Effects of diesel exhaust on allergic airway inflammation in mice

doi:10.1016/S0091-6749(98)70021-1

Journal of Allergy and Clinical Immunology

Volume 102, Issue 5, November 1998, Pages 805-812

https://doi.org/10.1016/S0091-6749(98)70021-1 Get rights and content

Abstract

Background: Eosinophilic infiltration and goblet cell hyperplasia were induced by the intratracheal instillation of diesel exhaust particles and ovalbumin in mice. However, it is unknown whether its results differ from the effects of the inhalation of diesel exhaust and allergen. Objectives: The purpose of this study was to compare the effects of diesel exhaust inhalation and intratracheal instillation of diesel exhaust particles in a murine asthma model. Methods: ICR mice were exposed to 3 mg soot per cubic meter of diesel exhaust for 6 weeks. After the first week, animals were sensitized by intraperitoneal injection of ovalbumin and aluminum hydroxide gel. After 5 weeks of diesel exhaust exposure, the mice were challenged with ovalbumin. The animals were killed 1, 2, 3, and 7 days after the challenge and investigated for airway inflammation, hyperplasia of goblet cells, airway hyperresponsiveness, local cytokine expression, and antigen-specific IgE and IgG1 production. Results: Exposure to diesel exhaust enhanced infiltration of eosinophils and neutrophils in murine airways even 1 day after the challenge. An increment of goblet cells under the bronchial epithelium was followed by the recruitment of inflammatory cells. Furthermore, exposure to diesel exhaust combined with ovalbumin sensitization enhanced respiratory resistance and expression of IL-5 in lung tissue and IgG1 production but not IgE. However, diesel exhaust alone did not induce pathologic changes in mice. Conclusions: Diesel exhaust enhanced allergic airway inflammation, hyperplasia of goblet cells, and airway hyperresponsiveness caused by ovalbumin sensitization. (J Allergy Clin Immunol 1998;102:805-12.)

Section snippets

Materials

Acetylcholine, diethyl ether, thimerosal, phenylmethane sulfonyl fluoride, and Tween 20 were purchased from Nacarai Tesque (Kyoto, Japan). Rat anti-mouse IgE horseradish peroxidase–conjugated streptavidin, BSA, EDTA, 4-methyl-umbelliferyl-β-galactoside, and ovalbumin (grade V) were obtained from Sigma Chemical Co, Ltd (St Louis, Mo). Biotinylated rabbit anti-mouse IgG1 and β-D-galactosidase–conjugated streptavidin were purchased from Zymed Laboratories (San Francisco, Calif). Leupeptin and

Histologic changes in murine airways after ovalbumin challenge with DE exposure

DE exposure alone (DE-saline) did not induce the infiltration of eosinophils in murine lungs. However, DE exposure enhanced eosinophilic infiltration caused by ovalbumin sensitization (Fig 1).

. Histologic changes of eosinophilic inflammation in airway after ovalbumin (OVA) challenge with or without diesel exhaust exposure (DE) . Mice were exposed to clean air or diesel exhaust for 5 to 6 weeks with ovalbumin sensitization. Lungs were removed 1, 2, 3, and 7 days after ovalbumin challenge. Degree

DISCUSSION

DE inhalation enhanced airway inflammation in association with marked eosinophil and neutrophil infiltration and airway hyperresponsiveness caused by antigen sensitization. Hyperplasia of goblet cells in the bronchial epithelium was followed by the recruitment of eosinophils. DE markedly enhanced the expression of IL-5 in murine lungs and the production of ovalbumin-specific IgG1 caused by ovalbumin sensitization. However, DE inhalation alone for 5 weeks did not induce airway inflammation and

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We investigated whether surrogate PM particles like carbon black (CB), diesel exhaust particle (DEP), coal fly ash (CFA) can recapitulate the allergic airway inflammatory response induced by urban particulate matter.
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Urban particulate matter with its unique physiochemical properties and heterogeneous composition elicits a mixed Th2/Th17 allergic airway response that is not seen after similar exposures to surrogate PM particles.
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Different types of environmental contaminants, including diesel exhaust particulates (DEPs), are known to affect the immune system in vivo and in vitro in adults (Inadera, 2006). DEPs can increase IL levels in vivo (Miyabara et al., 1998; Takano et al., 1997), depress immune responsiveness to bacterial antigens (Yang et al., 1999), impede phagocytosis-driven bacterial clearance (Yin et al., 2002), and weaken innate immunity by inhibiting secretion of interleukins (e.g., IL-1β) and tumor necrosis factor (e.g., TNF-α) (Yin et al., 2002). Despite the lack of conclusive evidence of a causal relationship between the increasing exposures to EDCs and increasing PTB rates, accumulating literature on EDC-driven modulation of biological processes overlaps with PTB-inducing processes.
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^☆: From the Research Team for Health Effects of Air Pollutants, National Institute for Environmental Studies, Ibaraki, Japan.

^☆☆: Reprint requests: Yuichi Miyabara, PhD, Research Team for Health Effects of Air Pollutants, National Institute for Environmental Studies (NIES), 16-2 Onogawa, Tsukuba, Ibaraki 305-0053, Japan.

^★: 0091-6749/98 $5.00 + 0 1/1/92699

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Effects of diesel exhaust on allergic airway inflammation in mice☆,☆☆,★

Abstract

Section snippets

Materials

Histologic changes in murine airways after ovalbumin challenge with DE exposure

DISCUSSION

Atmos Environ

Free Radic Biol Med

Free Radic Biol Med

J Immunol Methods

J Allergy Clin Immunol

Toxicology

J Allergy Clin Immunol

J Allergy Clin Immunol

Cell Immunol

J Allergy Clin Immunol

Toxicol Appl Pharmacol

Toxicology

Has the prevalence of asthma increased in children? Evidence from national study of health and growth 1973-86

Br Med J

Estimation of levels of personal exposure to suspended particulate matter and nitrogen dioxide in Tokyo

Environ Sci

Air pollution and asthma

Postgrad Med J

The role of air pollution in asthma

Clin Exp Allergy