UM
Elevated Expression of Serum Amyloid A 3 Protects Colon Epithelium Against Acute Injury Through TLR2-Dependent Induction of Neutrophil IL-22 Expression in a Mouse Model of Colitis
Zhang, Gufang; Liu, Jin; Wu, Lehao; Fang, Yu; Sun, Lei; Qian, Feng; Chen, Daijie; Ye, Richard D.
2018-06-29
Source PublicationFRONTIERS IN IMMUNOLOGY
ISSN1664-3224
Volume9
AbstractInduced expression of serum amyloid A (SAA) is a hallmark of many inflammatory diseases, but whether SAA exacerbates inflammation or protects tissues against injury remains unclear. In dextran sulfate sodium (DSS)-induced colitis, SAA3 is the predominant isoform of inducible SAA proteins that also include SAA1 and SAA2, and mice with genetic deletion of Saa3 exhibits increased production of proinflammatory cytokines, decreased expression of IL-22 along with aggravated epithelium disruption, and reduced colon length compared with wild-type littermates. Colonic neutrophils have been identified as a major source of IL-22 in these mice. Administration of exogenous SAA3 as recombinant protein to Saa3(-/-) mice improves neutrophil IL-22 production, colonic epithelial integrity, and secretion of the antimicrobial peptides Reg3 beta and Reg3 gamma. Stimulation of mouse bone marrow neutrophils with mouse SAA3 or human SAA1 leads to expansion of IL-22-producing neutrophils. Unlike previously reported IL-22 induction through IL-23, the SAA3-induced neutrophil IL-22 expression utilizes a TLR2-dependent mechanism that does not depend on IL-23. Adoptive transfer of the SAA3-treated neutrophils to Saa3(-/-) mice ameliorates DSS-induced colitis and improves colonic epithelial integrity. These findings suggest that in the DSS-induced mouse colitis model, SAA isoforms are expressed to different extent in colon and deletion of Saa3 renders these mice more susceptible to DSS-induced injury. The presence of SAA3 in the inflamed colon mucosal serves to protect epithelial barrier in part through expansion of IL-22-producing neutrophils. It is speculated that SAA3 stimulation of autologous neutrophils may have therapeutic potential for inflammatory bowel disease.
Keywordserum amyloid A inflammation innate immunity cytokines colitis neutrophils
DOI10.3389/fimmu.2018.01503
URLView the original
Indexed BySCI
Language英语
WOS Research AreaImmunology
WOS SubjectImmunology
WOS IDWOS:000436870800001
PublisherFRONTIERS MEDIA SA
The Source to ArticleWOS
Fulltext Access
Citation statistics
Cited Times [WOS]:6   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionUniversity of Macau
Recommended Citation
GB/T 7714
Zhang, Gufang,Liu, Jin,Wu, Lehao,et al. Elevated Expression of Serum Amyloid A 3 Protects Colon Epithelium Against Acute Injury Through TLR2-Dependent Induction of Neutrophil IL-22 Expression in a Mouse Model of Colitis[J]. FRONTIERS IN IMMUNOLOGY,2018,9.
APA Zhang, Gufang.,Liu, Jin.,Wu, Lehao.,Fang, Yu.,Sun, Lei.,...&Ye, Richard D..(2018).Elevated Expression of Serum Amyloid A 3 Protects Colon Epithelium Against Acute Injury Through TLR2-Dependent Induction of Neutrophil IL-22 Expression in a Mouse Model of Colitis.FRONTIERS IN IMMUNOLOGY,9.
MLA Zhang, Gufang,et al."Elevated Expression of Serum Amyloid A 3 Protects Colon Epithelium Against Acute Injury Through TLR2-Dependent Induction of Neutrophil IL-22 Expression in a Mouse Model of Colitis".FRONTIERS IN IMMUNOLOGY 9(2018).
Related Services
Recommend this item
Bookmark
Usage statistics
Export to Endnote
Google Scholar
Similar articles in Google Scholar
[Zhang, Gufang]'s Articles
[Liu, Jin]'s Articles
[Wu, Lehao]'s Articles
Baidu academic
Similar articles in Baidu academic
[Zhang, Gufang]'s Articles
[Liu, Jin]'s Articles
[Wu, Lehao]'s Articles
Bing Scholar
Similar articles in Bing Scholar
[Zhang, Gufang]'s Articles
[Liu, Jin]'s Articles
[Wu, Lehao]'s Articles
Terms of Use
No data!
Social Bookmark/Share
All comments (0)
No comment.
 

Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.