DC Field | Value | Language |
---|---|---|
dc.contributor.author | Corry, DB | ko |
dc.contributor.author | Kiss, A | ko |
dc.contributor.author | Song, LZ | ko |
dc.contributor.author | Song, L | ko |
dc.contributor.author | Xu, J | ko |
dc.contributor.author | Lee, Seung-Hyo | ko |
dc.contributor.author | Werb, Z | ko |
dc.contributor.author | Kheradmand, F | ko |
dc.date.accessioned | 2008-07-15T05:24:05Z | - |
dc.date.available | 2008-07-15T05:24:05Z | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.issued | 2004-04 | - |
dc.identifier.citation | FASEB JOURNAL, v.18, no.6, pp.995 - 995 | - |
dc.identifier.issn | 0892-6638 | - |
dc.identifier.uri | http://hdl.handle.net/10203/5826 | - |
dc.description.abstract | The mechanisms that initiate allergic lung inflammation are relevant to expression of diseases such as asthma, but the factors underlying resolution of inflammation are equally important. Previously, we demonstrated the importance of matrix metalloproteinase 2 (MMP2) for airway egression of lung eosinophils, a critical anti-inflammatory mechanism without which mice are rendered highly susceptible to lethal asphyxiation. Here we show that leukocyte MMP9 is the dominant airway MMP controlling inflammatory cell egression. The allergic lung phenotype of MMP9(-/-) mice was similar to WT and was not altered by concomitant deletion of the MMP2 gene ( double knockout; dko). However, inflammatory cells accumulated aberrantly in the lungs of allergen-challenged MMP9(-/-) and dko mice and fewer eosinophils and neutrophils were present in bronchoalveolar lavage. These aberrant cellular trafficking patterns were explained by disruption of transepithelial chemokine gradients, in MMP2(-/-) mice affecting only eotaxin (CCL11), but in MMP9(-/-) and dko mice involving eotaxin, MARC (CCL7), and TARC (CCL17). Thus, by establishing multiple transepithelial chemokine gradients, MMP9 is broadly implicated in the resolution of allergic inflammation, an essential protective mechanism that overlaps with a more limited role played by MMP2. | - |
dc.description.sponsorship | This study was supported by grants from the National Institutes of Health (HL 72419 and K025 HL 72062 to F.K., HL 69585 to D.C., and AI 53194 to Z.W.), and by funds from the Sandler Family Sustaining Foundation. | en |
dc.language | English | - |
dc.language.iso | en_US | en |
dc.publisher | FEDERATION AMER SOC EXP BIOL | - |
dc.subject | BRONCHIAL EPITHELIAL-CELLS | - |
dc.subject | MATRIX METALLOPROTEINASES | - |
dc.subject | AIRWAY HYPERREACTIVITY | - |
dc.subject | ADAPTIVE IMMUNITY | - |
dc.subject | GELATINASE B | - |
dc.subject | MURINE MODEL | - |
dc.subject | IN-VIVO | - |
dc.subject | ASTHMA | - |
dc.subject | MICE | - |
dc.subject | EOSINOPHILS | - |
dc.title | Overlapping and independent contributions of MMP2 and MMP9 to lung allergic inflammatory cell egression through decreased CC chemokines | - |
dc.type | Article | - |
dc.identifier.wosid | 000221108800025 | - |
dc.identifier.scopusid | 2-s2.0-3543136879 | - |
dc.type.rims | ART | - |
dc.citation.volume | 18 | - |
dc.citation.issue | 6 | - |
dc.citation.beginningpage | 995 | - |
dc.citation.endingpage | 995 | - |
dc.citation.publicationname | FASEB JOURNAL | - |
dc.identifier.doi | 10.1096/fj.03-1412fje | - |
dc.embargo.liftdate | 9999-12-31 | - |
dc.embargo.terms | 9999-12-31 | - |
dc.contributor.localauthor | Lee, Seung-Hyo | - |
dc.contributor.nonIdAuthor | Corry, DB | - |
dc.contributor.nonIdAuthor | Kiss, A | - |
dc.contributor.nonIdAuthor | Song, LZ | - |
dc.contributor.nonIdAuthor | Song, L | - |
dc.contributor.nonIdAuthor | Xu, J | - |
dc.contributor.nonIdAuthor | Werb, Z | - |
dc.contributor.nonIdAuthor | Kheradmand, F | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | chemotaxis | - |
dc.subject.keywordAuthor | cytokines | - |
dc.subject.keywordAuthor | gelatinase B | - |
dc.subject.keywordAuthor | matrix metalloproteinase-9 | - |
dc.subject.keywordPlus | BRONCHIAL EPITHELIAL-CELLS | - |
dc.subject.keywordPlus | MATRIX METALLOPROTEINASES | - |
dc.subject.keywordPlus | AIRWAY HYPERREACTIVITY | - |
dc.subject.keywordPlus | ADAPTIVE IMMUNITY | - |
dc.subject.keywordPlus | GELATINASE B | - |
dc.subject.keywordPlus | MURINE MODEL | - |
dc.subject.keywordPlus | IN-VIVO | - |
dc.subject.keywordPlus | ASTHMA | - |
dc.subject.keywordPlus | MICE | - |
dc.subject.keywordPlus | EOSINOPHILS | - |
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