title: Functional alterations of splenocytes in severe acute pancreatitis.
abstract: OBJECTIVE
  Recently, the concept of "Th1 (T helper cell type 1)/Th2 (T helper cell type 2) balance" was introduced for understanding the pathophysiologic response during septic or preseptic conditions. To clarify unknown Th1/Th2 balance during acute pancreatitis, functional alterations of the splenocyte were investigated in rat experimental severe acute pancreatitis.
  
  
  METHODS
  Spleens were removed from rats 24 h after the induction of severe necrotizing pancreatitis by retrograde injection of 3% sodium deoxycholate. Total splenocytes were harvested and cultured in the presence or absence of concanavalin A (con A) for 24 h. Proliferative capacities and cytokine-releasing capacities were evaluated.
  
  
  RESULTS
  In splenocytes harvested 24 h after the induction of pancreatitis, proliferative capacity with con A stimulation was significantly lower than that of sham operation. Interleukin-2 (IL-2) release with con A stimulation and interferon-gamma release with or without con A stimulation were significantly decreased in splenocytes from the rats with pancreatitis compared with those from sham operation. Interleukin-10 (IL-10) release with con A stimulation was also significantly decreased in splenocytes from the rats with pancreatitis compared with those from sham operation. The IL-2/IL-10 concentration ratio secreted by the splenocytes from the rats with pancreatitis was significantly lower than that from those undergoing the sham operation.
  
  
  CONCLUSIONS
  These results suggest that splenocyte function is markedly suppressed in experimental severe acute pancreatitis and that Th1/Th2 balance tends to Th1 suppression as a whole. Dysfunction of lymphocytes including splenocytes may play a certain role in the development of subsequent septic complications in this disease.
authors.affiliation: First Department of Surgery, Kobe University School of Medicine, Kobe 650-0017, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Ueda
authors.forename: Yoshifumi
authors.initials: Y
authors.lastname: Takeyama
authors.forename: Takeo
authors.initials: T
authors.lastname: Yasuda
authors.forename: Kozo
authors.initials: K
authors.lastname: Takase
authors.forename: Junsuke
authors.initials: J
authors.lastname: Nishikawa
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Kuroda
mesh_terms: D000208:Acute Disease; D000818:Animals; D000906:Antibodies; D002455:Cell Division / Q000276:immunology; D007150:Immunohistochemistry; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D007376:Interleukin-2 / Q000032:analysis / Q000276:immunology / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D008297:Male; D010195:Pancreatitis / Q000276:immunology*; D051381:Rats; D017208:Rats, Wistar; D012720:Severity of Illness Index; D013154:Spleen / Q000166:cytology* / Q000276:immunology* / Q000378:metabolism; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D000906:Antibodies; D007376:Interleukin-2; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma