Brugia filariasis differentially modulates persistent Helicobacter pylori gastritis in the gerbil model
| Autor: | Mark T. Whary, James G. Fox, Zhongming Ge, Heather Martin, Sureshkumar Muthupalani, Thomas R. Klei, Krishna P. Shakya |
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| Přispěvatelé: | Massachusetts Institute of Technology. Division of Comparative Medicine, Fox, James G., Martin, Heather R., Muthupalani, Sureshkumar, Ge, Zhongming, Whary, Mark T. |
| Rok vydání: | 2010 |
| Předmět: |
Brugia pahangi
Spirillaceae Immunology Helminthiasis Microbiology Severity of Illness Index Article Helicobacter Infections parasitic diseases Gastric mucosa medicine Animals Helicobacter RNA Messenger Microscopy biology Helicobacter pylori Histocytochemistry Gene Expression Profiling biology.organism_classification medicine.disease Filariasis Interleukin 10 Disease Models Animal Infectious Diseases medicine.anatomical_structure Gastric Mucosa Gastritis Cytokines medicine.symptom Gerbillinae |
| Zdroj: | PubMed Central |
| ISSN: | 1769-714X |
| Popis: | 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) |
| Databáze: | OpenAIRE |
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