title: Nitric oxide released from iNOS in polymorphonuclear leukocytes makes them deformable in an autocrine manner.
abstract: The objective of this study was to determine whether endogenous nitric oxide (NO) derived from reaction catalyzed by the inducible isoform of NO synthase (iNOS: NOS II) in polymorphonuclear leukocytes (PMNs) makes the PMNs deformable. Previous studies have shown that NO increases the deformability of PMNs and decreases the sequestration of PMNs in the lungs. However, there was little information regarding the effect of PMN-derived NO on the cells' deformability. In the present study PMNs were isolated from the blood of rats 24h after ip injection of saline (control) or lipopolysaccharide (LPS), and expression of iNOS in the PMNs of the LPS group was confirmed by immunocytochemistry. PMN deformability was evaluated by measuring the pressure generated during their passage through a microfilter at a constant flow rate. The nitrite/nitrate content of the solution in which the isolated PMNs were incubated was measured by the Griess method. In the control group, no iNOS was detectable in the PMNs, and the nitrite/nitrate level in the PMN incubation solution was low. Deformability was unchanged after incubation with specific iNOS inhibitor aminoguanidine, but decreased after incubation with N-formyl-methionyl-leucyl-phenyl-alanine. In the LPS group, PMN deformability was decreased compared to that of the control group. iNOS was detectable in the PMNs, and the deformability further decreased after incubation with aminoguanidine. These results suggest that endogenous NO generated during reactions catalyzed by iNOS in PMNs makes them deformable in an autocrine manner.
authors.affiliation: Department of Medicine, Kitasato University School of Medicine, Kitasato 1-15-1, Sagamihara, Kanagawa, Japan. hiro@kitasato-u.ac.jp
authors.forename: Hirosuke
authors.initials: H
authors.lastname: Kobayashi
authors.forename: Tailin
authors.initials: T
authors.lastname: Cui
authors.forename: Miyuki
authors.initials: M
authors.lastname: Ando
authors.forename: Ryuji
authors.initials: R
authors.lastname: Hataishi
authors.forename: Takao
authors.initials: T
authors.lastname: Imasaki
authors.forename: Hisashi
authors.initials: H
authors.lastname: Mitsufuji
authors.forename: Izumi
authors.initials: I
authors.lastname: Hayashi
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Tomita
mesh_terms: D000818:Animals; D019898:Autocrine Communication; D048429:Cell Size; D005374:Filtration; D006146:Guanidines / Q000494:pharmacology; D007150:Immunohistochemistry; D008070:Lipopolysaccharides / Q000494:pharmacology; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000166:cytology* / Q000201:enzymology* / Q000378:metabolism; D009569:Nitric Oxide / Q000096:biosynthesis / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II; D018583:Pliability; D051381:Rats; D017208:Rats, Wistar
chemical_list: D006146:Guanidines; D008070:Lipopolysaccharides; D009569:Nitric Oxide; D009240:N-Formylmethionine Leucyl-Phenylalanine; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; C004479:pimagedine