Helminth infection modulates systemic pro-inflammatory cytokines and chemokines implicated in type 2 diabetes mellitus pathogenesis.
BACKGROUND:The prevalence of helminth infections exhibits an inverse association with the prevalence of Type 2 diabetes mellitus (T2DM), and helminths are postulated to mediate a protective effect against T2DM. However, the biological mechanism behind this effect is not known. AIMS/METHODS:We postul...
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Format: | Article |
Language: | English |
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Public Library of Science (PLoS)
2020-03-01
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Series: | PLoS Neglected Tropical Diseases |
Online Access: | https://doi.org/10.1371/journal.pntd.0008101 |
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author | Anuradha Rajamanickam Saravanan Munisankar Chandrakumar Dolla Pradeep A Menon Kannan Thiruvengadam Thomas B Nutman Subash Babu |
author_facet | Anuradha Rajamanickam Saravanan Munisankar Chandrakumar Dolla Pradeep A Menon Kannan Thiruvengadam Thomas B Nutman Subash Babu |
author_sort | Anuradha Rajamanickam |
collection | DOAJ |
description | BACKGROUND:The prevalence of helminth infections exhibits an inverse association with the prevalence of Type 2 diabetes mellitus (T2DM), and helminths are postulated to mediate a protective effect against T2DM. However, the biological mechanism behind this effect is not known. AIMS/METHODS:We postulated that helminth infections act by modulating the pro-inflammatory cytokine and chemokine milieu that is characteristic of T2DM. To examine the association of cytokines and chemokines in helminth-diabetes co-morbidity, we measured the plasma levels of a panel of pro-inflammatory cytokines and chemokines in individuals with Strongyloides stercoralis infection (Ss+) and T2DM at the time of Ss diagnosis and then 6 months after definitive anthelmintic treatment along with uninfected control individuals with T2DM alone (Ss-). PRINCIPAL FINDINGS:Ss+ individuals exhibited significantly diminished levels of the pro-inflammatory cytokines-IL-1α, IL-1β, IL-6, IL-12, IL-18, IL-23, IL-27, G-CSF and GM-CSF and chemokines-CCL1, CCL2, CCL3, CCL11, CXCL1, CXCL2, CXCL8, CXCL9, CXCL10 and CXCL11. In contrast, Ss+ individuals exhibited significantly elevated levels of IL-1Ra. Anthelmintic treatment resulted in increased levels of all of the cytokines and chemokines. CONCLUSIONS:Thus, helminth infections alleviate and anthelmintic therapy partially restores the plasma cytokine and chemokine levels in helminth-diabetes co-morbidity. Our data therefore offer a plausible biological mechanism for the protective effect of helminth infections against T2DM. |
first_indexed | 2024-12-18T00:55:13Z |
format | Article |
id | doaj.art-e561419d542a41d1b86aff44cac93559 |
institution | Directory Open Access Journal |
issn | 1935-2727 1935-2735 |
language | English |
last_indexed | 2024-12-18T00:55:13Z |
publishDate | 2020-03-01 |
publisher | Public Library of Science (PLoS) |
record_format | Article |
series | PLoS Neglected Tropical Diseases |
spelling | doaj.art-e561419d542a41d1b86aff44cac935592022-12-21T21:26:32ZengPublic Library of Science (PLoS)PLoS Neglected Tropical Diseases1935-27271935-27352020-03-01143e000810110.1371/journal.pntd.0008101Helminth infection modulates systemic pro-inflammatory cytokines and chemokines implicated in type 2 diabetes mellitus pathogenesis.Anuradha RajamanickamSaravanan MunisankarChandrakumar DollaPradeep A MenonKannan ThiruvengadamThomas B NutmanSubash BabuBACKGROUND:The prevalence of helminth infections exhibits an inverse association with the prevalence of Type 2 diabetes mellitus (T2DM), and helminths are postulated to mediate a protective effect against T2DM. However, the biological mechanism behind this effect is not known. AIMS/METHODS:We postulated that helminth infections act by modulating the pro-inflammatory cytokine and chemokine milieu that is characteristic of T2DM. To examine the association of cytokines and chemokines in helminth-diabetes co-morbidity, we measured the plasma levels of a panel of pro-inflammatory cytokines and chemokines in individuals with Strongyloides stercoralis infection (Ss+) and T2DM at the time of Ss diagnosis and then 6 months after definitive anthelmintic treatment along with uninfected control individuals with T2DM alone (Ss-). PRINCIPAL FINDINGS:Ss+ individuals exhibited significantly diminished levels of the pro-inflammatory cytokines-IL-1α, IL-1β, IL-6, IL-12, IL-18, IL-23, IL-27, G-CSF and GM-CSF and chemokines-CCL1, CCL2, CCL3, CCL11, CXCL1, CXCL2, CXCL8, CXCL9, CXCL10 and CXCL11. In contrast, Ss+ individuals exhibited significantly elevated levels of IL-1Ra. Anthelmintic treatment resulted in increased levels of all of the cytokines and chemokines. CONCLUSIONS:Thus, helminth infections alleviate and anthelmintic therapy partially restores the plasma cytokine and chemokine levels in helminth-diabetes co-morbidity. Our data therefore offer a plausible biological mechanism for the protective effect of helminth infections against T2DM.https://doi.org/10.1371/journal.pntd.0008101 |
spellingShingle | Anuradha Rajamanickam Saravanan Munisankar Chandrakumar Dolla Pradeep A Menon Kannan Thiruvengadam Thomas B Nutman Subash Babu Helminth infection modulates systemic pro-inflammatory cytokines and chemokines implicated in type 2 diabetes mellitus pathogenesis. PLoS Neglected Tropical Diseases |
title | Helminth infection modulates systemic pro-inflammatory cytokines and chemokines implicated in type 2 diabetes mellitus pathogenesis. |
title_full | Helminth infection modulates systemic pro-inflammatory cytokines and chemokines implicated in type 2 diabetes mellitus pathogenesis. |
title_fullStr | Helminth infection modulates systemic pro-inflammatory cytokines and chemokines implicated in type 2 diabetes mellitus pathogenesis. |
title_full_unstemmed | Helminth infection modulates systemic pro-inflammatory cytokines and chemokines implicated in type 2 diabetes mellitus pathogenesis. |
title_short | Helminth infection modulates systemic pro-inflammatory cytokines and chemokines implicated in type 2 diabetes mellitus pathogenesis. |
title_sort | helminth infection modulates systemic pro inflammatory cytokines and chemokines implicated in type 2 diabetes mellitus pathogenesis |
url | https://doi.org/10.1371/journal.pntd.0008101 |
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