The role of nitric oxide in inflammatory reactions

Abstract

Nitric oxide (NO) was initially described as a physiological mediator of endothelial cell relaxation, an important role in hypotension. NO is an intercellular messenger that has been recognized as one of the most versatile players in the immune system. Cells of the innate immune system--macrophages, neutrophils and natural killer cells--use pattern recognition receptors to recognize the molecular patterns associated with pathogens. Activated macrophages then inhibit pathogen replication by releasing a variety of effector molecules, including NO. In addition to macrophages, a large number of other immune-system cells produce and respond to NO. Thus, NO is important as a toxic defense molecule against infectious organisms. It also regulates the functional activity, growth and death of many immune and inflammatory cell types including macrophages, T lymphocytes, antigen-presenting cells, mast cells, neutrophils and natural killer cells. However, the role of NO in nonspecific and specific immunity in vivo and in immunologically mediated diseases and inflammation is poorly understood. This Minireview will discuss the role of NO in immune response and inflammation, and its mechanisms of action in these processes.

Biological activity and toxicity of the Chinese herb Magnolia officinalis Rehder & E. Wilson (Houpo) and its constituents

“…Synthesised by many cell types involved in immunity and inflammation, through the inducible NO· synthase (iNOS), in response to pro-inflammatory cytokines and bacterial LPS, NO· is a major defense molecule, toxic against infectious organisms, and is a key player in the pathogenesis of a variety of inflammatory diseases (Lee et al, 2011). NO· notably regulates the functional activity, growth and death of many immune and inflammatory cell types including macrophages, T lymphocytes, antigen-presenting cells, mast cells, neutrophils, and natural killer cells (Coleman, 2001;Ricciardolo et al, 2004;Garcia and Stein, 2006;Tripathi et al, 2007). The factor NF-κB (Section 3.1) promotes the transcription of genes involved in pro-inflammatory responses.…”

Stimulation of Unprimed Macrophages with Immune Complexes Triggers a Low Output of Nitric Oxide by Calcium-dependent Neuronal Nitric-oxide Synthase

“…However, the generation of low output NO by macrophages is emerging as an important event in the initiation or modulation of inflammatory responses. At lower levels, secreted NO plays an important role as a secondary messenger and can influence a wide variety of physiological and pathophysiological processes (11). Some processes affected by macrophage-derived NO include vasodilation, neural transmission, osteoclast homeostasis, and stimulation of other immune cells for enhanced inflammatory responses (12)(13)(14)(15).…”

Effects of chitosan on nitric oxide production and inducible nitric oxide synthase activity and mRNA expression in weaned piglets

“…It is generated in various tissues from l-arginine by different forms of nitric oxide synthase: neuronal NOS, iNOS, and endothelial NOS (Nathan and Stuehr 1990). As a toxic defense molecule against infectious organisms, NO regulates the functional activity, growth, and death of many immune and inflammatory cells, including macrophages, T lymphocytes, antigen presenting cells, mast cells, neutrophils, and natural killer cells (Tripathi et al 2007). Inducible NOS, which was originally discovered in activated macrophages and predominantly functions in the innate immune system, is expressed in dendritic cells, NK cells, monocytes, macrophages among other immune cells (Bogdan 2001;David et al 2012).…”