UM
Suppression of Lipopolysaccharide-Induced Inflammatory Response by Fragments from Serum Amyloid A
Zhou, Huibin; Chen, Mingjie; Zhang, Gufang; Ye, Richard D.
2017-08
Source PublicationJOURNAL OF IMMUNOLOGY
ISSN0022-1767
Volume199Issue:3Pages:1105-1112
AbstractSerum amyloid A (SAA) is known as an acute-phase protein and a biomarker for inflammatory diseases. Published studies have shown that SAA possesses proinflammatory cytokine-like activity and is chemotactic for phagocytes, but the structural basis for these activities remains unidentified. In this article, we report that truncated SAA1 proteins lacking N-and C-terminal sequences exhibit reduced proinflammatory activity and strongly suppress LPS-induced expression of IL-1 beta, IL-6, and TNF-alpha in macrophages. A truncated SAA1 containing aa 11-58 was examined further and found to facilitate p38 MAPK phosphorylation while reducing LPS-stimulated phosphorylation of ERK and JNK. In LPS-challenged mice, aa 11-58 reduced the severity of acute lung injury, with significantly less neutrophil infiltration in the lungs and attenuated pulmonary expression of IL-1b, IL-6, and TNF-a. Coadministration of aa 11-58 markedly improved mouse survival in response to a lethal dose of LPS. A potent induction of IL-10 was observed in a TLR2-dependent, but TLR4-independent, manner in macrophages stimulated with aa 11-58. However, the aa 11-58 fragment of SAA1 was unable to induce chemotaxis or calcium flux through formyl peptide receptor 2. These results indicate that the N-and C-terminal sequences contain structural determinants for the proinflammatory and chemotactic activities of SAA1, and their removal switches SAA1 to an anti-inflammatory role. Given that proteolytic processing of SAA is associated with the pathological changes in several diseases, including secondary amyloidosis, our findings may shed light on the structure-function relationship of SAA1 with respect to its role in inflammation.
DOI10.4049/jimmunol.1700470
URLView the original
Indexed BySCI
Language英语
WOS Research AreaImmunology
WOS SubjectImmunology
WOS IDWOS:000406182600029
PublisherAMER ASSOC IMMUNOLOGISTS
The Source to ArticleWOS
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Cited Times [WOS]:6   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionUniversity of Macau
Recommended Citation
GB/T 7714
Zhou, Huibin,Chen, Mingjie,Zhang, Gufang,et al. Suppression of Lipopolysaccharide-Induced Inflammatory Response by Fragments from Serum Amyloid A[J]. JOURNAL OF IMMUNOLOGY,2017,199(3):1105-1112.
APA Zhou, Huibin,Chen, Mingjie,Zhang, Gufang,&Ye, Richard D..(2017).Suppression of Lipopolysaccharide-Induced Inflammatory Response by Fragments from Serum Amyloid A.JOURNAL OF IMMUNOLOGY,199(3),1105-1112.
MLA Zhou, Huibin,et al."Suppression of Lipopolysaccharide-Induced Inflammatory Response by Fragments from Serum Amyloid A".JOURNAL OF IMMUNOLOGY 199.3(2017):1105-1112.
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