MHC class II activation and interferon-γ mediate the inhibition of neutrophils and eosinophils by staphylococcal enterotoxin type A (SEA) Ana P. Ferreira-Duarte, Anelize S. Pinheiro-Torres, Gabriel F. Anhê, Antônio Condino-Neto, Edson Antunes, Ivani A. DeSouza Frontiers in Cellular and Infection Microbiology, 2017 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; 1-4 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 g/ml). SEA also significantly reduced the intracellular Ca 2+ 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 g/ml). In conclusion, SEA inhibits neutrophil and eosinophil by MHC class II-dependent mechanism, which may be modulated by concomitant release of IFN-.
Airway exposure to staphylococcal enterotoxin A potentiates allergen-induced bone marrow eosinophilia and trafficking to peripheral blood and airways Dalize M. Squebola-Cola, Glaucia C. Mello, Lorenzo Pissinatti, André A. Schenka, Gabriel F. Anhê, Ivani A. DeSouza, Antonio Condino-Neto, Edson Antunes American Journal of Physiology Lung Cellular and Molecular Physiology, 2013 Bone marrow (BM) eosinopoiesis is a common feature during allergen exposure in atopic individuals. Airway exposure to staphylococcal superantigens aggravates allergic airway disease and increases the output of BM eosinophils. However, the exact mechanisms regulating eosinophil mobilization and trafficking to the peripheral circulation and airways remain to be elucidated. Therefore, this study aimed to investigate the mechanisms determining the BM eosinopoiesis in allergic mice under exposure to staphylococcal enterotoxin A (SEA). Ovalbumin (OVA)-sensitized male BALB/C mice were intranasally exposed to SEA (1 μg), and at 4, 12, 24, and 48 h later animals were challenged with OVA (10 μg, twice a day). Measurement of IL-5, eotaxin, and granulocyte-macrophage colony-stimulating factor (GM-CSF) levels, flow cytometry for CCR3+, VLA4+, and CCR3+VLA4+, as well as adhesion assays to VCAM-1 were performed in BM. Prior airway exposure to SEA time dependently increased the BM eosinophil number in OVA-challenged mice. Eosinophils gradually disappear from peripheral blood, being recruited over time to the airways, where they achieve a maximal infiltration at 24 h. SEA exposure increased the levels of IL-5 and eotaxin (but not GM-CSF) in BM of OVA-challenged mice. Marked increases in CCR3+and CCR3+VLA4+expressions in BM eosinophils of OVA-challenged mice were observed, an effect largely reduced by prior exposure to SEA. Adhesion of BM eosinophils to VCAM-1 was increased in OVA-challenged mice, but prior SEA exposure abrogated this enhanced cell adhesion. Accumulation of BM eosinophils by airway SEA exposure takes place through IL-5- and CCR3-dependent mechanisms, along with downregulation of CCR3/VL4 and impaired cell adhesion to VCAM-1.
Resident macrophages modulate the neutrophil migration induced by staphylococcal enterotoxin B into the mouse peritoneal cavity Journal of Natural Toxins, 1996
Pharmacological characterization of the mouse paw edema induced by staphylococcal enterotoxin B Journal of Natural Toxins, 1996
