期刊论文详细信息
Frontiers in Cellular and Infection Microbiology
Productive and Penicillin-Stressed Chlamydia pecorum Infection Induces Nuclear Factor Kappa B Activation and Interleukin-6 Secretion In Vitro
Schoborg, Robert V.1  Leonard, Cory A.2  Borel, Nicole2 
[1] Department of Biomedical Sciences, Center for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA;Department of Pathobiology, Institute of Veterinary Pathology, University of Zurich, Zurich, Switzerland
关键词: Chlamydia pecorum;    nuclear factor kappa B;    Interleukin-6;    chlamydial persistence;    HeLa Cells;   
DOI  :  10.3389/fcimb.2017.00180
学科分类:生物科学(综合)
来源: Frontiers
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【 摘 要 】

Nuclear factor kappa B (NFkB) is an inflammatory transcription factor that plays an important role in the host immune response to infection. The potential for chlamydiae to activate NFkB 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 nuclear factor kappa B (NFkB) activation in vitro. C. pecorum infection induced both NFkB nuclear translocation and activation at 2 hours post infection, an effect strongly enhanced by suppression of host de novo protein synthesis. C. suis and C. trachomatis showed less capacity for NFkB activation compared to C. pecorum, suggesting a species-specific variation in NFkB activation. At 24 hpi, C. pecorum induced significant NFkB activation, an effect not abolished by penicillin (beta lactam)-induced chlamydial stress. C. pecorum-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 NFkB participates in the early inflammatory response to C. pecorum and that stressed chlamydiae can promote inflammation.

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