Brugia filariasis differentially modulates persistent Helicobacter pylori gastritis in the gerbil model
In select Helicobacter pylori-infected populations with low gastric cancer, nematode coinfections are common and both helicobacter gastritis and filariasis are modeled in gerbils. We evaluated gastritis, worm counts, tissue cytokine gene expression levels and Th1/Th2-associated antibody responses in...
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Format: | Article |
Language: | en_US |
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Elsevier B.V.
2011
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Online Access: | http://hdl.handle.net/1721.1/67284 https://orcid.org/0000-0001-9307-6116 |
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author | Martin, Heather R. Shakya, Krishna P. Muthupalani, Sureshkumar Ge, Zhongming Klei, Thomas R. Whary, Mark T. Fox, James G. |
author2 | Massachusetts Institute of Technology. Division of Comparative Medicine |
author_facet | Massachusetts Institute of Technology. Division of Comparative Medicine Martin, Heather R. Shakya, Krishna P. Muthupalani, Sureshkumar Ge, Zhongming Klei, Thomas R. Whary, Mark T. Fox, James G. |
author_sort | Martin, Heather R. |
collection | MIT |
description | In select Helicobacter pylori-infected populations with low gastric cancer, nematode coinfections are common and both helicobacter gastritis and filariasis are modeled in gerbils. We evaluated gastritis, worm counts, tissue cytokine gene expression levels and Th1/Th2-associated antibody responses in H. pylori and Brugia pahangi mono- and coinfected gerbils. H. pylori-associated gastritis indices were significantly lower 21 weeks post-infection in coinfected gerbils (p ≤ 0.05) and were inversely proportional to worm counts (r2 = −0.62, p < 0.003). Additionally, IFN-γ, IL-1β, CXCL1, IL-4 and IL-10 mRNA levels in the gastric antrum reflected a significant host response to gastric H. pylori and as well as systemic filariasis (p ≤ 0.05). Despite increasing worm burden (p < 0.05), gastritis progressed in coinfected gerbils (p < 0.03) becoming equivalent to H. pylori-infected gerbils at 42 weeks (p = 0.7). Pro- and anti-inflammatory mediator mRNA levels were notably downregulated in B. pahangi infected gerbils below uninfected control values, suggesting hyporesponsiveness to B. pahangi. Consistent with an increasing Th1 response to H. pylori, IgG2a (p < 0.01), IL-1β (p = 0.04) and CXCL1 (p = 0.006) responses significantly increased and IL-4 (p = 0.05) and IL-10 (p = 0.04) were decreased in coinfected gerbils at 42 weeks. Initial systemic responses to B. pahangi resulted in attenuated gastritis in coinfected gerbils, but subsequent filarid-associated hyporesponsiveness appears to have promoted H. pylori gastritis. |
first_indexed | 2024-09-23T14:06:45Z |
format | Article |
id | mit-1721.1/67284 |
institution | Massachusetts Institute of Technology |
language | en_US |
last_indexed | 2024-09-23T14:06:45Z |
publishDate | 2011 |
publisher | Elsevier B.V. |
record_format | dspace |
spelling | mit-1721.1/672842022-09-28T18:32:05Z Brugia filariasis differentially modulates persistent Helicobacter pylori gastritis in the gerbil model Martin, Heather R. Shakya, Krishna P. Muthupalani, Sureshkumar Ge, Zhongming Klei, Thomas R. Whary, Mark T. Fox, James G. Massachusetts Institute of Technology. Division of Comparative Medicine Fox, James G. Martin, Heather R. Muthupalani, Sureshkumar Ge, Zhongming Whary, Mark T. Fox, James G. In select Helicobacter pylori-infected populations with low gastric cancer, nematode coinfections are common and both helicobacter gastritis and filariasis are modeled in gerbils. We evaluated gastritis, worm counts, tissue cytokine gene expression levels and Th1/Th2-associated antibody responses in H. pylori and Brugia pahangi mono- and coinfected gerbils. H. pylori-associated gastritis indices were significantly lower 21 weeks post-infection in coinfected gerbils (p ≤ 0.05) and were inversely proportional to worm counts (r2 = −0.62, p < 0.003). Additionally, IFN-γ, IL-1β, CXCL1, IL-4 and IL-10 mRNA levels in the gastric antrum reflected a significant host response to gastric H. pylori and as well as systemic filariasis (p ≤ 0.05). Despite increasing worm burden (p < 0.05), gastritis progressed in coinfected gerbils (p < 0.03) becoming equivalent to H. pylori-infected gerbils at 42 weeks (p = 0.7). Pro- and anti-inflammatory mediator mRNA levels were notably downregulated in B. pahangi infected gerbils below uninfected control values, suggesting hyporesponsiveness to B. pahangi. Consistent with an increasing Th1 response to H. pylori, IgG2a (p < 0.01), IL-1β (p = 0.04) and CXCL1 (p = 0.006) responses significantly increased and IL-4 (p = 0.05) and IL-10 (p = 0.04) were decreased in coinfected gerbils at 42 weeks. Initial systemic responses to B. pahangi resulted in attenuated gastritis in coinfected gerbils, but subsequent filarid-associated hyporesponsiveness appears to have promoted H. pylori gastritis. National Institutes of Health (U.S.) (NIH grant R01 AI 0337750) National Institutes of Health (U.S.) (Grant P30-ES002109) National Institutes of Health (U.S.) (Grant P01 CA 028842) National Institutes of Health (U.S.) (Grant T32 RR 07036) 2011-11-21T21:38:06Z 2011-11-21T21:38:06Z 2010-09 Article http://purl.org/eprint/type/JournalArticle 1286-4579 http://hdl.handle.net/1721.1/67284 Martin, Heather R. et al. “Brugia filariasis differentially modulates persistent Helicobacter pylori gastritis in the gerbil model.” Microbes and Infection 12 (2010): 748-758. https://orcid.org/0000-0001-9307-6116 en_US http://dx.doi.org/10.1016/j.micinf.2010.05.005 Microbes and Infection Creative Commons Attribution-Noncommercial-Share Alike 3.0 http://creativecommons.org/licenses/by-nc-sa/3.0/ application/pdf Elsevier B.V. PubMed Central |
spellingShingle | Martin, Heather R. Shakya, Krishna P. Muthupalani, Sureshkumar Ge, Zhongming Klei, Thomas R. Whary, Mark T. Fox, James G. Brugia filariasis differentially modulates persistent Helicobacter pylori gastritis in the gerbil model |
title | Brugia filariasis differentially modulates persistent Helicobacter pylori gastritis in the gerbil model |
title_full | Brugia filariasis differentially modulates persistent Helicobacter pylori gastritis in the gerbil model |
title_fullStr | Brugia filariasis differentially modulates persistent Helicobacter pylori gastritis in the gerbil model |
title_full_unstemmed | Brugia filariasis differentially modulates persistent Helicobacter pylori gastritis in the gerbil model |
title_short | Brugia filariasis differentially modulates persistent Helicobacter pylori gastritis in the gerbil model |
title_sort | brugia filariasis differentially modulates persistent helicobacter pylori gastritis in the gerbil model |
url | http://hdl.handle.net/1721.1/67284 https://orcid.org/0000-0001-9307-6116 |
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