Source:http://linkedlifedata.com/resource/pubmed/id/17911623
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
2007-10-3
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pubmed:abstractText |
In the murine model of Cryptococcus neoformans infection Th1 (IL-12/IFN-gamma) and Th17 (IL-23/IL-17) responses are associated with protection, whereas an IL-4-dependent Th2 response exacerbates disease. To investigate the role of the Th2 cytokine IL-13 during pulmonary infection with C. neoformans, IL-13-overexpressing transgenic (IL-13Tg(+)), IL-13-deficient (IL-13(-/-)), and wild-type (WT) mice were infected intranasally. Susceptibility to C. neoformans infection was found when IL-13 was induced in WT mice or overproduced in IL-13Tg(+) mice. Infected IL-13Tg(+) mice had a reduced survival time and higher pulmonary fungal load as compared with WT mice. In contrast, infected IL-13(-/-) mice were resistant and 89% of these mice survived the entire period of the experiment. Ag-specific production of IL-13 by susceptible WT and IL-13Tg(+) mice was associated with a significant type 2 cytokine shift but only minor changes in IFN-gamma production. Consistent with enhanced type 2 cytokine production, high levels of serum IgE and low ratios of serum IgG2a/IgG1 were detected in susceptible WT and IL-13Tg(+) mice. Interestingly, expression of IL-13 by susceptible WT and IL-13Tg(+) mice was associated with reduced IL-17 production. IL-13 was found to induce formation of alternatively activated macrophages expressing arginase-1, macrophage mannose receptor (CD206), and YM1. In addition, IL-13 production led to lung eosinophilia, goblet cell metaplasia and elevated mucus production, and enhanced airway hyperreactivity. This indicates that IL-13 contributes to fatal allergic inflammation during C. neoformans infection.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-1767
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pubmed:author |
pubmed-author:AlberGottfriedG,
pubmed-author:BlessingManfredM,
pubmed-author:BrombacherFrankF,
pubmed-author:HansenGesineG,
pubmed-author:KöhlerGabrieleG,
pubmed-author:MüllerUweU,
pubmed-author:McKenzieAndrew N JAN,
pubmed-author:PolteTobiasT,
pubmed-author:SchützeNicoleN,
pubmed-author:StenzelWernerW,
pubmed-author:StraubingerReinhard KRK,
pubmed-author:WernerChristophC
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
179
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5367-77
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pubmed:meshHeading |
pubmed-meshheading:17911623-Animals,
pubmed-meshheading:17911623-Antibodies, Fungal,
pubmed-meshheading:17911623-Cryptococcosis,
pubmed-meshheading:17911623-Cryptococcus neoformans,
pubmed-meshheading:17911623-Cytokines,
pubmed-meshheading:17911623-Female,
pubmed-meshheading:17911623-Immunoglobulin Isotypes,
pubmed-meshheading:17911623-Inflammation,
pubmed-meshheading:17911623-Interleukin-13,
pubmed-meshheading:17911623-Lung Diseases, Fungal,
pubmed-meshheading:17911623-Macrophage Activation,
pubmed-meshheading:17911623-Macrophages, Alveolar,
pubmed-meshheading:17911623-Mice,
pubmed-meshheading:17911623-Mice, Inbred BALB C,
pubmed-meshheading:17911623-Mice, Knockout,
pubmed-meshheading:17911623-Mice, Transgenic,
pubmed-meshheading:17911623-Respiratory Hypersensitivity
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pubmed:year |
2007
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pubmed:articleTitle |
IL-13 induces disease-promoting type 2 cytokines, alternatively activated macrophages and allergic inflammation during pulmonary infection of mice with Cryptococcus neoformans.
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pubmed:affiliation |
Institute of Immunology, College of Veterinary Medicine, University of Leipzig, Leipzig, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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