Source:http://linkedlifedata.com/resource/pubmed/id/12355446
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
2002-9-30
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pubmed:abstractText |
A comparison of the growth of Leishmania mexicana in IL-4(-/-), IL-4Ralpha(-/-) and wild-type BALB/c mice demonstrated a disease exacerbative role for IL-13 as well as IL-4. Thus, while both IL-4(-/-) and IL-4Ralpha(-/-) mice were more resistant than wild-type controls to infection with L. mexicana, IL-4Ralpha(-/-) mice, which are unresponsive to IL-13 as well as IL-4, were significantly more resistant to parasite growth than their IL-4(-/-) counterparts. Cytokine and antibody analysis revealed a Th1-biased specific response in both infected IL-4(-/-) and IL-4Ralpha(-/-) mice compared with wild-type animals. Reconstituting SCID mice with IL-4(-/-), IL-4Ralpha(-/-) or wild-type splenocytes prior to infection demonstrated that the early onset of lesion growth was dependent on the presence of lymphocytes responding to IL-4 and/or IL-13, as lesions failed to develop in only the SCID IL-4Ralpha(-/-) reconstituted mice. An independent role for IL-13 in L. mexicana infection was demonstrated by comparing disease progression in IL-13(-/-), IL-4(-/-)/IL-13(-/-) and wild-type B6/129 mice. In contrast to IL-4(-/-)/IL-13(-/-) mice, which were resistant, IL-13(-/-) mice developed lesions similar in size to wild-type animals up to week 8 post-infection. However, in contrast to wild-type mice in which disease continued to progress, lesions eventually healed in IL-13(-/-) mice, in association with the development of a Th1 response. Collectively our results suggest that IL-4 plays a critical role in early lesion development, and that IL-13 plays a crucial part in maintaining a chronic non-healing infection.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Protozoan,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-13,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-4
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0014-2980
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
32
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2923-33
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12355446-Animals,
pubmed-meshheading:12355446-Antibodies, Protozoan,
pubmed-meshheading:12355446-Cytokines,
pubmed-meshheading:12355446-Interleukin-13,
pubmed-meshheading:12355446-Interleukin-4,
pubmed-meshheading:12355446-Leishmania mexicana,
pubmed-meshheading:12355446-Leishmaniasis, Cutaneous,
pubmed-meshheading:12355446-Lymphocyte Activation,
pubmed-meshheading:12355446-Mice,
pubmed-meshheading:12355446-Mice, Inbred BALB C,
pubmed-meshheading:12355446-Mice, SCID,
pubmed-meshheading:12355446-Receptors, Interleukin-4
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pubmed:year |
2002
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pubmed:articleTitle |
An essential role for IL-13 in maintaining a non-healing response following Leishmania mexicana infection.
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pubmed:affiliation |
Department of Immunology, University of Strathclyde, Strathclyde Institute for Biomedical Sciences, 27 Taylor Street, Glasgow G4 0NR, Scotland, GB, UK. j.alexander@strath.ac.uk
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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