An antioxidant agent prevents NO2-induced inhibition of mast cell mediator release: Evidence that the mechanism involves free radicals

The mast-cell-specific proteolytic enzymes tryptase and chymase were identified in and isolated from cholesteatoma in a ratio similar to that found in human skin. We assume that this ratio reflects a similar distribution of tryptase-containing and tryptase/chymase-containing mast cells in both these tissues. It seems conceivable that mechanisms able to trigger excessive and/or continuous mast cell degranulation in the middle ear might be causative for the formation of cholesteatoma either directly or via primed chronic inflammatory reactions. By their ability to amplify degranulation of mast cells, mast cell proteinases, in particular chymase, may contribute to the chain of events leading to the formation of cholesteatoma.

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Isolation and characterization of trypsin-like and chymotrypsin-like proteinases from human cholesteatoma

Hochstrasser

Gebhard

et al. 1994

Eur Arch Otorhinolaryngol

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Down-Regulation of Canine Airway Mast Cell Function Following Exposure to Ozone in Vivo

1996

Experimental Lung Research

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The influence of ozone on the function of airway cells involved in allergic responses is of particular interest due to the increasing prevalence of this environmental oxidant pollutant. In the present studies, the peripheral airways of Ascaris-sensitive dogs were expose to ozone (1 ppm, 5 min) or air (control) and the exposed segments were lavaged 30 min later. The kinetics and magnitude of release of PGD2 and histamine from canine peripheral airway mast cells (PAMC) was determined following in vitro challenge with Ascaris antigen or calcium ionophore approximately 4 h from the time of the in vivo exposures. Histamine content was significantly lower in PAMC retrieved from ozone- versus air-exposed segments (3.0 +/- 0.1 vs. 5.2 +/- 0.5 pg/cell). Absolute release of histamine at 20 min was decreased by 47 and 43% in ozone-exposed cells stimulated with antigen or ionophore, respectively. Maximal synthesis and release of PGD2 in response to antigen (345 +/- 22 pg/10(3) PAMC) or ionophore (1055 +/- 104 pg/10(3) PAMC) was inhibited by 32 and 55%, respectively, in cells from ozone-exposed segments. Inhibition of prostanoid synthesis was not observed in alveolar macrophages in the lavage samples, nor could decreased PGD2 be attributed to enhanced catabolism. These data indicate a differential down-regulatory influence of ozone on subsequent release of granular mediators and newly synthesized PGD2 from PAMC following brief in vivo exposure that lasts for several hours.

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Enhancement of Histamine Release from Rat Peritoneal Mast Cells Exposed to Formaldehyde

Fujimaki

Shiraishi

Katayama

1992

Inhalation Toxicology

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While formaldehyde is an indoor and outdoor pollutant, little is known about the effect of formaldehyde exposure on induction of allergic and inflammatory reactions.To examine the effects of in vitro exposure to formaldehyde on rat mast cell functions, purified peritoneal mast cells (PMC) were exposed to 1, 5, 10, and 50 ppm formaldehyde for 30 min and then incubated with secretagogues. Histamine release from PMC stimulated with A23787 or anti-rat IgE was significantly enhanced at 5 ppm formaldehyde. Substance P-induced histamine release was affected at 10 and 50 ppm formaldehyde; however, no enhancement of substance P-induced histamine release was seen below 5 ppm. The effects of modulators of mediator release on enhanced histamine release from formaldehyde-exposed PMC induced by immunological and nonimmunological stimulation were also examined. Pretreatment with cholera toxin or dexamethasone did not prevent the formaldehyde-induced enhancement in histamine release. Howevec pretreatment with p-bromophenacyl bromide, an inhibitor of phospholipase Ab prevented the stimulatory effects of formaldehyde on A23187 and antirat IgE-induced histamine release. These results suggest that formaldehyde gas can modify mast cell mediator release and may be partly relevant in the induction of many inflammatory and allergic diseases.

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An antioxidant agent prevents NO2-induced inhibition of mast cell mediator release: Evidence that the mechanism involves free radicals

Cited by 3 publications

References 13 publications

Isolation and characterization of trypsin-like and chymotrypsin-like proteinases from human cholesteatoma

Isolation and characterization of trypsin-like and chymotrypsin-like proteinases from human cholesteatoma

Down-Regulation of Canine Airway Mast Cell Function Following Exposure to Ozone in Vivo

Enhancement of Histamine Release from Rat Peritoneal Mast Cells Exposed to Formaldehyde

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