Source:http://linkedlifedata.com/resource/pubmed/id/11859129
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2002-2-22
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pubmed:abstractText |
Resistance to many intestinal nematodes is dependent on the induction of polarized type 2 cytokine responses, whereas type 1 responses can exacerbate these infections. The contributions of IL-4 and IL-13 to the development of resistance have been well described for a variety of intestinal parasites; however, the role of IL-10 has not been previously investigated. In this study we infected IL-10-, IL-10/IL-4-, IL-10/IL-12-, IL-4-, and IL-12-deficient mice with Trichuris muris to determine whether IL-10 contributes to the development of immunity. Interestingly, T. muris-infected IL-10-, IL-4-, and IL-10/IL-4-deficient mice failed to expel the parasite, and animals deficient in IL-10 displayed marked morbidity and mortality. In contrast, double IL-10/IL-12-deficient mice were completely resistant and mounted a highly polarized type 2 cytokine response, demonstrating that the increased susceptibility of IL-10-deficient mice was dependent on IL-12. Further study suggested that the susceptibility of IL-10- and IL-10/IL-4-deficient mice was probably attributable to a marked increase in type 1 cytokine production in those animals. The mortality observed in T. muris-infected IL-10- and IL-10/IL-4-deficient mice correlated with increased inflammation, loss of Paneth cells, and absence of mucus in the cecum. Interestingly, survival was enhanced in T. muris-infected IL-10/IL-4-deficient mice if a broad spectrum antibiotic was administered, suggesting that an outgrowth of opportunistic bacteria was contributing to the high degree of morbidity and mortality. Overall, these studies reveal a critical role for IL-10 in the polarization of Th2 responses, development of resistance during T. muris infection, and maintenance of barrier function in the colon.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Bacterial Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Neomycin,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
168
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2383-92
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:11859129-Animals,
pubmed-meshheading:11859129-Anti-Bacterial Agents,
pubmed-meshheading:11859129-Cecum,
pubmed-meshheading:11859129-Cells, Cultured,
pubmed-meshheading:11859129-Cytokines,
pubmed-meshheading:11859129-Gastrointestinal Diseases,
pubmed-meshheading:11859129-Interferon-gamma,
pubmed-meshheading:11859129-Interleukin-10,
pubmed-meshheading:11859129-Interleukin-4,
pubmed-meshheading:11859129-Mice,
pubmed-meshheading:11859129-Mice, Inbred C57BL,
pubmed-meshheading:11859129-Mice, Knockout,
pubmed-meshheading:11859129-Mucus,
pubmed-meshheading:11859129-Neomycin,
pubmed-meshheading:11859129-Paneth Cells,
pubmed-meshheading:11859129-RNA, Messenger,
pubmed-meshheading:11859129-Survival Rate,
pubmed-meshheading:11859129-Trichuriasis,
pubmed-meshheading:11859129-Tumor Necrosis Factor-alpha,
pubmed-meshheading:11859129-Weight Loss
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pubmed:year |
2002
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pubmed:articleTitle |
IL-10 is critical for host resistance and survival during gastrointestinal helminth infection.
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pubmed:affiliation |
Immunology Disease Resistance Laboratory, Animal and Natural Resources Institute, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, MD 20705, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.
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