Document Detail


Chlamydia trachomatis evokes a relative anti-inflammatory response in a free Ca2+ dependent manner in human macrophages.
MedLine Citation:
PMID:  19782401     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
Chlamydia trachomatis infections manifest as unique, chronic inflammatory diseases, indicating a relative compromise in the capacity of early immune responders such as macrophages to resolve the infection. We decided to investigate whether or not the chronic inflammatory manifestations are influenced by a disturbance in the pattern of inflammatory:anti-inflammatory cytokine elaboration early in the infection cycle in macrophages and assess the possible modulatory role of Ca(2+) signals in the process. Although the basal and functional levels of IL-12 and IL-10 are not identical in concentration, chlamydia initiated a significant decline in IL-12. This led to a difference in the ratio of time-course decline in IL-12 compared with IL-10 in a Ca(2+)-poor medium, while there was significant increase in IL-10 in a Ca(2+)-rich medium. Also, when macrophages were infected after treatment with drugs that either facilitated Ca(2+) influx into cells or inhibited efflux from intracellular stores into cytosol, there was a significant enhancement of the elaboration of IL-10 compared with IL-12. The immobilization of cytosolic Ca(2+) by BAPTA-AM resulted in the decline of macrophage IL-12 and IL-10 in both infected and uninfected cases. There was evidence that infectivity and status of chlamydial elementary bodies harvested from macrophages during these experiments were consistent with chronic forms as assessed by HSP-60:MOMP ratio. The implication of these findings is that chlamydia infection of macrophages, together with its capacity to moderate macrophage intracellular Ca(2+) levels, may evoke a net anti-inflammatory response that presumably favors chronic chlamydia infections.
Authors:
Anthony A Azenabor; Jenniffer York
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-09-25
Journal Detail:
Title:  Comparative immunology, microbiology and infectious diseases     Volume:  33     ISSN:  1878-1667     ISO Abbreviation:  Comp. Immunol. Microbiol. Infect. Dis.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-24     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7808924     Medline TA:  Comp Immunol Microbiol Infect Dis     Country:  England    
Other Details:
Languages:  eng     Pagination:  513-28     Citation Subset:  IM    
Copyright Information:
Copyright © 2009 Elsevier Ltd. All rights reserved.
Affiliation:
Department of Health Sciences, University of Wisconsin, Milwaukee, WI 53211, USA. aazenabo@uwm.edu
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