title: Nitric oxide and infection: another view.
abstract: Nitric oxide (NO) has been nicknamed "murderer" and "mediator" because it has toxic and signaling properties. We review these two aspects of NO synthesis from the perspective of the clinical infectious disease specialist by considering the potential of NO as an endothelium-derived relaxing factor (EDRF) in inflammation and sepsis and its potential as an antimicrobial system. We deviate from observations in recent authoritative reviews and point to important species differences that make it unlikely that NO serves as an EDRF mediating inflammatory vasodilatation in humans or that NO synthesized by humans phagocytes has an antimicrobial function. We propose that in humans, No synthesis is more confined and compartmentalized than in certain other animal species, and therefore, unwelcome toxicity, vasodilatation, or disturbance of paracrine signaling mechanisms (i.e., modulation of phagocytic cell functions) are avoidable during inflammation.
authors.affiliation: Department of Medicine, University of Zürich Medical School, Switzerland.
authors.forename: G
authors.initials: G
authors.lastname: Schoedon
authors.forename: M
authors.initials: M
authors.lastname: Schneemann
authors.forename: R
authors.initials: R
authors.lastname: Walter
authors.forename: N
authors.initials: N
authors.lastname: Blau
authors.forename: S
authors.initials: S
authors.lastname: Hofer
authors.forename: A
authors.initials: A
authors.lastname: Schaffner
mesh_terms: D000818:Animals; D001424:Bacterial Infections / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D008264:Macrophages / Q000378:metabolism; D009569:Nitric Oxide / Q000096:biosynthesis / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
chemical_list: D009569:Nitric Oxide