AUTHOR=Leonard Cory A. , Schoborg Robert V. , Borel Nicole 

TITLE=Productive and Penicillin-Stressed Chlamydia pecorum Infection Induces Nuclear Factor Kappa B Activation and Interleukin-6 Secretion In Vitro

JOURNAL=Frontiers in Cellular and Infection Microbiology

VOLUME=7

YEAR=2017

URL=https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2017.00180

DOI=10.3389/fcimb.2017.00180

ISSN=2235-2988

ABSTRACT=<p>Nuclear factor kappa B (NFκB) is an inflammatory transcription factor that plays an important role in the host immune response to infection. The potential for chlamydiae to activate NFκB has been an area of interest, however most work has focused on chlamydiae impacting human health. Given that inflammation characteristic of chlamydial infection may be associated with severe disease outcomes or contribute to poor overall fitness in farmed animals, we evaluated the ability of porcine chlamydiae to induce NFκB activation <italic>in vitro</italic>. <italic>C. pecorum</italic> infection induced both NFκB nuclear translocation and activation at 2 hours post infection (hpi), an effect strongly enhanced by suppression of host <italic>de novo</italic> protein synthesis. <italic>C. suis</italic> and <italic>C. trachomatis</italic> showed less capacity for NFκB activation compared to <italic>C. pecorum</italic>, suggesting a species-specific variation in NFκB activation. At 24 hpi, <italic>C. pecorum</italic> induced significant NFκB activation, an effect not abolished by penicillin (beta lactam)-induced chlamydial stress. <italic>C. pecorum</italic>-dependent secretion of interleukin 6 was also detected in the culture supernatant of infected cells at 24 hpi, and this effect, too, was unchanged by penicillin-induced chlamydial stress. Taken together, these results suggest that NFκB participates in the early inflammatory response to <italic>C. pecorum</italic> and that stressed chlamydiae can promote inflammation.</p>