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Publication : IL-17A Is an Important Effector of the Immune Response of the Mammary Gland to Escherichia coli Infection.

First Author  Porcherie A Year  2016
Journal  J Immunol Volume  196
Issue  2 Pages  803-12
PubMed ID  26685206 Mgi Jnum  J:251266
Mgi Id  MGI:6102334 Doi  10.4049/jimmunol.1500705
Citation  Porcherie A, et al. (2016) IL-17A Is an Important Effector of the Immune Response of the Mammary Gland to Escherichia coli Infection. J Immunol 196(2):803-12
abstractText  The cytokine IL-17A has been shown to play critical roles in host defense against bacterial and fungal infections at different epithelial sites, but its role in the defense of the mammary gland (MG) has seldom been investigated, although infections of the MG constitute the main pathology afflicting dairy cows. In this study, we showed that IL-17A contributes to the defense of the MG against Escherichia coli infection by using a mouse mastitis model. After inoculation of the MG with a mastitis-causing E. coli strain, the bacterial load increased rapidly, triggering an intense influx of leukocytes into mammary tissue and increased concentrations of IL-6, IL-22, TNF-alpha, and IL-10. Neutrophils were the first cells that migrated intensely to the mammary tissue, in line with an early production of CXCL2. Depletion of neutrophils induced an increased mammary bacterial load. There was a significant increase of IL-17-containing CD4(+) alphabeta T lymphocyte numbers in infected glands. Depletion of IL-17A correlated with an increased bacterial colonization and IL-10 production. Intramammary infusion of IL-17A at the onset of infection was associated with markedly decreased bacterial numbers, decreased IL-10 production, and increased neutrophil recruitment. Depletion of CD25(+) regulatory T cells correlated with a decreased production of IL-10 and a reduced bacterial load. These results indicate that IL-17A is an important effector of MG immunity to E. coli and suggest that an early increased local production of IL-17A would improve the outcome of infection. These findings point to a new lead to the development of vaccines against mastitis.
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