title: Seasonal variations in inflammatory responses to sepsis and  stress in mice.
abstract: OBJECTIVE
  In this study, we analyzed seasonal variations of immunoreactivity using a model of septic shock and a model of immunosuppression induced by chronic stress in mice.
  
  
  METHODS
  Retrospective comparative study using animals of experiments performed between 2001 and 2006 to identify seasonal variations in inflammatory responsiveness of mice.
  
  
  METHODS
  University-based research laboratory.
  
  
  METHODS
  C57Bl/6 mice and BALB/c mice.
  
  
  METHODS
  For analyzing septic shock, we used the hyperinflammatory model of colon ascendens stent peritonitis. Immunosuppression was induced by 4.5 days of intermittent combined acoustic and restraint stress.
  
  
  RESULTS
  We show that mice kept with 12:12-hr light/dark rhythm had an enhanced risk to die of experimentally-induced hyperinflammatory peritonitis performed in summer or autumn compared with the other seasons. This finding was associated with an exaggerated proinflammatory response of C57Bl/6 mice in summer or autumn compared with moderate inflammatory reactivity in winter and spring. Consistent with these results, we report that the severity of a stress-induced immunosuppression is less pronounced in BALB/c mice that were exposed to chronic psychological stress in the summer compared with exposure in winter. Coping with chronic psychological stress of these animals was correlated with less pronounced corticosterone release, less severe lymphocytopenia, and a lower ex vivo inducibility of interleukin-10, thereby attenuating a stress-mediated immunosuppressive state. Mice subjected to chronic stress in the summer season showed increased coping compared with mice that were stressed in the winter season.
  
  
  CONCLUSIONS
  Our results suggest that seasonal changes of the host's hypothalamus-pituitary-adrenal axis response influence the risk of infection and the susceptibility to stress, which interferes with the outcome after infection.
authors.affiliation: Departments of Immunology, University of Greifswald, Greifswald, Germany.
authors.forename: Cornelia
authors.initials: C
authors.lastname: Kiank
authors.forename: Pia
authors.initials: P
authors.lastname: Koerner
authors.forename: Wolfram
authors.initials: W
authors.lastname: Kessler
authors.forename: Tobias
authors.initials: T
authors.lastname: Traeger
authors.forename: Stefan
authors.initials: S
authors.lastname: Maier
authors.forename: Claus-Dieter
authors.initials: CD
authors.lastname: Heidecke
authors.forename: Christine
authors.initials: C
authors.lastname: Schuett
mesh_terms: D000818:Animals; D005260:Female; D007249:Inflammation / Q000209:etiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D012621:Seasons; D012772:Shock, Septic / Q000276:immunology* / Q000401:mortality; D013315:Stress, Psychological / Q000276:immunology*