Lymphocyte subsets and cellular immunity in patients with chronic pancreatitis.
BACKGROUND
An abnormal immune response may play a pathogenetic role in chronic pancreatitis. However, to date characterization of the systemic immunological changes in patients with chronic pancreatitis has not been undertaken.


METHODS
Lymphocyte phenotypes and proliferation ((3)H-thymidine) after stimulation with mitogens and interleukin-2 were studied in peripheral mononuclear cells from 11 patients with chronic pancreatitis (alcohol-induced n = 6; idiopathic pancreatitis n = 5). The natural killer cell activity was investigated in a (51)Cr release cytotoxicity assay. In vitro cytokine release of stimulated mononuclear cells was measured.


RESULTS
Flow cytometric studies showed a significant decrease in the percentage of circulating CD8+, CD56+ and CD25+ cells in patients with chronic pancreatitis independent of the etiology. Comparing all patients with chronic pancreatitis to controls, the proliferation rate was not significantly increased, but patients with pain (n = 5) showed increased proliferation in comparison to patients without pain (n = 6). No significant difference in natural killer cytotoxicity was observed. The in vitro release of tumor necrosis factor-alpha and interleukin-10 by stimulated mononuclear cells was increased.


CONCLUSIONS
Chronic pancreatitis is accompanied by systemic immune dysregulation. The observed changes in peripheral mononuclear cells reveal additional evidence that the cell-mediated immune response may contribute to the development of pain and tissue destruction in chronic pancreatitis.
Ockenga
J
J
Department of Gastroenterology and Hepatology, Medical School of Hannover, Germany. Ocken@aol.com
Jacobs
R
R
Kemper
A
A
Benschop
R J
RJ
Schmidt
R E
RE
Manns
M P
MP
D000328:Adult; D002908:Chronic Disease; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007111:Immunity, Cellular; D016131:Lymphocyte Subsets; D008297:Male; D008875:Middle Aged; D010146:Pain / Q000209:etiology; D010195:Pancreatitis / Q000276:immunology* / Q000473:pathology; D010641:Phenotype