IL-17 and IFNγ decrease in the gut of rats with experimental fibrosis. “Possible association with bacterial translocation”
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1
Universidad de Guadalajara, Centro Universitario de Ciencias de la Salud, Biología Molecular, Instituto de Enfermedades Crónico Degenerativas, Mexico
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2
Universidad de Guadalajara, Centro Universitario de Ciencias de la Salud, Fisiología, Laboratorio de Inmunología, Mexico
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3
Universidad de Guadalajara, Centro Universitario de Ciencias de la Salud, Fisiología, Unidad de Investigación Cardiovascular, Mexico
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4
Fisiología, Centro de Investigación en Inmunología y Dermatología, Mexico
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5
Universidad de Guadalajara, Centro Universitario de Ciencias de la Salud,, Fisiología, Grupo de Inmunogenética Funcional, Mexico
Background. Bacterial translocation (BT) in cirrhotic patients, is a trigger of peritonitis and septicemia, with a mortality rate of 30-50%. Alterations in the “intestine” immune response is a new field of study. BT has been reported in experimental models of liver fibrosis CCl4 and Thioacetamide (TAA). However, Th1 cytokines (IFN γ) and Th17 (IL-17) have been little explored in the gut of rats with experimental liver fibrosis. Aim. To analyze the expression of IL-17 and IFNγ in the gut of rats with fibrosis by TAA. Methods. Liver fibrosis was induced by thioacetamide administration (200 mg/kgi.p.). Fibrotic animals were euthanized after 3.5 and 8 weeks. Small and large gut tissue homogenates were used to detect IL-17 and IFNγ by Western-blotting. Gut sections were stained with hematoxylin/eosin to evaluate histological alterations. Results. Intestine IL-17 showed two molecular forms in the blots; 25KDa (glycosylated form) and 18KDa (non-glycosylated form). Both forms decreased 50% and 80% respectively compared with control group. These changes were evident in both early fibrosis and established cirrhosis. IFNγ decreased 65% compared to control group in the cirrhotic stage. Histological analyses showed hyperplasia of Peyer’s patches, epithelial inflammatory infiltrate and mucus hypersecretion. Conclusion. Gut bacterial overgrowth is associated with bacterial translocation process, which is closely linked to the dramatic decrease of IL-17 and IFNγ in the gut of rats with experimental fibrosis. These cytokines orchestrates antiparasitic important events at intestinal mucosal level and also activation of macrophages and neutrophil recruitment.
References
Wiest, R. and Garcia-Tsao, G; Bacterial translocation (BT) in cirrhosis. Hepatology(2005), 41: 422–433. doi: 10.1002/hep.20632
Ramón Bataller, David A. Brenner; Liver Fibrosis; J Clin Invest. 2005; 115(2):209–218 doi:10.1172/JCI24282
Keywords:
IL-17,
IFN- γ,
Liver Cirrhosis,
Bacterial Translocation,
rat model
Conference:
15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013.
Presentation Type:
Abstract
Topic:
Immune-mediated disease pathogenesis
Citation:
Bueno Topete
MR,
Sanchez Ravelero
E,
ZEPEDA Morales
AM,
Rodríguez
EE,
Del Toro Arreola
S,
García Benavides
L,
Fafutis Morris
M,
Domínguez Rosales
JA and
Muñoz Valle
JF
(2013). IL-17 and IFNγ decrease in the gut of rats with experimental fibrosis. “Possible association with bacterial translocation”.
Front. Immunol.
Conference Abstract:
15th International Congress of Immunology (ICI).
doi: 10.3389/conf.fimmu.2013.02.00205
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Received:
14 Mar 2013;
Published Online:
22 Aug 2013.
*
Correspondence:
Dr. Miriam R Bueno Topete, Universidad de Guadalajara, Centro Universitario de Ciencias de la Salud, Biología Molecular, Instituto de Enfermedades Crónico Degenerativas, Guadalajara, Jalisco, 44340, Mexico, ruthmyriamtop@hotmail.com