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Retinoid derivatives offer anti‐inflammatory benefits by promoting neutrophil apoptosis and inhibiting proinflammatory mediator production in a model of bovine respiratory disease
Author(s) -
Duquette Stephanie,
Fischer Carrie D,
Feener Troy D,
Barreda Daniel R,
Morck Douglas W,
Nickerson James,
Buret Andre G
Publication year - 2013
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.27.1_supplement.356.4
Subject(s) - proinflammatory cytokine , retinoid , apoptosis , inflammation , retinoic acid , immunology , context (archaeology) , mediator , medicine , chemistry , biology , cell culture , biochemistry , paleontology , genetics
Clearance of apoptotic neutrophils (PMN) following infection is critical for the resolution of inflammation. Despite demonstrating immunomodulatory properties, the effects of retinoids in PMN in the context of an inflammatory response remain unknown. Objective to evaluate the immunomodulatory properties of two retinoids, oxidatively‐transformed carotene‐β (OxC‐β) and retinoic acid (RA) in a model of Mannheimia haemolytica ‐induced bovine respiratory disease, which is characterized by severe inflammation. Results in vitro , RA and OxC‐β induced caspase‐and time‐dependent apoptosis, but not necrosis, in bovine PMN, but not epithelial cells or fibroblasts. Neither RA nor OxC‐β affected PMN function. In M. haemolytica ‐infected calves (2×10 7 CFU), animals that received a 28‐day dietary OxC‐β treatment (10 mg/kg) had elevated apoptotic leukocytes and reduced LTB 4 levels in their lower airways 3h post‐infection vs infected‐untreated calves. Conclusion RA and OxC‐β promote cell‐specific apoptosis and inhibit the production of pro‐inflammatory LTB 4 , both mechanisms that promote the resolution of inflammation, thereby suggesting an anti‐inflammatory role for retinoid derivatives. Supported by NSERC and AIHS.