title: [Suppressed increase of C3 receptors on polymorphonuclear leukocytes by stimulation with C5a in diabetes mellitus].
abstract: This study was undertaken to clarify the susceptibility to infection of patients with diabetes mellitus. The complement system is activated through the classical and/or the alternative pathways to produce many kinds of anaphylatoxins in the inflammatory process. One of the anaphylatoxins, C5a, possesses both the strong biological activity of a chemotactic factor and the increasing effect of CR1 and CR3 expression on polymorphonuclear leukocytes (PMNs). It is well known that the complement receptors, CR1 and CR3, on PMNs play important roles in the phagocytosis. We studied the changes of the expression of these receptors on PMNs in non-insulin dependent diabetes mellitus after the stimulation with recombinant human C5a. PMNs from 11 patients with non-insulin dependent diabetes mellitus and 11 normal controls were tested. There was no significant difference of CR1 and CR3 expression on PMNs after the addition of 10 ng/ml C5a between patients with diabetes mellitus and normal controls. However, by the stimulation with 50 ng/ml C5a, the increase of the CR3 expression on PMNs of patients with diabetes mellitus was significantly smaller than normal controls (p < 0.02). The increase of the expression of CR1 on PMNs was not significantly different the two groups. It is suggested that the small increase of the CR3 expression on PMNs by the stimulation with C5a is one of the factors of the susceptibility to infection in patients with diabetes mellitus.
authors.affiliation: First Department of Internal Medicine, Kyoto Prefectural University of Medicine.
authors.forename: T
authors.initials: T
authors.lastname: Doi
authors.forename: S
authors.initials: S
authors.lastname: Takemura
authors.forename: M
authors.initials: M
authors.lastname: Ueda
authors.forename: M
authors.initials: M
authors.lastname: Deguchi
authors.forename: N
authors.initials: N
authors.lastname: Ichio
authors.forename: K
authors.initials: K
authors.lastname: Yanagida
authors.forename: H
authors.initials: H
authors.lastname: Onodera
authors.forename: S
authors.initials: S
authors.lastname: Sugino
authors.forename: M
authors.initials: M
authors.lastname: Kondo
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002478:Cells, Cultured; D015936:Complement C5a / Q000502:physiology*; D003924:Diabetes Mellitus, Type 2 / Q000276:immunology* / Q000378:metabolism; D004198:Disease Susceptibility; D005260:Female; D006801:Humans; D008297:Male; D008565:Membrane Proteins; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology*; D011951:Receptors, Complement / Q000378:metabolism*
chemical_list: D008565:Membrane Proteins; D011951:Receptors, Complement; C085567:complement C3a receptor; D015936:Complement C5a