Interlukin -17 Promotes Granuloma Formation and Epithelial- Mesenchymal Transition (EMT) of Hepatic Cells in Experimental Schistosomiasis mansoni
El-Melegy, M., Badawy, N., Serag El-ddin, M. (2019). Interlukin -17 Promotes Granuloma Formation and Epithelial- Mesenchymal Transition (EMT) of Hepatic Cells in Experimental Schistosomiasis mansoni. EKB Journal Management System, 28(3), 111-118. doi: 10.21608/ejmm.2019.283063
Manal A. El-Melegy; Nadia S. Badawy; Marwa M. Serag El-ddin. "Interlukin -17 Promotes Granuloma Formation and Epithelial- Mesenchymal Transition (EMT) of Hepatic Cells in Experimental Schistosomiasis mansoni". EKB Journal Management System, 28, 3, 2019, 111-118. doi: 10.21608/ejmm.2019.283063
El-Melegy, M., Badawy, N., Serag El-ddin, M. (2019). 'Interlukin -17 Promotes Granuloma Formation and Epithelial- Mesenchymal Transition (EMT) of Hepatic Cells in Experimental Schistosomiasis mansoni', EKB Journal Management System, 28(3), pp. 111-118. doi: 10.21608/ejmm.2019.283063
El-Melegy, M., Badawy, N., Serag El-ddin, M. Interlukin -17 Promotes Granuloma Formation and Epithelial- Mesenchymal Transition (EMT) of Hepatic Cells in Experimental Schistosomiasis mansoni. EKB Journal Management System, 2019; 28(3): 111-118. doi: 10.21608/ejmm.2019.283063

Interlukin -17 Promotes Granuloma Formation and Epithelial- Mesenchymal Transition (EMT) of Hepatic Cells in Experimental Schistosomiasis mansoni

Egyptian Journal of Medical Microbiology
Volume 28, Issue 3, July 2019, Page 111-118  XML PDF (1.09 MB)
Document Type: New and original researches in the field of Microbiology.
DOI: 10.21608/ejmm.2019.283063
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Authors
Manal A. El-Melegy email 1; Nadia S. Badawy2; Marwa M. Serag El-ddin3
1Departments of Parasitologyو Faculty of Medicine, Menoufia University, Egypt
2Department of Histology and Cell Biology,Faculty of Medicine, Menoufia University, Egypt
3Deparetment of Histopathology, Faculty of Medicine, Menoufia University, Egypt
Abstract
Background: Schistosomiasis mansoni is a severe tropical disease. The most serious pathological effect is liver fibrosis. Interlukin 17 (IL-17) affects liver fibrosis. Objectives: This work was done to estimate the correlation between Schistosoma mansoni granuloma size and IL-17 level in the serum of the schistosomiasis infected mice , and to find its role in liver fibrosis. Methodology: The experiment lasted ten weeks. Sixty Swiss albino mice were used. Mice were divided into equally six groups. Control negative group G0 and infected five groups (G2,G4,G6,G8,G10) with Schistosoma mansoni cercarie. One group was sacrificed every two weeks .Two control mice were sacrificed with each group. Sera were collected for IL-17 assessment by ELISA, liver tissues were examined histopathologically by H&E stain and granulomas size were measured in the different experimental groups. Alpha smooth muscle actin (α SMA),Desmin and Glial Fibrillary Acidic Protein (GFAP) were used to assess the role of IL- 17 in liver fibrosis. Results: There was a highly significant increase (p<0.001) in IL-17 level in G6 (6 weeks post infection (wpi). A highly significant (p<0.001) positive correlation between the level of IL-17 in sera of the infected groups and granuloma size . Immune stains revealed that hepatocytes expressed stellate cell markers (αSMA ,desmin and GFAP). Moreover, the immunopathology was markedly correlated to IL-17 level. Where, there were a highly significant (p ˂ 0.001) increase of serum IL-17 and strong positive expression of α SMA, desmin and GFAP in mice of G6. Conclusion: These results proved that IL-17 promotes granuloma formation through epithelial mesenchymal transition (EMT) of hepatocytes which play a role in liver fibrosis. Our findings suggested that EMT is a talented therapeutic goal to decrease liver fibrosis for further study.
Keywords
Schistosoma mansoni; granuloma; IL-17; α SMA; EMT; fibrosis
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