CCL5 regulation of mucosal chlamydial immunity and infection
<p>Abstract</p> <p>Background</p> <p>Following genital chlamydial infection, an early T helper type 1 (Th1)-associated immune response precedes the activation and recruitment of specific Th1 cells bearing distinct chemokine receptors, subsequently leading to the clearan...
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BMC
2008-08-01
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Series: | BMC Microbiology |
Online Access: | http://www.biomedcentral.com/1471-2180/8/136 |
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author | Igietseme Joseph U Taub Dennis D Singh Shailesh Singh Udai P Sakthivel Senthilkumar K Lillard James W |
author_facet | Igietseme Joseph U Taub Dennis D Singh Shailesh Singh Udai P Sakthivel Senthilkumar K Lillard James W |
author_sort | Igietseme Joseph U |
collection | DOAJ |
description | <p>Abstract</p> <p>Background</p> <p>Following genital chlamydial infection, an early T helper type 1 (Th1)-associated immune response precedes the activation and recruitment of specific Th1 cells bearing distinct chemokine receptors, subsequently leading to the clearance of <it>Chlamydia</it>. We have shown that CCR5, a receptor for CCL5, is crucial for protective chlamydial immunity. Our laboratory and others have also demonstrated that CCL5 deficiencies found in man and animals can increase the susceptibility and progression of infectious diseases by modulating mucosal immunity. These findings suggest the CCR5-CCL5 axis is necessary for optimal chlamydial immunity. We hypothesized CCL5 is required for protective humoral and cellular immunity against <it>Chlamydia</it>.</p> <p>Results</p> <p>The present study revealed that CCR5 and CCL5 mRNAs are elevated in the spleen, iliac lymph nodes (ILNs), and genital mucosa following <it>Chlamydia muriduram </it>challenge. Antibody (Ab)-mediated inhibition of CCL5 during genital chlamydial infection suppressed humoral and Th1 > Th2 cellular responses by splenic-, ILN-, and genital mucosa-derived lymphocytes. Antigen (Ag)-specific proliferative responses of CD4<sup>+ </sup>T cells from spleen, ILNs, and genital organs also declined after CCL5 inhibition.</p> <p>Conclusion</p> <p>The suppression of these responses correlated with delayed clearance of <it>C. muriduram</it>, which indicate chlamydial immunity is mediated by Th1 immune responses driven in part by CCL5. Taken together with other studies, the data show that CCL5 mediates the temporal recruitment and activation of leukocytes to mitigate chlamydial infection through enhancing adaptive mucosal humoral and cellular immunity.</p> |
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institution | Directory Open Access Journal |
issn | 1471-2180 |
language | English |
last_indexed | 2024-12-14T04:42:18Z |
publishDate | 2008-08-01 |
publisher | BMC |
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series | BMC Microbiology |
spelling | doaj.art-cb0bc72762804da38338c5c3266cc14f2022-12-21T23:16:47ZengBMCBMC Microbiology1471-21802008-08-018113610.1186/1471-2180-8-136CCL5 regulation of mucosal chlamydial immunity and infectionIgietseme Joseph UTaub Dennis DSingh ShaileshSingh Udai PSakthivel Senthilkumar KLillard James W<p>Abstract</p> <p>Background</p> <p>Following genital chlamydial infection, an early T helper type 1 (Th1)-associated immune response precedes the activation and recruitment of specific Th1 cells bearing distinct chemokine receptors, subsequently leading to the clearance of <it>Chlamydia</it>. We have shown that CCR5, a receptor for CCL5, is crucial for protective chlamydial immunity. Our laboratory and others have also demonstrated that CCL5 deficiencies found in man and animals can increase the susceptibility and progression of infectious diseases by modulating mucosal immunity. These findings suggest the CCR5-CCL5 axis is necessary for optimal chlamydial immunity. We hypothesized CCL5 is required for protective humoral and cellular immunity against <it>Chlamydia</it>.</p> <p>Results</p> <p>The present study revealed that CCR5 and CCL5 mRNAs are elevated in the spleen, iliac lymph nodes (ILNs), and genital mucosa following <it>Chlamydia muriduram </it>challenge. Antibody (Ab)-mediated inhibition of CCL5 during genital chlamydial infection suppressed humoral and Th1 > Th2 cellular responses by splenic-, ILN-, and genital mucosa-derived lymphocytes. Antigen (Ag)-specific proliferative responses of CD4<sup>+ </sup>T cells from spleen, ILNs, and genital organs also declined after CCL5 inhibition.</p> <p>Conclusion</p> <p>The suppression of these responses correlated with delayed clearance of <it>C. muriduram</it>, which indicate chlamydial immunity is mediated by Th1 immune responses driven in part by CCL5. Taken together with other studies, the data show that CCL5 mediates the temporal recruitment and activation of leukocytes to mitigate chlamydial infection through enhancing adaptive mucosal humoral and cellular immunity.</p>http://www.biomedcentral.com/1471-2180/8/136 |
spellingShingle | Igietseme Joseph U Taub Dennis D Singh Shailesh Singh Udai P Sakthivel Senthilkumar K Lillard James W CCL5 regulation of mucosal chlamydial immunity and infection BMC Microbiology |
title | CCL5 regulation of mucosal chlamydial immunity and infection |
title_full | CCL5 regulation of mucosal chlamydial immunity and infection |
title_fullStr | CCL5 regulation of mucosal chlamydial immunity and infection |
title_full_unstemmed | CCL5 regulation of mucosal chlamydial immunity and infection |
title_short | CCL5 regulation of mucosal chlamydial immunity and infection |
title_sort | ccl5 regulation of mucosal chlamydial immunity and infection |
url | http://www.biomedcentral.com/1471-2180/8/136 |
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