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Reduced secretion of IL‐lβ by peritoneal cells from patients on continuous ambulatory peritoneal dialysis
Author(s) -
HART P. H.,
JONES C. A.,
L.JONES K.,
FINLAYJONES J.J.
Publication year - 1993
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.1993.10
Subject(s) - continuous ambulatory peritoneal dialysis , medicine , peritonitis , lipopolysaccharide , secretion , peritoneal dialysis , in vivo , peripheral blood mononuclear cell , monocyte , immunology , inflammation , in vitro , endocrinology , biology , biochemistry , microbiology and biotechnology
Summary The endogenous and lipopolysaccharide stimulated interleukin (IL)‐1β production in vitro by peritoneal monocytes/macrophages from patients on continuous ambulatory peritoneal dialysis (CAPD) was examined during episodes of infection and inflammation. Measurement of immunoreactive IL‐1β and bioactive IL‐1 in both supernatants and cell lysates after culture for 18 h revealed that these cells secreted a significantly lower proportion of total IL‐1 than that measured for elutriated blood monocytes. For the inflammatory peritoneal cells, the proportion of total IL‐1β that was cell‐associated resembled that reported for more differentiated pulmonary alveolar macrophages and for adherent monocytes cultured for 18 h prior to stimulation. A similar reduced ability to secrete IL‐1β was detected for unfractionated peritoneal cells from CAPD patients without peritonitis upon direct comparison with the IL‐1β production by blood mononuclear cells from the same patients. These results suggested that at a time when a pro‐inflammatory response by extravasated host monocytes/macrophages was required by CAPD patients with peritonitis, only a minor proportion of total IL‐1β would be available extracellularly. This study highlights the rapidity with which extravasated monocytes lose their ability to secrete IL‐lβ and raises the possibility that an important site of utilization of IL‐1β in vivo may be intracellular in its location.