title: Effects of acute cold stress on phagocytosis of apoptotic cells: the role of corticosterone.
abstract: OBJECTIVE
  Stress can alter many aspects of the immune response, and many studies have been conducted on the effects of stress on inflammatory processes, but little is known about its influence on the resolution of inflammation in tissue homeostasis, which includes the clearance of apoptotic cells by macrophages in a non-phlogistic way. In the present study, we investigated the effect of acute cold stress on the phagocytosis of apoptotic cells by macrophages.
  
  
  METHODS
  Mice were submitted to acute cold stress (4 degrees C for 4 h) and the capacity of peritoneal macrophages to phagocyte apoptotic thymocytes and to secrete anti-inflammatory cytokines was evaluated. Plasma corticosterone and catecholamine levels were investigated to assess their effect on the phagocytic capacity of macrophages in vitro.
  
  
  RESULTS
  We showed that acute cold stress decreases phagocytosis of apoptotic cells at the inflammatory site by lipopolysaccharide-activated macrophages but did not affect resting macrophages. The inhibitory effect on phagocytosis is accompanied by a reduced level of TGF-beta and higher IL-10 secretion. After stress, plasma concentrations of corticosterone increased 6-fold, epinephrine 2-fold and norepinephrine 1.7-fold compared to control mice. In vitro experiments showed that the decrease in phagocytosis after stress could be attributed, at least in part, to the effects of corticosterone; epinephrine and norepinephrine had no effect.
  
  
  CONCLUSIONS
  The current study shows that acute cold stress decreases phagocytosis of apoptotic cells from an inflammatory environment by macrophages, and this inhibition is mediated by the intracellular glucocorticoid receptor.
authors.affiliation: Department of Biochemistry and Immunology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil. renata.sesti@gmail.com
authors.forename: Renata
authors.initials: R
authors.lastname: Sesti-Costa
authors.forename: Gyselle Chrystina
authors.initials: GC
authors.lastname: Baccan
authors.forename: Silvana
authors.initials: S
authors.lastname: Chedraoui-Silva
authors.forename: Bernardo
authors.initials: B
authors.lastname: Mantovani
mesh_terms: D000208:Acute Disease; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000276:immunology*; D002395:Catecholamines / Q000378:metabolism; D003080:Cold Temperature / Q000009:adverse effects; D003345:Corticosterone / Q000378:metabolism*; D004195:Disease Models, Animal; D004837:Epinephrine / Q000378:metabolism; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology; D018836:Inflammation Mediators / Q000494:pharmacology; D016753:Interleukin-10 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D009638:Norepinephrine / Q000378:metabolism; D010587:Phagocytosis / Q000276:immunology*; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D013312:Stress, Physiological / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000378:metabolism; D015854:Up-Regulation / Q000276:immunology
chemical_list: D002395:Catecholamines; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D011965:Receptors, Glucocorticoid; D016212:Transforming Growth Factor beta; D016753:Interleukin-10; D003345:Corticosterone; D009638:Norepinephrine; D004837:Epinephrine