Possible Role of Nitric Oxide in IgE-Mediated Allergic Cutaneous Reaction in Mice

Abstract

The role of nitric oxide (NO) in the development of allergic cutaneous reactions in mice was investigated. A biphasic cutaneous reaction composed of an immediate-phase edema and a late-phase edema was evoked by epicutaneous application of 2,4-dinitrofluorobenzene on the ear of mice passively sensitized with mouse anti-dinitrophenol monoclonal IgE. Two NO synthase inhibitors, L-N^G-nitroarginine methyl ester (L-NAME) and N^G-monomethyl-L-arginine, significantly inhibited both phases of the IgE-mediated biphasic cutaneous reaction. Simultaneous treatment with L-arginine attenuated the inhibitory effect of L-NAME. An NO donor, 3-morpholinosydononimine-N-ethylcarbamide, caused a potent edematous reaction in the mouse ear. Furthermore, L-NAME inhibited the cutaneous reactions caused by both interleukin-1β and tumor necrosis factor-α, putative mediators of the late-phase edema in the biphasic cutaneous reaction. These results indicate that a gaseous mediator, NO, participates, at least in part, in the development of ear edema in the IgE-mediated biphasic cutaneous reaction in mice.

Inducible Nitric Oxide Synthase Downmodulates Contact Hypersensitivity by Suppressing Dendritic Cell Migration and Survival

“…It has also been reported that an iNOS inhibitor exerted a suppressive effect on the CHS response to 2,4,6-trinitrochlorobenzene (TNCB) (Musoh et al, 1998), although this effect was limited to the first few hours of the response, and neither NO production, NO-expressing cells, nor NOS isoenzymes were identified. Thus, the mode of action of iNOS in CHS remains a matter of debate.…”

Effect of Y-24180, an antagonist at platelet-activating factor (PAF) receptors, on IgE-mediated cutaneous reactions in mice

“…The inhibition by WEB2086 also may support participation of PAF in the induction of the LPR. Recently, it has been known the involvement of nitric oxide (NO) in the biphasic cutaneous reactions [21] and of tumor necrosis factor-a (TNF-a) and interleukin-1b (IL-1b) in the LPR [12,22]. Although interaction between PAF and NO on mast cells is unknown, several PAF antagonists suppress the induction of NO synthase in macrophages [23].…”