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Anti‐inflammatory benefits of retinoids: retinoic acid and oxidatively‐transformed β‐carotene induce neutrophil apoptosis and inhibit leukotriene B 4 synthesis
Author(s) -
Duquette Stephanie,
Fischer Carrie D,
Morck Douglas W,
Barreda Daniel R,
Nickerson James G,
Buret Andre G
Publication year - 2012
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.26.1_supplement.835.10
Subject(s) - proinflammatory cytokine , apoptosis , inflammation , retinoid , retinoic acid , immunology , context (archaeology) , innate immune system , biology , chemistry , immune system , biochemistry , gene , paleontology
Clearance of apoptotic neutrophils following infection is critical for the resolution of inflammation. Little is known about the effects of retinoid products (vitamin A derivatives) in innate immune cells in the context of an inflammatory response. Hypothesis Retinoic acid (RA) or oxidatively‐transformed β‐carotene (OxβC), a retinoid derivative, may have immuno‐modulatory benefits by promoting neutrophil apoptosis and inhibiting proinflammatory signaling. Aim To evaluate the effects of RA and OxβC in model of Mannheimia haemolytica ‐induced bovine respiratory disease, a disease associated with severe inflammation. Results In vitro, RA and OxβC dose‐dependently induced apoptosis, but not necrosis, in circulating bovine neutrophils, but not in epithelial cells. In M. haemolytica‐ challenged calves (2×10 7 CFU), animals that received a 28‐day dietary OxβC treatment (10 mg/kg) had elevated apoptotic leukocytes and reduced LTB 4 levels in their lower airways 3 h post‐infection versus infected‐untreated calves. Conclusion RA and OxβC promote cell‐selective apoptosis and inhibit the synthesis of proinflammatory LTB 4 , which in turn may confer yet unrecognized anti‐inflammatory benefits. Supported by NSERC.