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Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
immunology and microbiology
Interleukin-4 (IL-4) and IL-13 suppress excessive neutrophil infiltration and hepatocyte damage during acute murine schistosomiasis japonica
Infection and Immunity, Volume 80, No. 1, Year 2012
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Description
Due to the importance of neutrophils and proinflammatory cytokines in schistosomal liver damage, we analyzed the mechanisms underlying neutrophil and proinflammatory responses in murine schistosomiasis japonica. We found that granulomatous inflammation around parasite eggs in the liver was greater in Schistosoma japonicum-infected IL-4 -/- IL-13 -/- (doubleknockout [DKO]) mice than in infected wild-type (WT) mice at 6 weeks, but not at 8 weeks, postinfection, suggesting the importance of Th2 responses in these typical hepatic lesions. Infected DKO mice also showed increased neutrophil infiltration accompanying more severe pathology, as shown by the enhanced necrosis of hepatocytes. This was not likely due to a Th1/Th2 imbalance, because there was no detectable increase in gamma interferon (IFN-γ) production in these DKO mice. mRNA expression of interleukin-17A (IL-17A), proinflammatory cytokines, and the neutrophil chemoattractant CXCL2 in liver was higher in infected DKO mice than in WT mice. However, in IL-4 -/- IL-13 -/- IL-17A -/- (triple-knockout [TKO]) mice, the absence of IL-17A was associated with only marginal differences in schistosomal liver damage, suggesting that IL-17A is only partially responsible for neutrophil-driven hepatic damage. Furthermore, the expression of mRNAs encoding proinflammatory cytokines was not under the control of IL-17A in TKO mice. These findings indicate that IL-4 and IL-13 suppress excessive neutrophil recruitment, proinflammatory cytokine production, and hepatic damage during the acute stage of S. japonicum infection, suggesting that neutrophils and proinflammatory cytokines are mainly responsible for hepatocyte damage during acute murine schistosomiasis japonica. However, neutrophil induction and the production of proinflammatory cytokines were not due solely to IL-17A. © 2012, American Society for Microbiology.
Authors & Co-Authors
Seki, Takenori
Japan, Tokyo
Graduate School of Medical and Dental Sciences
Kumagai, Takashi
Japan, Tokyo
Graduate School of Medical and Dental Sciences
Kwansa-Bentum, Bethel
Japan, Tokyo
Graduate School of Medical and Dental Sciences
Ghana, Accra
Noguchi Memorial Institute for Medical Research
Furushima-Shimogawara, Rieko
Japan, Tokyo
Graduate School of Medical and Dental Sciences
Anyan, William Kofi
Ghana, Accra
Noguchi Memorial Institute for Medical Research
Miyazawa, Yuuki
Japan, Tokyo
Graduate School of Medical and Dental Sciences
Iwakura, Yoichiro
Japan, Tokyo
The University of Tokyo
Japan, Kawaguchi
Japan Science and Technology Agency
Ohta, Nobuo
Japan, Tokyo
Graduate School of Medical and Dental Sciences
Statistics
Citations: 42
Authors: 8
Affiliations: 4
Identifiers
Doi:
10.1128/IAI.05581-11
ISSN:
00199567
e-ISSN:
10985522
Research Areas
Infectious Diseases