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1.
J Allergy Clin Immunol Glob ; 3(2): 100211, 2024 May.
Article in English | MEDLINE | ID: mdl-38419685

ABSTRACT

Background: Chronic rhinosinusitis (CRS) is a heterogeneous disease characterized by persistent sinonasal inflammation and sinus microbiome dysbiosis. Nasal polyps (NPs) are one of the main manifestations that cause diverse clinical symptoms of CRS. Objective: We sought to conduct a bibliometric and visual analysis of articles on CRS and NPs published between 2003 and 2022 to provide researchers with the current state of research and potential directions. Methods: We searched relevant articles from 2003 to 2022 in the Web of Science database. VOSviewer and the Bibliometrix R package were used to perform the bibliometric analysis. Results: A total of 3907 publications were retrieved. The United States made the highest contributions to global research, followed by China. Northwestern University had the most publications. The most published author was C. Bachert, followed by R. P. Schleimer and R. J. Schlosser. The authors with the most co-citations were C. Bachert, W. J. Fokkens, and P. Gevaert. Moreover, the journal with the most publications was the International Forum of Allergy & Rhinology, and the Journal of Allergy and Clinical Immunology was the most cited. "Covid-19," "biologics," and "type 2 inflammation" were the top current research hotspots. Conclusions: The United States and Northwestern University were the leading country and institution in researching CRS and NPs. C. Bachert was the most influential expert. The International Forum of Allergy & Rhinology and the Journal of Allergy and Clinical Immunology were leading journals. "Covid-19," "biologics," and "type 2 inflammation" were the trending topics.

2.
World Allergy Organ J ; 17(3): 100880, 2024 Mar.
Article in English | MEDLINE | ID: mdl-38390554

ABSTRACT

Chronic rhinosinusitis (CRS) is a disease highly associated with abnormal regulation of T and B cells. The underlying pathophysiology of inflammatory pathways has critical implications for the diagnosis and management of CRS. Soluble CD40-ligand (sCD40L) is a cleaved form of CD40L present in plasma which functions the same way as CD40L, which has been observed as an inflammatory biomarker in many diseases. CD40L-positive cells control B-cell maturation, proliferation, apoptosis, and antibody production by binding to its receptor CD40 on B-cells. And our results show for the first time that patients with CRS have lower serum sCD40L levels compared to healthy subjects and that decreased sCD40L levels in patients correlate with increased CD40L-positive cell counts in the sinonasal mucosa. In addition, eosinophilic chronic rhinosinusitis (eCRS) patients tend to exhibit more CD40L-positive cells in the sinonasal mucosa compared to non-eCRS patients. This supports the notion that local blockade of CD40/CD40L may suppress pathogenic T/B cell responses and reduce tissue inflammation. Significantly, sCD40L and CD40L may be involved in the development and progression of CRS by impairing peripheral blood B-cell function and enhancing the local inflammatory response in the sinonasal mucosa.

3.
Front Immunol ; 14: 1171308, 2023.
Article in English | MEDLINE | ID: mdl-37325657

ABSTRACT

Background: Chronic rhinosinusitis (CRS), whose prevalence and pathogenesis are age-related, is characterized by nasal tissue eosinophil infiltration. CD40-CD40 ligand (CD40L) pathway involves in the eosinophil-mediated inflammation, and inducible co-stimulator (ICOS)-ICOS ligand (ICOSL) signal can strengthen CD40-CD40L interaction. Whether CD40-CD40L and ICOS-ICOSL have a role in the development of CRS remains unknown. Objectives: The aim of this study is to investigate the association of CD40-CD40L and ICOS-ICOSL expression with CRS and underlying mechanisms. Methods: Immunohistology detected the expression of CD40, CD40L, ICOS, and ICOSL. Immunofluorescence was performed to evaluate the co-localizations of CD40 or ICOSL with eosinophils. Correlations between CD40-CD40L and ICOS-ICOSL as well as clinical parameters were analyzed. Flow cytometry was used to explore the activation of eosinophils by CD69 expression and the CD40 and ICOSL expression on eosinophils. Results: Compared with the non-eCRS subset, ECRS (eosinophilic CRS) subset showed significantly increased CD40, ICOS, and ICOSL expression. The CD40, CD40L, ICOS, and ICOSL expressions were all positively correlated with eosinophil infiltration in nasal tissues. CD40 and ICOSL were mainly expressed on eosinophils. ICOS expression was significantly correlated with the expression of CD40-CD40L, whereas ICOSL expression was correlated with CD40 expression. ICOS-ICOSL expression positively correlated with blood eosinophils count and disease severity. rhCD40L and rhICOS significantly enhanced the activation of eosinophils from patients with ECRS. Tumor necrosis factor-α (TNF-α) and interleukin-5 (IL-5) obviously upregulated CD40 expression on eosinophils, which was significantly inhibited by the p38 mitogen-activated protein kinase (MAPK) inhibitor. Conclusions: Increased CD40-CD40L and ICOS-ICOSL expressions in nasal tissues are linked to eosinophils infiltration and disease severity of CRS. CD40-CD40L and ICOS-ICOSL signals enhance eosinophils activation of ECRS. TNF-α and IL-5 regulate eosinophils function by increasing CD40 expression partly via p38 MAPK activation in patients with CRS.


Subject(s)
CD40 Ligand , Eosinophilia , Humans , Eosinophils/metabolism , Interleukin-5 , Tumor Necrosis Factor-alpha , CD40 Antigens , Eosinophilia/metabolism , Interleukin-2 , Inducible T-Cell Co-Stimulator Protein
4.
Article in Chinese | MEDLINE | ID: mdl-36987961

ABSTRACT

Objective:To explore the clinical correlation between peripheral blood basophil levels and chronic sinusitis (CRS) subtypes. Methods:One hundred and twenty-six patients with CRS and 103 healthy cases from physical examination admitted to the First Affiliated Hospital of Soochow University from January 2021 to October 2022 were retrospectively analyzed. According to the histopathological classification, CRS patients were divided into eosinophilic chronic sinusitis (eCRS) group (47 cases) and non eosinophilic chronic sinusitis (non-eCRS) group (79 cases). The differences among the three groups in peripheral blood inflammation cell counts, eosinophils-to-basophils ratio(bEBR), basophils-to-neutrophils ratio(BNR), basophils-to-lymphocytes ratio(BLR), basophils-to-monocytes ratio(BMR) were compared, and study the correlation between each index and Lund-Mackay score, and the correlation between basophils in peripheral blood and other inflammatory cells. Results:The counts of basophils in the peripheral blood of the healthy control group, eCRS group and non-eCRS group were 0.03±0.01, 0.04±0.02, 0.03±0.02, respectively, the eosinophils-to-basophils ratio(bEBR) were 5.64±4.22, 8.38±5.95, 4.55±3.90, the basophils-to-neutrophils ratio(BNR) were 0.01±0, 0.01±0.01, 0.01±0.01, and the basophils-to-lymphocytes ratio(BLR) were 0.01±0.01, 0.02±0.01, and 0.02±0.01, respectively, the basophils-to-monocytes ratio(BMR) were 0.08±0.04, 0.11±0.06, and 0.08 ±0.04 respectively. There was a statistically significant difference between eCRS group and healthy control group, non-eCRS group(P<0.01), while there was no statistically significant difference between non-eCRS group and healthy control group(P>0.05). Basophil counts (r=0.185 5, P<0.05), BLR(r=0.226 9, P<0.05), BMR(r=0.228 1, P<0.01) in patients with CRS were positively correlated with Lund Makey score. In addition, basophils were also positively correlated with eosinophils(r=0.479 2, P<0.01), lymphocytes(r=0.259 4, P<0.01), and monocytes(r=0.256 4, P<0.01) in patients with CRS. Conclusion:The peripheral blood basophil count, BLR and BMR were significantly increased in eCRS, and were significantly positively correlated with Lund -Makey score. It has the potential to develop into disease biomarkers and new therapeutic targets of eCRS.


Subject(s)
Nasal Polyps , Rhinitis , Sinusitis , Humans , Basophils , Retrospective Studies , Rhinitis/surgery , Eosinophils , Sinusitis/surgery , Chronic Disease , Nasal Polyps/pathology
5.
Mol Carcinog ; 62(6): 771-785, 2023 06.
Article in English | MEDLINE | ID: mdl-36988339

ABSTRACT

Replication factor C 5 (RFC5) is involved in a variety of biological functions of cancer. However, the expression pattern of RFC5 and the underlying mechanisms in colorectal cancer (CRC) remain elusive. Here, we show that RFC5 is significantly upregulated in CRC tissues and cells. Patients with CRC and increased RFC5 levels have an unfavorable prognosis. RFC5 can promote the proliferation, migration, and invasion of CRC cells and inhibit the apoptosis of CRC cells. Additionally, upstream of RFC5, we constructed the competing endogenous RNA network and confirmed that RFC5 in this network was inhibited by miR-3614-5p by directly targeting its 3'-untranslated regions. We verified that circ_0038985, which is positively correlated with RFC5, directly targeted miR-3614-5p. Overexpression of circ_0038985 promoted CRC cell migration and invasion, and these effects were partially reversed by the reintroduction of miR-3614-5p. Moreover, we found that RFC5 may promote the vascular endothelial growth factor A (VEGFa)/vascular endothelial growth factor receptor 2 (VEGFR2)/extracellular signal-regulated protein kinase (ERK) pathway. The knockdown of RFC5 reduced CRC tumorigenesis in vivo. Collectively, these data demonstrate that the circ_0038985/miR-3614-5p/RFC5 axis plays a critical role in the progression of CRC, and RFC5 may promote CRC progression by affecting the VEGFa/VEGFR2/ERK pathway.


Subject(s)
Colorectal Neoplasms , MicroRNAs , Humans , MicroRNAs/genetics , MicroRNAs/metabolism , Vascular Endothelial Growth Factor A/metabolism , Replication Protein C/genetics , Replication Protein C/metabolism , Cell Line, Tumor , Cell Proliferation/genetics , Colorectal Neoplasms/genetics , Colorectal Neoplasms/metabolism , Oncogenes
6.
Environ Sci Pollut Res Int ; 27(34): 43299-43311, 2020 Dec.
Article in English | MEDLINE | ID: mdl-32737779

ABSTRACT

Previous papers that study the relationship between air pollution and happiness have not paid much attention to subjective air pollution. This paper attempts to explore the influence of subjective air pollution on happiness, the heterogeneity of the effects, and people's subjective willingness for improving air quality. We match the data of Chinese General Social Survey with local air quality and mainly based on the method of regression discontinuity. Our study shows that the public's subjective air pollution perception has significant negative effects on their happiness. The negative effects on happiness of unhealthy people and middle-aged/old people are greater than that of healthy people and young people. Moreover, residents who are relatively vulnerable to the harm of air pollution appear to be more willing to pay for the improvement of air quality. These results indicate that in order to improve air quality more rationally and effectively, not only should the government concentrate on the improvement of objective air quality but also pay attention to the public's subjective feelings, as well as taking the subjective needs of local residents into consideration in the process of air pollution control.


Subject(s)
Air Pollution , Happiness , Adolescent , Aged , China , Conservation of Natural Resources , Emotions , Humans , Middle Aged
7.
Neurosci Lett ; 515(2): 125-30, 2012 May 02.
Article in English | MEDLINE | ID: mdl-22450048

ABSTRACT

A prime culprit in the pathogenesis of Alzheimer's disease (AD) is overproduction/aggregation of ß-amyloid (Aß), which is derived from ß-Amyloid Precursor Protein through sequential cleavages by ß-site APP cleaving protein 1 (BACE1) and γ-secretase. The level/activity of BACE1 is elevated in sporadic AD and identification of proteins that affect BACE1 is important in AD research. Here we found that M1 Muscarinic acetylcholine receptor (M1 mAChR), an important G protein-coupled receptor involved in cholinergic neuronal activity, can interact with BACE1 and mediate its proteosomal degradation. Moreover, overexpression and downregulation of M1 mAChR can decrease and increase the levels of BACE1, as well as the generation of Aß, respectively. These findings point to a novel coupling of BACE1 and M1 mAChR in AD and possibly schizophrenia.


Subject(s)
Amyloid Precursor Protein Secretases/metabolism , Aspartic Acid Endopeptidases/metabolism , Proteasome Endopeptidase Complex/metabolism , Receptor, Muscarinic M1/metabolism , Alzheimer Disease/metabolism , Cells, Cultured , HEK293 Cells , Humans
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