CINC blockade prevents neutrophil Ca2+ signaling upregulation and gut bacterial translocation in thermal injury

In this study, we have evaluated the role of cytokine-induced neutrophil ch emoattractant (CINC), in the upregulation of neutrophil Ca2+ signaling in n eutrophils from thermally injured rats treated with anti-CINC antibody. Add itionally, we have determined the effect of the treatment with CINC antibod y on the accumulation of activated neutrophils in the intestinal wall, and the effect of such accumulation on gut bacterial translocation. Measurement s of myeloperoxidase (MPO) activity and immunohistochemical localization of neutrophils determined neutrophil sequestration in the rat intestine. Agar culture analyses and a specific Escherichia coli beta -galactosidase gene polymerase chain reaction was carried out to detect gut indigenous bacteria l invasion into intestinal wall and extraintestinal mesenteric lymph nodes (MLN). The results showed that pretreatment of rats with anti-CINC antibody attenuated the thermal injury-induced enhancement in [Ca2+](i) responses i n neutrophils both in the basal and Formyl-Met-Leu-Phe stimulated condition s. Moreover, treatment with the CINC antibody decreased neutrophil infiltra tion into the gut and attenuated thermal injury-caused translocation of bac teria into the MLN. (C) 2000 Elsevier Science B.V. All rights reserved.