Chlamydophila pneumoniae re-infection triggers the production of IL-17A and IL-17E, important regulators of airway inflammation
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Investigation of the effects of interleukin (IL)-17 cytokines in Chlamydophila pneumoniae-infected mice.
Mice were infected with C. pneumoniae once or three times and the expression of IL-17 cytokines was followed by RT qPCR from day 1 to day 28 after infection and re-infection. After the treatment of mice with anti-IL-17A, ELISA was used to detect the differences in cytokine and chemokine production. The number and phenotype of the IL-17A-producing cells were determined by ELISPOT.
Chlamydophila pneumoniae induced IL-17A and IL-17F from day 2 after infection, and their levels remained elevated on day 28. The expression of IL-17C, IL-17D and IL-17E mRNA did not change significantly in response to a single infection. The in vivo neutralization of IL-17A resulted in a higher C. pneumoniae burden in the mouse lungs, a decreased cell influx, and diminished chemokine levels. The phenotype of IL-17A-producing cells was CD4+. The re-infection of mice led to an increased expression of IL-17E mRNA.
These results facilitate an understanding of the early inflammatory response after C. pneumoniae infection and suggest that C. pneumoniae re-infection induces the production of a high amount of IL-17E, which has an important role in the pathogenesis of allergic pulmonary diseases.
KeywordsAnimal models Chlamydophila pneumoniae IL-17
We thank Zsótér Gizella and Lévai Istvánné for excellent technical support. This work was supported by OTKA National Research Fund Grant PD 100442, and Grants TÁMOP-4.2.1./B-09/1/KONV-2010-0005, and TÁMOP-4.2.2./B-2013 from the New Széchenyi Plan.
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