The IL-6 response to Chlamydia from primary reproductive epithelial cells is highly variable and may be involved in differential susceptibility to the immunopathological consequences of chlamydial infection

BMC Immunology

Wilhelmina M Huston¹  John A Allan¹  Vivian Kienzle²  Shruti Menon²  Pooja Patel²  Scott H Stansfield²  Kelly Cunningham² 

[1] The Wesley Research Institute, The Wesley Hospital, 40 Chasely Street, Auchenflower, QLD 4066, Australia;Institute of Health and Biomedical Innovation, Queensland University of Technology, Q Block, 60 Musk Ave, Kelvin Grove, QLD 4059, Australia

关键词: Immunopathology;    IL-6;    Infertility;    Chlamydia;   

Others  :  1077743
DOI  :  10.1186/1471-2172-14-50

 received in 2013-08-12, accepted in 2013-11-14,  发布年份 2013

【 摘 要 】

Background

Chlamydia trachomatis infection results in reproductive damage in some women. The process and factors involved in this immunopathology are not well understood. This study aimed to investigate the role of primary human cellular responses to chlamydial stress response proteases and chlamydial infection to further identify the immune processes involved in serious disease sequelae.

Results

Laboratory cell cultures and primary human reproductive epithelial cultures produced IL-6 in response to chlamydial stress response proteases (CtHtrA and CtTsp), UV inactivated Chlamydia, and live Chlamydia. The magnitude of the IL-6 response varied considerably (up to 1000 pg ml^-1) across different primary human reproductive cultures. Thus different levels of IL-6 production by reproductive epithelia may be a determinant in disease outcome. Interestingly, co-culture models with either THP-1 cells or autologous primary human PBMC generally resulted in increased levels of IL-6, except in the case of live Chlamydia where the level of IL-6 was decreased compared to the epithelial cell culture only, suggesting this pathway may be able to be modulated by live Chlamydia. PBMC responses to the stress response proteases (CtTsp and CtHtrA) did not significantly vary for the different participant cohorts. Therefore, these proteases may possess conserved innate PAMPs. MAP kinases appeared to be involved in this IL-6 induction from human cells. Finally, we also demonstrated that IL-6 was induced by these proteins and Chlamydia from mouse primary reproductive cell cultures (BALB/C mice) and mouse laboratory cell models.

Conclusions

We have demonstrated that IL-6 may be a key factor for the chlamydial disease outcome in humans, given that primary human reproductive epithelial cell culture showed considerable variation in IL-6 response to Chlamydia or chlamydial proteins, and that the presence of live Chlamydia (but not UV killed) during co-culture resulted in a reduced IL-6 response suggesting this response may be moderated by the presence of the organism.

【 授权许可】

   
2013 Cunningham et al.; licensee BioMed Central Ltd.

【 图 表 】

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