Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 5 de 5
Filter
1.
Egypt J Immunol ; 29(4): 174-183, 2022 Oct.
Article in English | MEDLINE | ID: mdl-36208046

ABSTRACT

Schistosoma mansoni liver fibrosis is a complicated multicellular process involving numerous cytokines, chemokines, and growth factors. Transforming growth factor beta 1 (TGF-1) and interleukin (IL)-13 have been identified as critical pro-fibrotic mediators in many studies. IL-17A was linked to enhanced TGF- and IL-13-induced pathologies. This case-control study aimed to explore the effect of IL-17A on TGF- and IL-13-induced liver fibrosis during experimentally schistosomiasis mansoni infection. A total of 40 laboratory-bred female C57BL/6 mice were divided into four equal groups (G), G1 non-infected, G2 infected wild type (WT), G3 infected/anti-IL-17 monoclonal antibodies (mAb) and G4 treated mice. Mice were infected percutaneously with 40±5 cercariae per mouse. Neutralizing IL-17 mAb was administered to G3 intraperitoneally 3 weeks after infection and then every third day until 2 days before sacrification; mice of G4 were treated with a single dose of praziquantel. Serum levels of TGF-, IL-13, IL-17A, and proinflammatory cytokines were measured by ELISA. Liver granulomas were identified by hematoxylin-eosin stain and measured by an ocular micrometer. There was a significantly increased serum concentration of TGF-, IL-13, and IL-17A in infected WT mice (P<0.01), but praziquantel treatment reduced cytokine levels (P<0.03). Neutralization of IL-17A activity remarkably reduced serum concentrations of TGF- and IL-13 (P <0.03) resulting in improved liver functions and reduced granuloma size. Secretion of IL-IL-6 and TNF-were markedly enhanced by infection, however, mice that received anti-mouse IL-17 mAb displayed fewer inflammatory mediators (P<0.03). In conclusion, IL-17A might contribute to the progress of liver fibrosis by enhancing the profibrotic effect of TGF- and IL-13 in mice infected with S. mansoni.


Subject(s)
Interleukin-17/metabolism , Schistosoma mansoni , Schistosomiasis mansoni , Animals , Antibodies, Monoclonal/pharmacology , Antibodies, Monoclonal/therapeutic use , Case-Control Studies , Cytokines , Eosine Yellowish-(YS)/pharmacology , Eosine Yellowish-(YS)/therapeutic use , Female , Hematoxylin/pharmacology , Hematoxylin/therapeutic use , Humans , Inflammation Mediators/pharmacology , Inflammation Mediators/therapeutic use , Interleukin-13 , Liver , Liver Cirrhosis/complications , Mice , Mice, Inbred C57BL , Praziquantel/pharmacology , Praziquantel/therapeutic use , Transforming Growth Factor beta1
2.
Parasitol Res ; 121(1): 245-254, 2022 Jan.
Article in English | MEDLINE | ID: mdl-34757500

ABSTRACT

Parasitic infections of the gastrointestinal tract (GIT) may cause severe morbidity and even death in untreated patients. In certain cases, endoscopy may be the only possible option for diagnosis and management of GIT parasitic diseases. This study aimed to elucidate the role of endoscopy in the identification of GIT pathological changes during parasitic infections. Three hundred patients suffering from GIT manifestation were enrolled in this study. Stool samples were collected from all patients and examined for the presence of parasitic stages by direct and concentrated techniques. Parasite-infected patients were further examined by CBC and narrow-band endoscopic procedure. Stool examination has demonstrated parasitic stages in stool samples of 100 (33.3%) patients. Eighty-nine patients (89%) had a single parasitic infection while 11 patients (11%) had mixed infections. Complete blood examination of infected patients was within the normal ranges in almost all types of infections except for eosinophilia in some of them. Upper endoscopic examination revealed that parasitic infections led to various pathological changes in the esophagus (6%), stomach (42%), and duodenum (50%). Colonoscopy revealed abnormal findings at the rectum (25%) and the colon (32%). In conclusion, the endoscopic examination can be considered an important diagnostic option for the detection of pathological changes in GIT during chronic parasitic diseases and can be included in the differential diagnosis of other GIT pathological changes detected by endoscopy.


Subject(s)
Gastrointestinal Diseases , Parasites , Animals , Endoscopy, Gastrointestinal , Gastroscopy , Humans
3.
J Egypt Soc Parasitol ; 41(2): 485-96, 2011 Aug.
Article in English | MEDLINE | ID: mdl-21980785

ABSTRACT

Brucellosis is a worldwide zoonotic gram-negative bacterium of worldwide distribution. Its role in causing miscarriage in animals is well documented. Data on its role in human abortion are very few. This paper was carried out on selected women with abortion or history of abortion to clarify the role of brucellosis in human abortion. A total of 129 women were selected from Al-Zahraa University Hospital and other obstetric and gynecological hospitals in the vicinity of Greater Cairo. The patients were subjected to clinical, gynecological, and serodiagnosis (STAT and ELISA) of brucellosis. Also, routine urine (Nuclepore technique) and stool (Kato thick smear) was done as well as skin tests and ELISA for common hepatic parasites. The results showed that 59 had brucellosis, 27 had toxoplasmosis, 15 had fascioliasis and 29 had other cause(s) of abortion. Meanwhile, none had visceral leishmaniasis or schistosomiasis mansoni. the signs and symptoms of all patients were hepatosplenomegaly (31.1%), lower back abdominal pain (23.13%), lassitude, headache (each, 21.7%), lymphadenopathy (20.1%), vomiting (17.1%), loss of appetite, myalgia or diarrhea or constipation (each, 15.42 %), weight loss (14.6%), chest pain (13.9%), night sweating or dizziness (11.65%), fever or right sided abdominal pain (each, 10.7%), chills (7.71%), urticaria or monoarthralgia (each, 3.85%). These signs and symptoms were confusing for specific clinical picture of brucellosis. Brucellosis patients were successfully treated with a combination of Rifampicin 600 mg. once daily and Septrin 800 mg twice daily for 6 weeks. Cure was achieved clinically and serologically. Patients with toxoplasmosis or fascioliasis were also treated with Fasinex and Mirazid respectively. Other parasites were also treated.


Subject(s)
Brucellosis/drug therapy , Brucellosis/prevention & control , Infectious Disease Transmission, Vertical/prevention & control , Pregnancy Complications, Infectious/drug therapy , Abortion, Spontaneous/microbiology , Abortion, Spontaneous/prevention & control , Adolescent , Adult , Anti-Bacterial Agents/therapeutic use , Female , Humans , Middle Aged , Pregnancy , Rifampin/therapeutic use , Risk Factors , Trimethoprim, Sulfamethoxazole Drug Combination/therapeutic use , Young Adult
4.
J Egypt Soc Parasitol ; 38(2): 371-84, 2008 Aug.
Article in English | MEDLINE | ID: mdl-18853612

ABSTRACT

The present study evaluated the hypothesis that genetic diversity in SAG5 genes was generated by recombination events. Three lines of evidence suggested that recombination occurred in SAG5 genes in T. gondii. The permutation test revealed strong signature of intragenic recombination, pairwise comparisons of nucleotide sequences of SAG5 genes revealed that SAG5A alleles have chimerical structures composed of segments derived through recombination events between different alleles, and phylogenetic trees reconstructed based on SAG5 sequences using neighbor-joining and maximum parsimony methods, showed statistically well-supported consensus clusters of T. gondii strains specific to each SAG5 gene. Topological discrepancies between trees based on the N-terminal variable domain and C-terminal conserved domain sequences, were observed, suggesting intragenic recombinetion between SAG5A and SAG5B/C genes. The results showed that recombination within SAG5 in T. gondii was a major evolutionary mechanism generating both allelic variation at SAG5 locus and contributing to genotypic diversity and to emergence of new T. gondii variants, allowing them to evade the host immune defence mechanism.


Subject(s)
Genetic Variation , Protozoan Proteins/genetics , Toxoplasma/genetics , Alleles , Animals , Base Sequence , Chimera , Genes, Protozoan , Genotype , Molecular Sequence Data , Recombination, Genetic
5.
Infect Immun ; 72(5): 2772-9, 2004 May.
Article in English | MEDLINE | ID: mdl-15102787

ABSTRACT

Invasion of enterocytes by pathogenic microbes evokes both innate and adaptive immune responses, and microbial pathogens have developed strategies to overcome the initial host immune defense. beta-Defensins are potentially important endogenous antibiotic-like effectors of innate immunity expressed by intestinal epithelia. In this study, the interplay between the enteric protozoan parasite Cryptosporidium parvum and host epithelial beta-defensin expression was investigated. Using human and murine models of infection, we demonstrated that C. parvum infection differentially regulates beta-defensin gene expression. Downregulation of murine beta-defensin-1 mRNA and protein was observed in both in vitro and in vivo models of infection. Infection of the human colonic HT29 cell line with the parasite resulted in differential effects on various members of the defensin gene family. Partial reduction in human beta-defensin-1 (hBD-1), induction of hBD-2, and no effect on hBD-3 gene expression was observed. Recombinant hBD-1 and hBD-2 peptides exhibited significant antimicrobial activity against C. parvum sporozoites in vitro. These findings demonstrate that C. parvum infection of enterocytes may affect the expression of various defensins in different ways and suggest that the overall outcome of the effect of antimicrobial peptides on early survival of the parasite may be complex.


Subject(s)
Cryptosporidiosis/genetics , Cryptosporidiosis/immunology , Cryptosporidium parvum , beta-Defensins/genetics , Animals , Cell Line , Cytokines/metabolism , Down-Regulation , Gene Expression Regulation , Humans , Inflammation Mediators/metabolism , Interferon-gamma/deficiency , Interferon-gamma/genetics , Mice , Mice, Inbred BALB C , Mice, Inbred C57BL , Mice, Knockout , RNA, Messenger/genetics , RNA, Messenger/metabolism , beta-Defensins/metabolism
SELECTION OF CITATIONS
SEARCH DETAIL
...