期刊论文详细信息
Frontiers in Cellular and Infection Microbiology
MHC Class II Activation and Interferon-γ Mediate the Inhibition of Neutrophils and Eosinophils by Staphylococcal Enterotoxin Type A (SEA)
Pinheiro-Torres, Anelize S.1  Ferreira-Duarte, Ana P.1  Antunes, Edson1  , Gabriel F.2  Anhê3  nio3  Condino-Neto, Antô4 
[1] Department of Biology and Physiology, Faculty of Medicine of Jundiai, Brazil;Department of Immunology, Institute of Biomedical Sciences, University of SãDepartment of Pharmacology, State University of Campinas, Brazil;o Paulo, Brazil
关键词: Adhesion;    Chemotaxis;    Bone Marrow;    Interleukin-8;    Eotaxin;   
DOI  :  10.3389/fcimb.2017.00518
学科分类:生物科学(综合)
来源: Frontiers
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【 摘 要 】

Staphylococcal enterotoxins are classified as superantigens that act by linking T-cell receptor with MHC class II molecules, which are expressed on classical antigen-presenting cells (APC). Evidence shows that MHC class II is also expressed in neutrophils and eosinophils. This study aimed to investigate the role of MHC class II and IFN- on chemotactic and adhesion properties of neutrophils and eosinophils after incubation with SEA. Bone marrow (BM) cells obtained from BALB/c mice were resuspended in culture medium, and incubated with SEA (3-30 ng/ml; 1 to 4 h), after which chemotaxis and adhesion were evaluated. Incubation with SEA significantly reduced the chemotactic and adhesive responses in BM neutrophils activated with IL-8 (200 ng/ml). Likewise, SEA significantly reduced the chemotactic and adhesive responses of BM eosinophils activated with eotaxin (300 ng/ml). The inhibitory effects of SEA on cell chemotaxis and adhesion were fully prevented by prior incubation with an anti-MHC class II blocking antibody (2 µg/ml). SEA also significantly reduced the intracellular Ca2+ levels in IL-8- and eotaxin-activated BM cells. No alterations of MAC-1, VLA4 and LFA-1 expressions were observed after SEA incubation. In addition, SEA elevated by 3.5-fold (P<0.05) the INF- levels in BM cells. Incubation of BM leukocytes with IFN- (10 ng/ml, 2 h) reduced both neutrophil and eosinophil chemotaxis and adhesion, which were prevented by prior incubation with anti-MHC class II antibody (2 µg/ml). In conclusion, SEA inhibits neutrophil and eosinophil by MHC class II-dependent mechanism, which may be modulated by concomitant release of IFN-.

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