Abstract:
:Mer signaling participates in a novel inhibitory pathway in TLR activation. The purpose of the present study was to examine the role of Mer signaling in the down-regulation of TLR4 activation-driven immune responses in mice, i.t.-treated with LPS, using the specific Mer-blocking antibody. At 4 h and 24 h after LPS treatment, expression of Mer protein in alveolar macrophages and lung tissue decreased, sMer in BALF increased significantly, and Mer activation increased. Pretreatment with anti-Mer antibody did not influence the protein levels of Mer and sMer levels. Anti-Mer antibody significantly reduced LPS-induced Mer activation, phosphorylation of Akt and FAK, STAT1 activation, and expression of SOCS1 and -3. Anti-Mer antibody enhanced LPS-induced inflammatory responses, including activation of the NF-κB pathway; the production of TNF-α, IL-1β, and MIP-2 and MMP-9 activity; and accumulation of inflammatory cells and the total protein levels in BALF. These results indicate that Mer plays as an intrinsic feedback inhibitor of the TLR4- and inflammatory mediator-driven immune responses during acute lung injury.
journal_name
J Leukoc Bioljournal_title
Journal of leukocyte biologyauthors
Lee YJ,Han JY,Byun J,Park HJ,Park EM,Chong YH,Cho MS,Kang JLdoi
10.1189/jlb.0611289subject
Has Abstractpub_date
2012-06-01 00:00:00pages
921-32issue
6eissn
0741-5400issn
1938-3673pii
jlb.0611289journal_volume
91pub_type
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pub_type: 杂志文章
doi:10.1189/jlb.0112048
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journal_title:Journal of leukocyte biology
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journal_title:Journal of leukocyte biology
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doi:
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