In vivo (Athens, Greece) · 2013
IL-17E production is elevated in the lungs of Balb/c mice in the later stages of Chlamydia muridarum infection and re-infection.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Mosolygó Tímea, Spengler Gabriella, Endrész Valéria, Laczi Krisztián, Perei Katalin, Burián Katalin
Аннотация
BACKGROUND: Pathogens can influence allergic respiratory diseases. We previously found that multiple infections with Chlamydophila pneumoniae induce the production of interleukin-17A (IL-17A) and IL-17E, which have roles in the pathogenesis of asthma. The present work was designed to investigate our hypothesis that infections with another pathogen can induce the production of IL-17A and IL-17E.
MATERIALS AND METHODS: At an internal of 28 days, mice were infected twice with Chlamydia muridarum; the kinetics of IL-17A and IL-17E expression was subsequently determined at the mRNA and protein levels. The amounts of IL-17 cytokines produced by the stimulated spleen cells were determined by enzyme-linked immunosorbent assay (ELISA). The presence of IL-17E in the lungs was revealed by an indirect immunofluorescence test.
RESULTS: The infection with C. muridarum induced the production of IL-17A at the early stages of infection. The quantity of IL-17E was highest on days 28 and 56 after the first infection (28 days after the second infection). In the later stages of infection, IL-17E was produced by epithelial cells. The re-stimulated peripheral spleen cells produced IL-17A.
CONCLUSION: Multiple infection with C. muridarum induces the production of a high amount of IL-17E, which plays an important part in the pathogenesis of allergic pulmonary diseases.
MATERIALS AND METHODS: At an internal of 28 days, mice were infected twice with Chlamydia muridarum; the kinetics of IL-17A and IL-17E expression was subsequently determined at the mRNA and protein levels. The amounts of IL-17 cytokines produced by the stimulated spleen cells were determined by enzyme-linked immunosorbent assay (ELISA). The presence of IL-17E in the lungs was revealed by an indirect immunofluorescence test.
RESULTS: The infection with C. muridarum induced the production of IL-17A at the early stages of infection. The quantity of IL-17E was highest on days 28 and 56 after the first infection (28 days after the second infection). In the later stages of infection, IL-17E was produced by epithelial cells. The re-stimulated peripheral spleen cells produced IL-17A.
CONCLUSION: Multiple infection with C. muridarum induces the production of a high amount of IL-17E, which plays an important part in the pathogenesis of allergic pulmonary diseases.