Source:http://linkedlifedata.com/resource/pubmed/id/10226071
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
1999-6-7
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pubmed:abstractText |
The Th2 cytokine interleukin (IL)-13 is believed to play an important role in the development of allergy, although it has also been ascribed anti-inflammatory roles in several experimental models. In this study, we have examined the effects of human recombinant IL-13 on eosinophilic lung inflammation in the guinea pig. IL-13 (1 to 100 ng, given by intratracheal instillation) did not elicit airway eosinophil recruitment. A pronounced accumulation of eosinophils, as well as monocyte/macrophages, was elicited by intratracheal instillation of guinea pig tumor necrosis factor alpha (gpTNF-alpha). Intratracheal administration of IL-13 (1 to 100 ng) given immediately prior to exposure to gpTNF-alpha resulted in a dose-related suppression of eosinophil and monocyte/macrophage accumulation in the airways, as assessed by bronchoalveolar lavage (BAL) and eosinophil peroxidase activity in whole-lung homogenates. IL-13 treatment also reduced BAL fluid (BALF) leukocyte accumulation induced by subsequent aerosol antigen challenge of sensitized guinea pigs. Antigen challenge also resulted in elevated levels of immunoreactive eotaxin and eosinophil-stimulating activity in BALF, although only the latter was reduced significantly by IL-13 instillation prior to challenge. In contrast to the suppressive effects of IL-13, instillation of human recombinant IL-4 (100 ng) alone elicited an increase in BALF monocyte/macrophage numbers, and IL-4 was unable to inhibit gpTNF-alpha-induced leukocyte accumulation. Hence, IL-13 (but not human IL-4) exhibits an anti-inflammatory action in the airways of gpTNF-alpha- or antigen-challenged guinea pigs, by mechanisms that may involve the decreased generation of eosinophil-stimulating activity in the airways.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents...,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Eosinophil Peroxidase,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-13,
http://linkedlifedata.com/resource/pubmed/chemical/Peroxidases,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1044-1549
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
20
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1007-12
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pubmed:dateRevised |
2009-9-29
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pubmed:meshHeading |
pubmed-meshheading:10226071-Animals,
pubmed-meshheading:10226071-Anti-Inflammatory Agents, Non-Steroidal,
pubmed-meshheading:10226071-Antigens,
pubmed-meshheading:10226071-Bronchoalveolar Lavage Fluid,
pubmed-meshheading:10226071-Cell Aggregation,
pubmed-meshheading:10226071-Eosinophil Peroxidase,
pubmed-meshheading:10226071-Eosinophils,
pubmed-meshheading:10226071-Female,
pubmed-meshheading:10226071-Guinea Pigs,
pubmed-meshheading:10226071-Humans,
pubmed-meshheading:10226071-Interleukin-13,
pubmed-meshheading:10226071-Lung,
pubmed-meshheading:10226071-Male,
pubmed-meshheading:10226071-Peroxidases,
pubmed-meshheading:10226071-Pneumonia,
pubmed-meshheading:10226071-Recombinant Proteins,
pubmed-meshheading:10226071-Tumor Necrosis Factor-alpha
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pubmed:year |
1999
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pubmed:articleTitle |
Anti-inflammatory actions of interleukin-13: suppression of tumor necrosis factor-alpha and antigen-induced leukocyte accumulation in the guinea pig lung.
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pubmed:affiliation |
Department of Pharmacy and Pharmacology, University of Bath; Leukocyte Biology, Imperial College School of Medicine at the National Heart and Lung Institute, London, United Kingdom. m.l.watson@bath.ac.uk
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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