Nitric oxide as a regulator of inflammatory processes

Wallace, John L.

doi:10.1590/s0074-02762005000900002

Cited by 117 publications

(75 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Even if MPO is an important part of the antimicrobial defence, the increased formation of hypohalous acid may aggravate tissue damage during the inflammation processes. In this context, we could hypothesize that NO serves as a negative regulator of MPO activity, in agreement with previous data demonstrating that NO inhibits many iron-containing enzymes [32].…”

Section: Discussionsupporting

confidence: 92%

“…The NO production by these cells in the bone microenvironment could regulate the osteoclast function, and, in addition, both PMN and platelets may also serve as targets for NO action. In fact, NO can down-regulate neutrophil aggregation and secretion and may protect from the damage induced by the potent reactive oxygen metabolites produced by PMN themselves, as previously described, since it has been reported to be a free radical scavenger [31][32][33]. Moreover, NO might inhibit platelet aggregation and adhesion, thus having an anti-inflammatory action [34].…”

Section: Discussionmentioning

confidence: 69%

See 1 more Smart Citation

The effects of disodium pamidronate on human polymorphonuclear leukocytes and platelets: An in vitro study

Salvolini¹,

Orciani²,

Vignini

et al. 2009

Cellular and Molecular Biology Letters

View full text Add to dashboard Cite

Recent reports have indicated that, as well as having antiresorptive effects, bisphosphonates could have an application as anti-inflammatory drugs. Our aim was to investigate whether this anti-inflammatory action could be mediated by the nitric oxide (NO) released by the leukocytes migrating to the site of inflammation. In particular, we investigated in vitro the intracellular calcium concentration ([Ca 2+ ] i ), the level of NO released by PMN and platelets, and the PMN myeloperoxidase activity after incubation with disodium pamidronate, since there was a postulated modulatory effect of this aminosubstituted bisphosphonate on leukocytes both in vitro and in vivo. Our data shows that the pamidronate treatment provoked a significant increase in the [Ca 2+ ] i parallel to the enhancement in NO release, suggesting a possible activation of constitutive nitric oxide synthase, while the myeloperoxidase activity was significantly reduced. In conclusion, we hypothesized that treatment with pamidronate could stimulate NO-production by cells present near the bone compartment, thus constituting a protective mechanism against bone resorption occurring during inflammation. In addition, PMN-and platelet-derived NO could act as a negative feed-back signal to restrict the inflammatory processes.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 69%

The effects of disodium pamidronate on human polymorphonuclear leukocytes and platelets: An in vitro study

Salvolini¹,

Orciani²,

Vignini

et al. 2009

Cellular and Molecular Biology Letters

View full text Add to dashboard Cite

show abstract

“…iNOS plays an important role in the inflammatory reaction by producing excessive NO (Renard and Raes, 1999). iNOS is involved in complex biological processes and is a wellknown host innate immune and inflammatory response to diverse pathogens (Wallace, 2005). COX-2 is another important enzyme induced by several stimuli such as LPS, cytokines, and growth factors and is expressed in response to inflammation.…”

Section: Resultsmentioning

confidence: 99%

Inhibitory Effect of Sargauum fulvellum Ethanolic Extract on LPS-Induced Inflammatory Reaction in RAW 264.7 Mouse Macrophages

Kim¹,

Kim²,

Jeong³

et al. 2013

Journal of Applied Biological Chemistry

View full text Add to dashboard Cite

Recently, algae has been considered as a potential antiinflammatory source due to its distinctive habitat environment exposing to light and high oxygen concentration. In present study, anti-inflammatory effect of brown alga, Sargassum fullvellum ethanol extract (SFEE), was examined. SFEE inhibited not only the production of nitric oxide and pro-inflammatory cytokines (IL-6, IL-1β, TNF-α) but also the expression of inducible nitric oxide synthase and cyclooxygenase 2 in LPS-induced RAW 264.7 cells without affecting cell viability. SFEE also suppressed the expression of nuclear factor kappa B (NF-κB), suggesting that SFEE could affect the expression of inflammation related cytokines and proteins through the regulation of NF-κB. Furthermore, formation of edema of the ear was 40% lower in mice treated with the highest dose (250 mg/kg) of SFEE than in the control mice. Thus, our study showed that SFEE may be a potential therapeutic anti-inflammatory drug.

show abstract

“…Nitric oxide is a key immunoregulatory molecule (reviewed in references 8,9). It plays a role in regulating T cell activation through ras/ERK signaling (10) and exerts anti-inflammatory effects by inhibiting NF-B (reviewed in references 8,9).…”

mentioning

confidence: 99%

S-Nitrosoglutathione Reductase Deficiency Confers Improved Survival and Neurological Outcome in Experimental Cerebral Malaria

et al. 2017

View full text Add to dashboard Cite

Artesunate remains the mainstay of treatment for cerebral malaria, but it is less effective in later stages of disease when the host inflammatory response and blood-brain barrier integrity dictate clinical outcomes. Nitric oxide (NO) is an important regulator of inflammation and microvascular integrity, and impaired NO bioactivity is associated with fatal outcomes in malaria. Endogenous NO bioactivity in mammals is largely mediated by S-nitrosothiols (SNOs). Based on these observations, we hypothesized that animals deficient in the SNO-metabolizing enzyme, S-nitrosoglutathione reductase (GSNOR), which exhibit enhanced S-nitrosylation, would have improved outcomes in a preclinical model of cerebral malaria. GSNOR knockout (KO) mice infected with Plasmodium berghei ANKA had significantly delayed mortality compared to WT animals (P Ͻ 0.0001), despite higher parasite burdens (P Ͻ 0.01), and displayed markedly enhanced survival versus the wild type (WT) when treated with the antimalarial drug artesunate (77% versus 38%; P Ͻ 0.001). Improved survival was associated with higher levels of protein-bound NO, decreased levels of CD4 ϩ and CD8 ϩ T cells in the brain, improved blood-brain barrier integrity, and improved coma scores, as well as higher levels of gamma interferon. GSNOR KO animals receiving WT bone marrow had significantly reduced survival following P. berghei ANKA infection compared to those receiving KO bone barrow (P Ͻ 0.001). Reciprocal transplants established that survival benefits of GSNOR deletion were attributable primarily to the T cell compartment. These data indicate a role for GSNOR in the host response to malaria infection and suggest that strategies to disrupt its activity will improve clinical outcomes by enhancing microvascular integrity and modulating T cell tissue tropism.

show abstract

Nitric oxide as a regulator of inflammatory processes

Abstract: Nitric oxide (NO)

Cited by 117 publications

References 47 publications

The effects of disodium pamidronate on human polymorphonuclear leukocytes and platelets: An in vitro study

The effects of disodium pamidronate on human polymorphonuclear leukocytes and platelets: An in vitro study

Inhibitory Effect of Sargauum fulvellum Ethanolic Extract on LPS-Induced Inflammatory Reaction in RAW 264.7 Mouse Macrophages

S-Nitrosoglutathione Reductase Deficiency Confers Improved Survival and Neurological Outcome in Experimental Cerebral Malaria

Contact Info

Product

Resources

About