title: Suppression of cellular immunity by surgical stress.
abstract: BACKGROUND
  Suppression of cellular immunity is one of the host responses to surgical stress. In cancer patients this immunosuppression may accelerate the growth and metastasis of residual cancer cells, so it is desirable to restrict immunosuppression by surgical stress to a minimum. However, the extent and duration of immunosuppression caused by operations on gastrointestinal cancer, as well as the mechanisms involved, have not been determined.
  
  
  METHODS
  To clarify these points, we investigated immunocyte function and measured the blood levels of hormones, cytokines, and acute phase reactants from before to after operation in 20 patients with stage I gastrointestinal cancer.
  
  
  RESULTS
  In patients exposed to surgical stress, peripheral blood lymphocyte numbers and function were suppressed until at least 2 weeks postoperatively. This immunosuppression was mainly due to a decrease of helper-inducer T cells, cytotoxic T cells, natural killer cells, and interleukin-2 receptor-positive cells, as well as an increase of suppressor T cells. In addition, hypersecretion of cortisol and overproduction of immunosuppressive acidic protein were observed.
  
  
  CONCLUSIONS
  Cellular immunosuppression by surgical stress was mainly due to an increase of lymphocyte subsets that depress cellular immunity coupled with a decrease of the subsets that promote it. Overproduction of cortisol and immunosuppressive acidic protein in response to surgical stress may play an important role in the development of immunosuppression.
authors.affiliation: Department of Surgery, Tokyo Women's Medical University, Daini Hospital, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Ogawa
authors.forename: M
authors.initials: M
authors.lastname: Hirai
authors.forename: T
authors.initials: T
authors.lastname: Katsube
authors.forename: M
authors.initials: M
authors.lastname: Murayama
authors.forename: K
authors.initials: K
authors.lastname: Hamaguchi
authors.forename: T
authors.initials: T
authors.lastname: Shimakawa
authors.forename: Y
authors.initials: Y
authors.lastname: Naritake
authors.forename: T
authors.initials: T
authors.lastname: Hosokawa
authors.forename: T
authors.initials: T
authors.lastname: Kajiwara
mesh_terms: D000209:Acute-Phase Proteins / Q000032:analysis; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D000368:Aged; D002395:Catecholamines / Q000097:blood; D016207:Cytokines / Q000097:blood; D005770:Gastrointestinal Neoplasms / Q000276:immunology / Q000601:surgery*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007108:Immune Tolerance; D008213:Lymphocyte Activation; D008875:Middle Aged; D013312:Stress, Physiological / Q000276:immunology*
chemical_list: D000209:Acute-Phase Proteins; D002395:Catecholamines; D016207:Cytokines; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone