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Tulathromycin promotes phagocytosis and mediates IL‐8, NO, and PGE2 secretion in bovine monocyte‐derived macrophages
Author(s) -
Beatty Jennifer Kathleen,
Fischer Carrie D,
Morck Douglas W,
Lucas Merlyn J,
Robb Edward J,
Buret Andre G
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.751.9
Subject(s) - phagocytosis , lipopolysaccharide , macrophage , secretion , monocyte , prostaglandin e2 , apoptosis , chemistry , microbiology and biotechnology , interleukin 8 , immunology , inflammation , nitric oxide , biology , in vitro , endocrinology , biochemistry
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 E 2 (PGE 2 ), 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. Aim 1) 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, PGE 2 , and NO. Results Light 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 PGE 2 in lipopolysaccharide (LPS)‐stimulated BMDM. Conclusion TUL promotes macrophage phagocytosis of apoptotic neutrophils and modulates COX‐2 protein expression and secreted levels of IL‐8, NO, and PGE 2 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.