Tulathromycin promotes phagocytosis and mediates IL‐8, NO, and PGE2 secretion in bovine monocyte‐derived macrophages

Abstract

Tulathromycin (TUL) is an antibiotic used in the treatment of bovine respiratory disease, whose efficacy may be due to anti‐inflammatory capabilities. In the lung, macrophage secretion of inflammatory mediators interleukin (IL)‐8, nitric oxide (NO), and prostaglandin E2 (PGE2), as well as phagocytosis apoptotic neutrophils, are imperative mechanisms contributing to the resolution of inflammation. Effects of TUL on modulation of macrophage function have yet to be investigated.Aim1) to determine the effects of TUL on neutrophil phagocytosis by bovine monocyte‐derived macrophages (BMDM) and 2) to examine the direct effects of TUL on the expression of cyclo‐oxygenase‐2 (COX‐2) and secreted levels of IL‐8, PGE2, and NO.ResultsLight microscopy suggested that TUL‐induced neutrophil apoptosis is associated with increased neutrophil phagocytosis by BMDM. Western blotting showed TUL increases expression of COX‐2, while ELISA and Greiss reaction showed that TUL decreased secreted levels of IL‐8, and NO and increased levels of PGE2 in lipopolysaccharide (LPS)‐stimulated BMDM.ConclusionTUL promotes macrophage phagocytosis of apoptotic neutrophils and modulates COX‐2 protein expression and secreted levels of IL‐8, NO, and PGE2 in LPS‐stimulated BMDM. Together, the findings illustrate novel mechanisms through which an antibiotic may deliver anti‐inflammatory benefits. This work is supported by NSERC.