Email this article INFLUENCE OF CHLAMYDIA TRACHOMATIS TYPE III SECRETION SYSTEM ON REGULATION OF CYTOKINE RESPONSE
- Authors: Fedina ED1, Kolkova NI1, Koroleva EA1, Shabalina LA1, Grabko VI1, Zigangirova NA1
-
Affiliations:
- Issue: Vol 89, No 4 (2012)
- Pages: 26-32
- Section: Articles
- Submitted: 09.06.2023
- Published: 15.12.2012
- URL: https://microbiol.crie.ru/jour/article/view/13683
- ID: 13683
Cite item
Full Text
Abstract
Aim. Develop in vitro model for studying production of cytokines by monocyte cells infected
with Chlamydia trachomatis mediated by type III secretion system (TTSS). Materials and methods.
Strain C. trachomatis L2/434/Bu was used in the experiments, culture of human monocytes U-937
was infected by this strain. Level of inflammatory cytokines was measured on flow analyzer Bio-
Plex 200 (Bio-Rad Laboratories). Low molecular compound LHC-342 which belongs to the class
of heterocyclic compounds was used as TTSS inhibitor. Results. 24 hours after the infection with
C. trachomatis culture 8 analyzed cytokines are induced in U-937 cells (IL-1, IL-4, IL-6, IL-8,
IL-10, GM-CSF, IFN-, TNF). The most pronounced increase was observed for IL-8, GM-CSF
and IFN-. Introduction of TTSS inhibitor into the culture of infected cells suppressed chlamydia
growth, but addition of FeSO4 restored the growth of chlamydiae. And activity associated
with translocation of effector TTSS protein IncA to inclusion membrane was suppressed. Under
the conditions of the obtained model of TTSS inhibition during intracellular development of C.
trachomatis a significant decrease of 2 pro-inflammatory cytokines - IL-6 and IL-1 - was observed.
Conclusion. Cytokine response plays a key role in the protective immune response in
chlamydia infection but at the same time induces immunopathologic conditions. The data obtained
give reasons to assume role of C. trachomatis TTSS in the induction of this component of immune
response that requires further detailed studies.
with Chlamydia trachomatis mediated by type III secretion system (TTSS). Materials and methods.
Strain C. trachomatis L2/434/Bu was used in the experiments, culture of human monocytes U-937
was infected by this strain. Level of inflammatory cytokines was measured on flow analyzer Bio-
Plex 200 (Bio-Rad Laboratories). Low molecular compound LHC-342 which belongs to the class
of heterocyclic compounds was used as TTSS inhibitor. Results. 24 hours after the infection with
C. trachomatis culture 8 analyzed cytokines are induced in U-937 cells (IL-1, IL-4, IL-6, IL-8,
IL-10, GM-CSF, IFN-, TNF). The most pronounced increase was observed for IL-8, GM-CSF
and IFN-. Introduction of TTSS inhibitor into the culture of infected cells suppressed chlamydia
growth, but addition of FeSO4 restored the growth of chlamydiae. And activity associated
with translocation of effector TTSS protein IncA to inclusion membrane was suppressed. Under
the conditions of the obtained model of TTSS inhibition during intracellular development of C.
trachomatis a significant decrease of 2 pro-inflammatory cytokines - IL-6 and IL-1 - was observed.
Conclusion. Cytokine response plays a key role in the protective immune response in
chlamydia infection but at the same time induces immunopathologic conditions. The data obtained
give reasons to assume role of C. trachomatis TTSS in the induction of this component of immune
response that requires further detailed studies.
References
- Buchholz K.R., Stephens R.S. Activation of the host cell proinflammatory interleukin-8 response by Chlamydia trachomatis. Cell. Microbiol. 2006, 11: 1768-1779.
- Dessus-Babus S., Knight S. T., Wyrick P. B. Chlamydial infection of polarized HeLa cells induces PMN chemotaxis but the cytokine profile varies between disseminating and nondisseminating strains. Cell. Microbiol. 2000, 4: 317-327.
- Franchi L., Stoolman J., Kanneganti T. D. et al. Critical role for Ipaf in Pseudomonas aeruginosa-induced caspase-1 activation. Eur. J. Immunol. 2007, 37: 3030-3039.
- Hudson D. L., Layton A. N., Field T. R. et al. Inhibition of type III secretion in Salmonella enterica serovar Typhimurium by smallmolecule inhibitors. Antimicrob. Agents Chemother. 2007, 51: 2631-2635.
- Mardh P. A. Tubal factor infertility, with special regard to chlamydial salpingitis. Curr. Opin. Infect. Dis. 2004, 2: 49-52.
- Miao E. A., Alpuche-Aranda C. M., Dors M. et al. Cytoplasmic flagellin activates caspase-1 and secretion of interleukin 1 via Ipaf. Nat. Immunol. 2006, 7: 569-575.
- Morrison R. P., Manning D. S., Caldwell H. D. Immunology of Chlamydia trachomatis infections. Immunoprotective and immunopathogenetic responses. In: T. S. Quinn (ed.). Sexually transmitted diseases. N.Y., Raven Press Ltd., 1992, p. 57-84.
- Prantner D., Nagarajan U.M. Role for the Chlamydial type III secretion apparatus in host cytokine expression. Infect. Immun. 2009, 1: 76-84.
- Rasmussen S. J., L. Eckmann A. J. Quayle et al. Secretion of proinflammatory cytokines by epithelial cells in response to Chlamydia infection suggests a central role for epithelial cells in chlamydial pathogenesis. J. Clin. Investig. 1997, 99: 77-87.
- Shin H., Cornelis G. R. Type III secretion translocation pores of Yersinia enterocolitica trigger maturation and release of proinflammatory IL-1. Cell. Microbiol. 2007, 9: 2893-2902.
- Steensberg A. The role of IL-6 in exerciseinduced immune changes and metabolism. Exerc. Immunol. Rev. 2003, 9: 40-47.
- Stephens R. S. The cellular paradigm of chlamydial pathogenesis. Trends in Microbiology. 2003, 1: 44-51.
- Sun G. W., Lu J., Pervaiz S. et al. Caspase-1-dependent macrophage death induced by Burkholderia pseudomallei. Cell. Microbiol. 2005, 7: 1447-1458.
- Sutterwala F. S., Mijares L. A., Li L. et al. Immune recognition of Pseudomonas aeruginosa mediated by the IPAF/NLRC4 inflammasome. J. Exp. Med. 2007, 204: 3235-3245.
Supplementary files
