Role of IL-17A in enhancing liver fibrosis induced by TGF-ß1 and IL-13 in Schistosoma mansoni infected mice.

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.

Endoscopic procedure as a diagnostic tool for intestinal parasitic pathological changes.

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.