Generation of nitric oxide by human neutrophils

Wright, Clifford D.; ̈lsch, Alexander Mu; Busse, Rudi; Oßwald, Hartmut

doi:10.1016/0006-291x(89)92506-0

Cited by 286 publications

(112 citation statements)

References 13 publications

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“…Our data indicate that nude mice macrophage populations cocultured with N592/IL-12/IL-15 produced NO and inhibited the growth of these tumor cells in vitro, through both NO-dependent and NO-independent mechanisms. In contrast, granulocytes, attracted at the tumor site by MIP-2 (murine equivalent of IL-8) (42), may also cooperate in NO production (42)(43)(44)(45), and in tumor destruction (46 -50). Both granulocytes and macrophages could also be responsible for the blood vessel injuries observed in N592/IL-12/IL-15 tumor (29,50).…”

Section: Discussionmentioning

confidence: 99%

The Combined Action of IL-15 and IL-12 Gene Transfer Can Induce Tumor Cell Rejection Without T and NK Cell Involvement

Carlo

Comes

Basso

et al. 2000

The Journal of Immunology

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The cooperative antitumor effects of IL-12 and IL-15 gene transfer were studied in the N592 MHC class I-negative small cell lung cancer cell line xenotransplanted in nude mice. N592 cells engineered to secrete IL-15 displayed a significantly reduced tumor growth kinetics, and a slightly reduced tumor take rate, while N592 engineered with IL-12 displayed only minor changes in their growth in nude mice. However, N592 cells producing both cytokines were completely rejected, and produced a potent local bystander effect, inducing rejection of coinjected wild-type tumor cells. N592/IL-12/IL-15 cells were completely and promptly rejected also in NK-depleted nude mice, while in granulocyte-depleted animals a slight delay in the rejection process was observed. Immunohistochemical analyses of the N592/IL-12/IL-15 tumor area in intact nude mice revealed the presence of infiltrating macrophages, granulocytes, and NK cells, and expression of inducible NO synthase and of secondary cytokines such as IL-1β, TNF-α, and IFN-γ, and at higher levels GM-CSF, macrophage-inflammatory protein-2, and monocyte chemoattractant protein-1. In NK cell-depleted nude mice, numerous macrophages and granulocytes infiltrated the tumor, and a strong expression of macrophage-inflammatory protein-2 and inducible NO synthase was also observed. Finally, macrophages cocultured with N592/IL-12/IL-15 produced NO in vitro, and inhibited tumor cell growth, further suggesting their role as effector cells in this model.

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Section: Discussionmentioning

confidence: 99%

The Combined Action of IL-15 and IL-12 Gene Transfer Can Induce Tumor Cell Rejection Without T and NK Cell Involvement

Carlo

Comes

Basso

et al. 2000

The Journal of Immunology

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“…NO can also be formed by an inducible isoenzyme in activated inflammatory cells, particularly macrophages (Marletta et Hibbs et al, 1988;Stuehr et al, 1989) and neutrophils (Rimele et al, 1988;Salvemini et al, 1989;Schmidt et al, 1989;Wright et al, 1989;McCall et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Time‐dependent enhancement or inhibition of endotoxin‐induced vascular injury in rat intestine by nitric oxide synthase inhibitors

László

Whittle

Moncada

1994

British J Pharmacology

135

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1 The effects of the nitric oxide (NO) synthase inhibitors, N0-nitro-L-arginine methyl ester (L-NAME) and NG-monomethyl-L-arginine (L-NMMA), on the vascular damage induced by the endotoxin, E. coli lipopolysaccharide (LPS), in the ileum and colon were investigated in the conscious rat over a 5 h period. 2 Administration of LPS (3 mg kg-', i.v.) increased ileal and colonic vascular injury after a lag period of 2 h, as determined by the leakage of radiolabelled albumin. 3 Administration of L-NAME (1-5 mg kg-', s.c.) concurrently with LPS, produced a dose-dependent increase in vascular albumin leakage in the intestinal tissues, when determined over a 5 h period. Vascular albumin leakage with LPS and L-NAME (5 mg kg-') was substantially increased after 1 h, reached maximal levels 3 h after administration, and then slowly declined. 4 L-NMMA (50 mg kg-1, s.c.), likewise elevated intestinal albumin leakage when administered concurrently with LPS, but this reached maximal levels after 1 h and rapidly declined over the subsequent 2 h. 5 In control rats, in the absence of LPS challenge, neither L-NAME (5 mg kg-', s.c.) nor L-NMMA (50 mg kg-', s.c.) increased intestinal vascular leakage of albumin over a 5 h period. 6 By contrast, when L-NAME (1-5 mg kg-', s.c.) or L-NMMA (12.5-50mg kg-', s.c.) was injected 3 h after LPS, a dose-dependent reduction in the LPS-provoked vascular albumin leakage was observed. 7 Pretreatment with L-arginine (300 mg kg-', s.c.) 15 min prior to the NO synthase inhibitors, reversed either the potentiation or the inhibition by L-NAME (5 mg kg-', s.c.) or L-NMMA (50 mg kg-', s.c.) of the LPS-induced intestinal vascular damage. 8 These findings indicate that initial suppression of the constitutive NO synthase by L-NAME or L-NMMA following challenge with LPS aggravates the acute vascular injury in the ileum and colon, suggesting a defensive role of NO. By contrast, the delayed administration of NO synthase inhibitors, at a time of known expression of the inducible NO synthase, provides protection against the subsequent damage to the intestinal vasculature.

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“…Recently, Wallerath et al [39] have demonstrated neuronal constitutive NOS in PMNs and inducible NOS in eosinophils. Several methods of determining NO · , including NMMA-inhibitable DCFH oxidation [33], NO-dependent oxidation of oxyHb to metHb [21,40], and formation of nitrite [41], have reported NO production by PMNs only in the presence of SOD or inhibitors of O 2 ·Ϫ synthesis. Depending on the type and level of PMN stimulation, O 2 ·Ϫ synthesis was 2-50 times NO · levels in these studies [21,41].…”

Section: Discussionmentioning

confidence: 99%

“…Several methods of determining NO · , including NMMA-inhibitable DCFH oxidation [33], NO-dependent oxidation of oxyHb to metHb [21,40], and formation of nitrite [41], have reported NO production by PMNs only in the presence of SOD or inhibitors of O 2 ·Ϫ synthesis. Depending on the type and level of PMN stimulation, O 2 ·Ϫ synthesis was 2-50 times NO · levels in these studies [21,41]. Because activated human PMNs produce both NO and O 2 ·Ϫ , which reacts at the rate of diffusion to produce ONOO Ϫ , it follows that NO · levels will increase as O 2 ·Ϫ levels are attenuated.…”

Section: Discussionmentioning

confidence: 99%

Effects of heme proteins on nitric oxide levels and cell viability in isolated PMNs: a mechanism of toxicity

Cassidy

Burleson

Delgado

et al. 2000

Journal of Leukocyte Biology

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Generation of nitric oxide by human neutrophils

Cited by 286 publications

References 13 publications

The Combined Action of IL-15 and IL-12 Gene Transfer Can Induce Tumor Cell Rejection Without T and NK Cell Involvement

The Combined Action of IL-15 and IL-12 Gene Transfer Can Induce Tumor Cell Rejection Without T and NK Cell Involvement

Time‐dependent enhancement or inhibition of endotoxin‐induced vascular injury in rat intestine by nitric oxide synthase inhibitors

Effects of heme proteins on nitric oxide levels and cell viability in isolated PMNs: a mechanism of toxicity

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