Intra-abdominal sepsis alters tumor necrosis factor-alpha and interleukin-1 beta binding to human neutrophils.
OBJECTIVE
To determine the effects of intraabdominal sepsis on polymorphonuclear leukocyte tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) receptor expression.


METHODS
Prospective, randomized comparison between patients undergoing elective colon surgery vs. patients with intra-abdominal sepsis.


METHODS
Tertiary-care center with all patients with intra-abdominal sepsis in a surgical ICU environment.


METHODS
Group 1 (n = 7) represents control patients who underwent elective colon surgery without intra-abdominal sepsis. Group 2 (n = 10) represents patients with intra-abdominal sepsis.


RESULTS
Polymorphonuclear leukocyte TNF-alpha and IL-1 beta receptor expression +/- stimulation of the oxidative burst was measured using 125I TNF-alpha and 125I IL-1 beta. Superoxide anion production and candicidal activity were measured in the presence of TNF-alpha and IL-1 beta. Group 2 patients expressed fewer TNF-alpha and IL-1 beta receptors on their cell surface, and stimulation of oxidative burst reduced TNF-alpha and IL-1 beta receptor expression in group 2 more than in group 1. Diminished TNF-alpha and IL-1 beta binding reduced superoxide anion production by group 2 polymorphonuclear leukocytes. Decreased TNF-alpha binding but not IL-1 beta, reduced polymorphonuclear leukocyte candicidal activity by group 2 polymorphonuclear leukocytes.


CONCLUSIONS
a) Intra-abdominal sepsis reduces polymorphonuclear leukocyte TNF-alpha and IL-1 beta receptor expression. b) Expression of these surface receptors is altered by stimulation of the polymorphonuclear leukocyte oxidative burst. c) Diminished TNF-alpha and IL-1 beta receptor expression is associated with functional impairments in polymorphonuclear leukocyte activity.
Simms
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Division of Surgical Research, Rhode Island Hospital, Providence 02903.
D'Amico
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D000005:Abdomen; D000368:Aged; D005260:Female; D016905:Gram-Negative Bacterial Infections / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D007108:Immune Tolerance; D007375:Interleukin-1 / Q000276:immunology / Q000378:metabolism*; D008024:Ligands; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism*; D011446:Prospective Studies; D011956:Receptors, Cell Surface / Q000096:biosynthesis* / Q000276:immunology / Q000378:metabolism; D011971:Receptors, Immunologic / Q000096:biosynthesis* / Q000276:immunology / Q000378:metabolism; D017472:Receptors, Interleukin-1; D018124:Receptors, Tumor Necrosis Factor; D016897:Respiratory Burst / Q000276:immunology; D013481:Superoxides / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000378:metabolism*
D007375:Interleukin-1; D008024:Ligands; D011956:Receptors, Cell Surface; D011971:Receptors, Immunologic; D017472:Receptors, Interleukin-1; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D013481:Superoxides