Staphylococcal enterotoxin A regulates bone marrow granulocyte trafficking during pulmonary inflammatory disease in XXXX .

@entity2304 @entity14541 @entity59 @entity639 @entity19 @entity15891 @entity4459 @entity6580 @entity8024 @entity3804 @entity637 @entity647
UNASSIGNED: Pulmonary neutrophil infiltration produced by Staphylococcal enterotoxin A (SEA) airway exposure is accompanied by marked granulocyte accumulation in bone marrow (BM). Therefore, the aim of this study was to investigate the mechanisms of BM cell accumulation, and trafficking to circulating blood and lung tissue after SEA airway exposure. Male BALB/C @entity19 were intranasally exposed to SEA (1 g), and at 4, 12 and 24h thereafter, BM, circulating blood, bronchoalveolar lavage (BAL) fluid and lung tissue were collected. Adhesion of BM granulocytes and flow cytometry for @entity3804 , @entity4459 and VLA-4 and cytokine and/or chemokine levels were assayed after SEA-airway exposure. Prior exposure to SEA promoted a marked PMN influx to BAL and lung tissue, which was accompanied by increased counts of immature and/or mature neutrophils and eosinophils in BM, along with blood neutrophilia. Airway exposure to SEA enhanced BM neutrophil @entity3804 expression, and adhesion to @entity6580 and/or @entity8024 -coated plates. Elevated levels of @entity2304 , @entity14541 , INF-y, @entity637 , KC/ @entity15891 and SDF-1a were detected in BM after SEA exposure. SEA exposure increased production of eosinopoietic cytokines ( @entity639 and @entity59 ) and BM eosinophil VLA-4 expression, but it failed to affect eosinophil adhesion to @entity6580 and @entity8024 . In conclusion, BM neutrophil accumulation after SEA exposure takes place by integrated action of cytokines and/or chemokines, enhancing the adhesive responses of BM neutrophils and its trafficking to lung tissues, leading to @entity647 . BM eosinophil accumulation in SEA-induced @entity647 may occur via increased eosinopoietic cytokines and VLA-4 expression.
