cell response to self NAs. CD72 is thus involved in discrimination of self-NAs from microbial NAs by specifically suppressing autoimmune responses to self-NAs.


Subject(s)
Animals , Antigens, Nuclear , Autoantibodies , Autoantigens , Autoimmune Diseases , Autoimmunity , B-Lymphocytes , Cytoplasm , Dendritic Cells , Discrimination, Psychological , Humans , Immunoreceptor Tyrosine-Based Inhibition Motif , Lectins, C-Type , Lupus Erythematosus, Systemic , Mice , RNA
7.
Rev. Soc. Bras. Med. Trop ; 51(6): 725-730, Nov.-Dec. 2018. tab, graf
Article in English | LILACS | ID: biblio-977100

ABSTRACT

Abstract Invasive aspergillosis is a common fungal infection in immunocompromised individuals. Some studies have shown that toll-like receptor and dectin-1 genetic polymorphisms may alter signaling pathways, thus increasing an individual's susceptibility to invasive aspergillosis. We investigated the pertinent literature to determine whether polymorphisms in the genes encoding toll-like receptors and dectin-1 increase the susceptibility to invasive aspergillosis. This study systematically reviewed the literature using the databases PubMed/PMC, Scopus, and Web of Science using the keywords invasive aspergillosis, polymorphism, Toll-like, and Dectin-1. From the initial search, 415 studies were found and according to our inclusion and exclusion criteria, eight studies were selected. Several studies described single-nucleotide polymorphisms (SNPs) that are associated with a greater susceptibility to invasive aspergillosis. These SNPs were found in the genes that encode toll-like receptors 1, 3, 4, and 5 and the gene that encodes dectin-1; upon activation, both cellular receptors initiate a signaling cascade that can result in the production of cytokines and chemokines. Thus, our literature review uncovered a significant association between polymorphisms in the genes that encode toll-like receptors and dectin-1 and invasive aspergillosis. More studies should be performed to better understand the relationship between toll-like receptor and dectin-1 genetic polymorphisms and invasive aspergillosis susceptibility.


Subject(s)
Humans , Aspergillosis/genetics , Genetic Predisposition to Disease/genetics , Polymorphism, Single Nucleotide/genetics , Lectins, C-Type/genetics , Toll-Like Receptors/genetics
8.
Chinese Medical Journal ; (24): 1731-1736, 2016.
Article in English | WPRIM | ID: wpr-251314

ABSTRACT

<p><b>BACKGROUND</b>The expression of dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin (DC-SIGN) in renal tubular epithelial cells has been thought to be highly correlated with the occurrence of several kidney diseases, but whether it takes place in renal tissues during hemorrhagic shock (HS) is unknown. The present study aimed to investigate this phenomenon and the inhibitory effect of Vitamin C (VitC).</p><p><b>METHODS</b>A Sprague-Dawley rat HS model was established in vivo in this study. The expression level and location of DC-SIGN were observed in kidneys. Also, the degree of histological damage, the concentrations of tumor necrosis factor-μ and interleukin-6 in the renal tissues, and the serum concentration of blood urea nitrogen and creatinine at different times (2-24 h) after HS (six rats in each group), with or without VitC treatment before resuscitation, were evaluated.</p><p><b>RESULTS</b>HS induced DC-SIGN expression in rat tubular epithelial cells. The proinflammatory cytokine concentration, histological damage scores, and functional injury of kidneys had increased. All these phenomena induced by HS were relieved when the rats were treated with VitC before resuscitation.</p><p><b>CONCLUSIONS</b>The results of the present study illustrated that HS could induce tubular epithelial cells expressing DC-SIGN, and the levels of proinflammatory cytokines in the kidney tissues improved correspondingly. The results also indicated that VitC could suppress the DC-SIGN expression in the tubular epithelial cells induced by HS and alleviate the inflammation and functional injury in the kidney.</p>


Subject(s)
Animals , Ascorbic Acid , Therapeutic Uses , Blotting, Western , Cell Adhesion Molecules , Metabolism , Epithelial Cells , Metabolism , Pathology , Immunohistochemistry , Kidney Tubules , Metabolism , Pathology , Lectins, C-Type , Metabolism , Male , Rats , Rats, Sprague-Dawley , Receptors, Cell Surface , Metabolism , Shock, Hemorrhagic , Drug Therapy , Metabolism
9.
Article in Chinese | WPRIM | ID: wpr-256595

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effect of low-selenium diet on the liver and kidneys of rats and explore the role of macrophage polarization into M1 and M2 phenotypes in liver and kidney injuries.</p><p><b>METHODS</b>Twenty-four rats (12 female and 12 male) were randomly divided into control group and low-selenium group and fed with normal chow (dietary selenium of 0.18 mg/kg) and low-selenium diet (dietary selenium of 0.02 mg/kg) for 109 days. After the feeding, the rats were sacrificed for HE staining to observe liver and kidney pathologies, and immunohistochemistry was performed for analyzing CCR7, CD206, CD163-positive cell numbers in the liver and kidneys.</p><p><b>RESULTS</b>The rats in low-selenium group showed severer fibrosis in the liver and kidney than the control group. In either male or female rats in low-selenium group, CCR7 and CD206 expressions in the liver were comparable with those in control group, but CD163 expression was lower than that in the control group (P<0.05 for both female and male rats). In the kidney, the proximal tubule showed a slightly higher while the distal tubule showed a slightly lower CCR7 expression in low selenium group than in the control group (P>0.05). In low-selenium group, a significantly lower CD163 expression in the distal tubule and a significantly higher CD206 expression in the proximal tubule were noted as compared with the control group (P<0.05 in both female and male rats). Compared with the control rats, the male rats in low-selenium group, but not the female rats, showed a significantly lower CD163 expression in the proximal tubule of the kidney (P<0.05); the female but not the male rats in low-selenium group show a higher CD206 expression in the distal tubule (P<0.05).</p><p><b>CONCLUSION</b>Low-selenium diet can cause liver and kidney fibrosis in rats and may inhibit macrophage activation into the M2 phenotype.</p>


Subject(s)
Animals , Antigens, CD , Metabolism , Antigens, Differentiation, Myelomonocytic , Metabolism , Diet , Female , Fibrosis , Kidney , Metabolism , Pathology , Lectins, C-Type , Metabolism , Liver , Metabolism , Pathology , Macrophage Activation , Male , Mannose-Binding Lectins , Metabolism , Rats , Receptors, CCR7 , Metabolism , Receptors, Cell Surface , Metabolism , Selenium
10.
Article in Chinese | WPRIM | ID: wpr-337398

ABSTRACT

Polymeric micelles have exhibited attractive properties as drug carriers, such as high stability in vivo and good biocompatibility, and been successfully used to dissolve various drugs of poor aqueous solubilities. In this study, we developed a new type of polymeric micelles with mannose-mediated targeting and pH-responsive drug release properties for anticancer drug delivery. The polymeric micelles were prepared from an amphiphilic polymer, poly (glycidyl methacrylate)-g-mannose (PGMA-Mannose). An anticancer drug, doxorubicin (DOX), was encapsulated into the micelles during the micellization, and could be released rapidly under acidic condition. The specificity of cellular uptake of the micelles by two different cell lines was studied using confocal laser scanning microscopy and the MTT assay. DOX-loaded micelles were efficiently trapped by mannose-receptor-overexpressing cancer cells MDA-MB-231, whereas mannose- receptor-poor cells HEK293 showed much lower endocytosis towards the micelles under the same conditions. Thus, DOX-loaded micelles displayed higher cytotoxicity to MDA-MB-231 cancer cells as compared with free DOX. The present study demonstrates that PGMA-Mannose micelles are a promising targeted drug delivery system for cancer therapy.


Subject(s)
Cell Line, Tumor , Doxorubicin , Pharmacology , Drug Delivery Systems , HEK293 Cells , Humans , Lectins, C-Type , Metabolism , Mannose , Chemistry , Mannose-Binding Lectins , Metabolism , Micelles , Receptors, Cell Surface , Metabolism
11.
Article in English | LILACS, VETINDEX | ID: biblio-954793

ABSTRACT

The blood plasma of numerous snake species naturally comprises endogenous phospholipase A2 inhibitors, which primarily neutralize toxic phospholipases A2 that may eventually reach their circulation. This inhibitor type is generally known as snake blood phospholipase A2 inhibitors (sbPLIs). Most, if not all sbPLIs are oligomeric glycosylated proteins, although the carbohydrate moiety may not be essential for PLA2 inhibition in every case. The presently known sbPLIs belong to one of three structural classes - namely sbαPLI, sbβPLI or sbγPLI - depending on the presence of characteristic C-type lectin-like domains, leucine-rich repeats or three-finger motifs, respectively. Currently, the most numerous inhibitors described in the literature are sbαPLIs and sbγPLIs, whereas sbβPLIs are rare. When the target PLA2 is a Lys49 homolog or an Asp49 myotoxin, the sbPLI is denominated a myotoxin inhibitor protein (MIP). In this brief overview, the most relevant data on sbPLIs will be presented. Representative examples of sbαPLIs and sbγPLIs from two Old World - Gloydius brevicaudus and Malayopython reticulatus - and two New World - Bothrops alternatus and Crotalus durissus terrificus - snake species will be emphasized.(AU)


Subject(s)
Animals , Plasma , Snakes , Blood , Lectins, C-Type , Phospholipase A2 Inhibitors
12.
Article in Chinese | WPRIM | ID: wpr-255161

ABSTRACT

<p><b>OBJECTIVE</b>To construct the expression vector pLCK-CD69-IRES-EGFP that contains mouse cell surface activation protein CD69 and enhanced green fluorescent protein(EGFP),and to generate CD69 transgenic mice based on this vector.</p><p><b>METHODS</b>First, RNA was extracted from mouse lung tissue and cDNA was synthesized via reverse transcription. PCR primer was designed through the PubMed searching, then mouse CD69 DNA fragment was amplified with PCR. Second, this DNA fragment was subcloned to the pInsulater-LCK-IRES-EGFP plasmid and constructed the transgenic vector after the verification of nucleotide sequence. Third, the expression vector was then transfected into 293 T cells and its expression in 293 T cells was observed under fluorescence microscope. Last, microinjection was performed to transfer the expression vector pLCK-CD69-IRES-EGFP into fertilized eggs, which were implanted into pseudo-pregnant recipient mice. After birth the tail samples of the pups were obtained for the purpose of genotyping to determine the transgenic founders. Fluorescence microscope and flow cytometer were used to measure the expression of CD69 on cells.</p><p><b>RESULTS</b>The construction of the expression vector pLCK-CD69-IRES-EGFP was verified by enzyme digestion and DNA sequencing. The transfected 293 T cell showed expression of the protein under fluorescence microscope. Identification of PCR for the tail tissue of the pups confirmed the present of CD69 transgene and resting lymphocytes demonstrated the expression of CD69.</p><p><b>CONCLUSION</b>The construction of expression vector pLCK-CD69-IRES-EGFP and generation of CD69 transgenic mice have been successfully processed, which lays a foundation of the solid pattern studies in inflammatory diseases.</p>


Subject(s)
Animals , Antigens, CD , Genetics , Antigens, Differentiation, T-Lymphocyte , Genetics , DNA, Complementary , Genetic Vectors , Genotype , Green Fluorescent Proteins , Genetics , Lectins, C-Type , Genetics , Mice , Mice, Transgenic , Plasmids , Polymerase Chain Reaction , Sequence Analysis, DNA , Transfection
13.
Protein & Cell ; (12): 297-306, 2015.
Article in English | WPRIM | ID: wpr-757590

ABSTRACT

Dendritic cells (DCs) comprise two functionally distinct subsets: plasmacytoid DCs (pDCs) and myeloid DCs (mDCs). pDCs are specialized in rapid and massive secretion of type I interferon (IFN-I) in response to nucleic acids through Toll like receptor (TLR)-7 or TLR-9. In this report, we characterized a CD56(+) DC population that express typical pDC markers including CD123 and BDCA2 but produce much less IFN-I comparing with pDCs. In addition, CD56(+) DCs cluster together with mDCs but not pDCs by genome-wide transcriptional profiling. Accordingly, CD56(+) DCs functionally resemble mDCs by producing IL-12 upon TLR4 stimulation and priming naïve T cells without prior activation. These data suggest that the CD56(+) DCs represent a novel mDC subset mixed with some pDC features. A CD4(+)CD56(+) hematological malignancy was classified as blastic plasmacytoid dendritic cell neoplasm (BPDCN) due to its expression of characteristic molecules of pDCs. However, we demonstrated that BPDCN is closer to CD56(+) DCs than pDCs by global gene-expression profiling. Thus, we propose that the CD4(+)CD56(+) neoplasm may be a tumor counterpart of CD56(+) mDCs but not pDCs.


Subject(s)
Biomarkers , Metabolism , CD56 Antigen , Genetics , Allergy and Immunology , Cell Lineage , Genetics , Allergy and Immunology , Dendritic Cells , Allergy and Immunology , Metabolism , Pathology , Gene Expression , Hematologic Neoplasms , Genetics , Allergy and Immunology , Pathology , Humans , Immunophenotyping , Interferon Type I , Metabolism , Interleukin-12 , Metabolism , Interleukin-3 Receptor alpha Subunit , Genetics , Allergy and Immunology , Lectins, C-Type , Genetics , Allergy and Immunology , Membrane Glycoproteins , Genetics , Allergy and Immunology , Myeloid Cells , Allergy and Immunology , Metabolism , Pathology , Receptors, Immunologic , Genetics , Allergy and Immunology , Terminology as Topic , Toll-Like Receptor 4 , Genetics , Allergy and Immunology , Toll-Like Receptor 7 , Genetics , Allergy and Immunology , Toll-Like Receptor 9 , Genetics , Allergy and Immunology
14.
Article in Chinese | WPRIM | ID: wpr-355331

ABSTRACT

<p><b>OBJECTIVE</b>To study the effect and mechanism of soluble dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin (sDC-SIGN) on the phagocytosis of Staphylococcus aureus (S. aureus) by immature dendritic cells (imDCs).</p><p><b>METHODS</b>Flow cytometry was employed to examine the effect of sDC-SIGN on the phagocytosis of S. aureus by imDCs. Enzyme-linked immunosorbent assay (ELISA) was used to analyze the binging of sDC-SIGN to S. aureus, lipoteichoic acid (LTA) and lipopolysaccharides (LPS) and investigate the effect of the ligands mannan and LTA and anti-DC-SIGN antibodies 1C6 and 4H3 on the binging of sDC-SIGN to S. aureus.</p><p><b>RESULTS</b>sDC-SIGN inhibited the phagocytosis of S. aureus by imDCs. sDC-SIGN bound to S. aureus in a Ca(2+)-dependent manner. sDC-SIGN concentration-dependently bound to LTA, but not to LTA, and the binging of sDC-SIGN to S. aureus was blocked by mannan, LTA, 1C6 and 4H3.</p><p><b>CONCLUSION</b>sDC-SIGN preferentially binds to the carbohydrate constituents on S. aureus to affect the binding between membrane-bound DC-SIGN and S. aureus, thus suppressing the phagocytosis of S. aureus by imDCs.</p>


Subject(s)
Cell Adhesion Molecules , Metabolism , Dendritic Cells , Cell Biology , Metabolism , Humans , Lectins, C-Type , Metabolism , Lipopolysaccharides , Phagocytosis , Receptors, Cell Surface , Metabolism , Staphylococcus aureus , Teichoic Acids
15.
Mem. Inst. Oswaldo Cruz ; 109(2): 250-255, abr. 2014. tab, graf
Article in English | LILACS | ID: lil-705822

ABSTRACT

Studies on human genetic variations are a useful source of knowledge about human immunodeficiency virus (HIV)-1 infection. The Langerin protein, found at the surface of Langerhans cells, has an important protective role in HIV-1 infection. Differences in Langerin function due to host genetic factors could influence susceptibility to HIV-1 infection. To verify the frequency of mutations in the Langerin gene, 118 samples from HIV-1-infected women and 99 samples from HIV-1-uninfected individuals were selected for sequencing of the promoter and carbohydrate recognition domain (CRD)-encoding regions of the Langerin gene. Langerin promoter analysis revealed two single nucleotide polymorphisms (SNPs) and one mutation in both studied groups, which created new binding sites for certain transcription factors, such as NFAT5, HOXB9.01 and STAT6.01, according to MatInspector software analysis. Three SNPs were observed in the CRD-encoding region in HIV-1-infected and uninfected individuals: p.K313I, c.941C>T and c.983C>T. This study shows that mutations in the Langerin gene are present in the analysed populations at different genotypic and allelic frequencies. Further studies should be conducted to verify the role of these mutations in HIV-1 susceptibility.


Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Young Adult , Antigens, CD/genetics , HIV Infections/genetics , HIV-1 , Lectins, C-Type/genetics , Mutation , Mannose-Binding Lectins/genetics , Polymorphism, Single Nucleotide/genetics , Promoter Regions, Genetic/genetics , Brazil , Genotype , Gene Frequency/genetics , Genetic Predisposition to Disease/genetics , Hydrophobic and Hydrophilic Interactions , Homeodomain Proteins/genetics , Polymerase Chain Reaction , Sequence Analysis, DNA , /genetics , Transcription Factors/genetics
16.
Article in Chinese | WPRIM | ID: wpr-302399

ABSTRACT

This study was purposed to explore the correlation of regenerating Islet-derived 3-alpha(Reg3α) protein level in plasma with the diagnosis and prognosis of the gastrointestinal acute graft-versus-host disease (GI-aGVHD) after all-HSCT, 103 patients who underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT) were observed in our hospital from December 2011 to December 2012. Peripheral blood samples were routinely collected at 9 d before allo-HSCT, 0 d, 14 d, 28 d after allo-HSCT as well as in aGVHD and at the 1 and 4 weeks after aGVHD therapy. The plasma concentrations of Reg3α were measured by using ELISA kit. The results indicated that among the 103 patients, 17 cases never developed aGVHD symptoms (no-aGVHD), 27 cases presented with non-aGVHD associated diarrhea, 10 cases presented with isolated skin aGVHD, 17 cases developed grades I-II GI-aGVHD, 32 cases with grades III-IV GI-aGVHD. The plasma concentrations of Reg3α in group of patients with GI-aGVHD and group of non-aGVHD diarrhea were 111.5 (54.7-180.2) and 23.9 (14.5-89.5) ng/ml respectively with significant difference (P < 0.001). The plasma concentrations of Reg3α in 17 patients of grades III-IV GI-aGVHD who experienced a complete or partial response and 7 patients who had no response to therapy at 4 weeks were 137.2(51.7-205.4) and 679.4(122.3-896.8) ng/ml respectively with the significant difference (P = 0.028). All of the patients who had no response to therapy died of aGVHD associated multiple organ failure. The area under the ROC curve was 0.902 when plasma concentration of Reg3α was set at 87.73 ng/ml. The sensitivity was 81.48% and the specificity was 82.86% when the critical value was used in diagnosis of grades III-IV GI-aGVHD. The probability of grades III-IV GI-aGVHD had statistical difference above and below 87.73 ng/ml after allo-HSCT (P < 0.001). It is concluded that the increase of plasma Reg3α level after transplantation suggests the incidence of grades III-IV GI-aGVHD. The high level of plasma Reg3α protein in patients with grades III-IV GI-aGVHD after the immunosuppressive treatment for four weeks indicates a poor prognosis. The plasma concentrations of Reg3α can be used as a specific biomarker of GI-aGVHD.


Subject(s)
Adolescent , Adult , Antigens, Neoplasm , Blood , Biomarkers, Tumor , Blood , Female , Graft vs Host Disease , Diagnosis , Hematopoietic Stem Cell Transplantation , Humans , Intestinal Diseases , Diagnosis , Lectins, C-Type , Blood , Male , Middle Aged , Pancreatitis-Associated Proteins , Plasma , Prognosis , Transplantation, Homologous , Young Adult
17.
Acta Pharmaceutica Sinica ; (12): 482-489, 2014.
Article in English | WPRIM | ID: wpr-245058

ABSTRACT

This study investigated the effect of arctigenin (Arc) on the cell activation, cytokines expression, proliferation, and cell-cycle distribution of mouse T lymphocytes. Mouse lymphocytes were prepared from lymph node and treated with Phorbol-12-myristate-13-acetate (PMA)/Ionimycin (Ion) and/or Arc. CD69, CD25, cytokines, proliferation and cell cycle were assayed by flow cytometry. The results showed that, at concentrations of less than 1.00 micromol x L(-1), Arc expressed non-obvious cell damage to cultured lymphocytes, however, it could significantly down-regulate the expression of CD69 and CD25, as well as TNF-alpha, IFN-gamma, IL-2, IL-4, IL-6 and IL-10 on PMA/Ion stimulated lymphocytes. At the same time, Arc could also inhibit the proliferation of PMA/Ion-activated lymphocytes and exhibited lymphocyte G 0/G1 phase cycle arrest. These results suggest that Arc possesses significant anti-inflammatory effects that may be mediated through the regulation of cell activation, cytokines expression and cell proliferation.


Subject(s)
Animals , Anti-Inflammatory Agents , Pharmacology , Antigens, CD , Metabolism , Antigens, Differentiation, T-Lymphocyte , Metabolism , Arctium , Chemistry , Cell Cycle Checkpoints , Cell Proliferation , Cytokines , Metabolism , Female , Furans , Pharmacology , Interferon-gamma , Metabolism , Interleukin-10 , Metabolism , Interleukin-2 , Metabolism , Interleukin-2 Receptor alpha Subunit , Metabolism , Interleukin-4 , Metabolism , Interleukin-6 , Metabolism , Ionomycin , Pharmacology , Lectins, C-Type , Metabolism , Lignans , Pharmacology , Lymphocyte Activation , Mice , Mice, Inbred BALB C , Plants, Medicinal , Chemistry , T-Lymphocytes , Cell Biology , Allergy and Immunology , Tetradecanoylphorbol Acetate , Pharmacology , Tumor Necrosis Factor-alpha , Metabolism
18.
Article in English | WPRIM | ID: wpr-190884

ABSTRACT

Dendritic cells (DCs) are professional antigen-presenting cells capable of initiating and regulating innate and adaptive immunity. The development of effective ways to produce a large number of DCs in laboratories made the use of DCs available in various vaccine approaches. Compared to conventional vaccines, focused on protective antibody responses, DC vaccines emphasize protective T cell immunity but might elicit strong antibody responses as well. In addition, the recent discoveries of functionally distinct DC subsets in various organs and tissues are likely to increase the potential of exploiting DCs in vaccines and immunotherapy. Vaccines composed of DCs generated ex vivo, pulsed with antigens, and matured prior to being re-infused to the body have been widely tried clinically but resulted in limited success due to various obstacles. In this review, new approaches that protein vaccines are selectively targeted to the endocytic C-type lectin receptors on surface of DCs in vivo are discussed.


Subject(s)
Adaptive Immunity , Antibody Formation , Antigen-Presenting Cells , Dendritic Cells , Immunotherapy , Lectins, C-Type , Receptors, Antigen , Vaccines
19.
Chinese Journal of Cardiology ; (12): 132-135, 2014.
Article in Chinese | WPRIM | ID: wpr-356425

ABSTRACT

<p><b>OBJECTIVE</b>To explore the anti-inflammatory mechanisms of high density lipoprotein (HDL) by observing the effects of apoprotein (apo)AI, a major protein component of HDL, on the inflammatory macrophage cell polarity.</p><p><b>METHODS</b>Cultured mice marrow-derived macrophages were stimulated with lipopolysaccharide and interferon after 10 µg/ml of apoAI were added to the macrophages for 24 hours. The expression of membrane molecules CD16/32, CD206 were detected by fluorescence activated cell sorting (FACS). ELISA was used to detect the secretion of IL-10 and IL-12. Real-time quantitative PCR was used to detect the mRNA expression of TLR4, MyD88 and IRF5.</p><p><b>RESULTS</b>Compared to macrophages stimulated by interferon and lipopolysaccharide but without pretreatment with apoAI, pre-incubation with apoAI significantly downregulated the expression of CD16/32 (91.17% ± 1.99% vs.50.47% ± 1.02%, P < 0.05), IL-12 [(747.27 ± 3.74)pg/ml vs. (73.80 ± 4.56)pg/ml, P < 0.05], upregulated the expression of CD206(0.33% ± 0.12% vs. 3.00% ± 0.36%, P < 0.05), IL -10 expression [(23.56 ± 4.30) pg/ml vs.(32.91 ± 2.47) pg/ml, P < 0.05], and reduced the mRNA expression of TLR4 (1.000 ± 0.025 vs.0.708 ± 0.003, P < 0.05) , MyD88 (1.591 ± 0.005 vs. 1.341 ± 0.005, P < 0.05) , IRF5 (0.954 ± 0.005 vs. 0.463 ± 0.003, P < 0.05) .</p><p><b>CONCLUSION</b>ApoAI enhances the switch of inflammatory macrophages to anti-inflammatory macrophages possibly through inhibiting TLR4-MyD88-IRF5 pathway.</p>


Subject(s)
Animals , Apolipoprotein A-I , Pharmacology , Cell Line , Female , Interferon Regulatory Factors , Metabolism , Interleukin-10 , Metabolism , Interleukin-12 , Metabolism , Lectins, C-Type , Metabolism , Macrophages , Allergy and Immunology , Metabolism , Mannose-Binding Lectins , Metabolism , Mice , Mice, Inbred C57BL , Myeloid Differentiation Factor 88 , Metabolism , Receptors, Cell Surface , Metabolism , Receptors, IgG , Metabolism , Toll-Like Receptor 4 , Metabolism
20.
Immune Network ; : 205-212, 2013.
Article in English | WPRIM | ID: wpr-223722

ABSTRACT

Dectin-1, which specifically recognizes beta-glucan of fungal cell walls, is a non-Toll-like receptor (TLR) pattern recognition receptor and a representative of C-type lectin receptors (CLRs). The importance of Dectin-1 in innate immune cells, such as dendritic cells and macrophages, has previously been well studied. However, the function of Dectin-1 in B cells is very poorly understood. To determine the role of Dectin-1 in B cell activation, we first investigated whether mouse B cells express Dectin-1 and then assessed the effect of Dectin-1 stimulation on B cell proliferation and antibody production. Mouse B cells express mRNAs encoding CLRs, including Dectin-1, and surface Dectin-1 was expressed in B cells of C57BL/6 rather than BALB/c strain. Dectin-1 agonists, heat-killed Candida albicans (HKCA) and heat-killed Saccharomyces cerevisiae (HKSC), alone induced B cell proliferation but not antibody production. Interestingly, HKSC, HKCA, and depleted zymosan (a selective Dectin-1 agonist) selectively enhanced LPS-driven IgG1 production. Taken together, these results suggest that, during fungal infection, beta-glucan-stimulated Dectin-1 may cooperate with TLR4 to specifically enhance IgG1 production by mouse B cells.


Subject(s)
Animals , Antibody Formation , B-Lymphocytes , Candida albicans , Cell Proliferation , Cell Wall , Dendritic Cells , Immunoglobulin G , Lectins, C-Type , Macrophages , Mice , RNA, Messenger , Saccharomyces cerevisiae , Sprains and Strains , Zymosan
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