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Review
. 2002 Jul;129(1):4-10.
doi: 10.1046/j.1365-2249.2002.01918.x.

Nitric oxide: a regulator of mast cell activation and mast cell-mediated inflammation

J W Coleman  1
Affiliations
Review

Nitric oxide: a regulator of mast cell activation and mast cell-mediated inflammation

J W Coleman. Clin Exp Immunol. 2002 Jul.

Abstract

Nitric oxide (NO) plays diverse roles in physiological and pathological processes. During immune and inflammatory responses, for example in asthma, NO is generated at relatively high and sustained levels by the inducible form of nitric oxide synthase (NOS-2). NOS-2 derived NO regulates the function, growth, death and survival of many immune and inflammatory cell types. In the case of mast cells, NO suppresses antigen-induced degranulation, mediator release, and cytokine expression. The action of NO on mast cells is time dependent, requiring several hours, and noncGMP mediated, most probably involving chemical modification of proteins. NO inhibits a number of mast cell-dependent inflammatory processes in vivo, including histamine mediated vasodilatation, vasopermeation and leucocyte-endothelial cell attachment. In human asthma and animal models of lung inflammation the role of NO is harder to define. However, although there are conflicting data, the balance of evidence favours a predominantly protective role for NO. Mimicking or targeting NO dependent pathways may prove to be a valuable therapeutic approach to mast cell mediated diseases.

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Figures

Fig. 1
Fig. 1
NO synthesis and reactions in immune and inflammatory cells. In response to inflammatory cytokines or bacterial lipopolysaccharide (LPS), the enzyme NOS-2 is expressed in many cell types to produce a sustained and high level production of NO. The NO is oxidized to RNOS of generic formula NOx. These nitrosate the thiol group in glutathione to produce S-nitrosoglutathione (GS-NO) or thiol groups in proteins to generate protein-S-NO. Under oxidative stress, NO interacts with superoxide (O2−) to produce the toxic peroxynitrite anion (OONO−).
Fig. 2
Fig. 2
The oxidative reactions and fate of NO.
Fig. 3
Fig. 3
Effects of GS-NO on antigen-induced cytokine mRNA expression in RBL-2H3 mast cells. The cells were incubated with the NO donor for different time periods, challenged with antigen, and the RNA extracted 2 h later for analysis by RNase protection assay. Experiment performed by R.D. Koranteng.
Fig. 4
Fig. 4
Inhibitory effects of NO on mast cell activation, mediator release and mast cell dependent vascular inflammatory events.
See this image and copyright information in PMC

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