Persistently Elevated Level of IL-8 inChlamydia trachomatisInfected HeLa 229 Cells is Dependent on Intracellular Available Iron
Author(s) -
Harsh Vardhan,
Raini Dutta,
Vikas Vats,
Rishein Gupta,
Rajneesh Jha,
Hem Chandra Jha,
Pragya Srivastava,
Apurb Rashmi Bhengraj,
Aruna Mittal
Publication year - 2009
Publication title -
mediators of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.37
H-Index - 97
eISSN - 1466-1861
pISSN - 0962-9351
DOI - 10.1155/2009/417658
Subject(s) - chlamydia trachomatis , proinflammatory cytokine , chlamydia , secretion , hela , biology , chemokine , immunology , tumor necrosis factor alpha , intracellular , interleukin 6 , microbiology and biotechnology , virology , inflammation , cell , endocrinology , genetics
Chlamydia trachomatis is a leading cause of sexually transmitted infection worldwide and responsible for myriad of immunopathological changes associated with reproductive health. Delayed secretion of proinflammatory chemokine interleukin (IL)-8 is a hallmark of chlamydial infection and is dependent on chlamydial growth. We examined the effect of iron chelators on IL-8 production in HeLa 229 (cervix epitheloid cell, CCL2) cells infected with C. trachomatis . IL-8 production was induced by Iron chelator DFO and Mimosine, however, synergy with chlamydial infection was obtained with DFO only. Temporal expression of proinflammatory secreted cytokines IL-1beta, TNF-alpha, and IL-8 did not show synchrony in Chlamydia trachomatis infected cells. Secretion of IL-8 from Hela cells infected with C. trachomatis was not dependent on IL-1 beta and TNF- alpha induction. These results indicate towards involvement of iron in chlamydia induced IL-8 production.
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