Open AccessTumour necrosis factor production and cell‐mediated immunityin anorexia nervosa
Author(s) -
SCHATTNER A.,
STEINBOCK M.,
TEPPER R.,
SCHONFELD A.,
VAISMAN N.,
HAHN T.
Publication year - 1990
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1990.tb05127.x
Subject(s) - phytohaemagglutinin , peripheral blood mononuclear cell , tumor necrosis factor alpha , medicine , endocrinology , cytokine , lipopolysaccharide , pathophysiology , immunology , anorexia nervosa , stimulation , biology , in vitro , eating disorders , biochemistry , psychiatry
SUMMARY Fourteen patients with anorexia nervosa (AN) were studied for the production of tumour necrosisfactor (TNF), the activation of the interferon (IFN) system and cell‐mediated cytotoxicity (CMC)and the results were compared with 16 age‐matched healthy women. AN patients had significantlyincreased spontaneous TNF production by peripheral blood mononuclear cells (PBMC) in vitro (16 ± 5 U/ml versus 4 ± 3 U/ml in the control group; P < 005), although no TNF was detectable in theplasma from either group. TNF production in vitro , following stimulation of PBMC byphytohaemagglutinin (PHA) or tumour cells, was similar in AN patients and controls; however, lipopolysaccharide (LPS) induced TNF production was found to be lower in AN ( P <0.1). CMC wassignificantly lower in AN patients (4 ± 2 versus 10 ± 3 in controls, expressed as lytic units/10 6 cells;P<0.05), but no difference could be found between AN and controls in IFN activity as reflected bythe level of the IFN‐induced enzyme 2′‐5′oligoadenylate synthetase (2‐5A) in PBMC. Beta‐endorphins in the plasma were higher in the AN group ( P < 0.05) but these levels could not becorrelated to those of lFN, CMC or TNF. Defective CMC and increased TNF production by PBMCin patients with anorexia nervosa may possibly result from the nutritional deficiencies andneuroendocrine abnormalities associated with the disease, and may contribute to the pathophysiology of AN.