Linked Life Data

11859129

Source:http://linkedlifedata.com/resource/pubmed/id/11859129

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2002-2-22
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
168
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2383-92
pubmed:dateRevised
2008-11-21
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
pubmed:year
2002
pubmed:articleTitle
IL-10 is critical for host resistance and survival during gastrointestinal helminth infection.
pubmed:affiliation
Immunology Disease Resistance Laboratory, Animal and Natural Resources Institute, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, MD 20705, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.