Enhanced nasal cytokine production in human beings after in vivo challenge with diesel exhaust particles

doi:10.1016/S0091-6749(96)70233-6

Journal of Allergy and Clinical Immunology

Volume 98, Issue 1, July 1996, Pages 114-123

https://doi.org/10.1016/S0091-6749(96)70233-6 Get rights and content

Abstract

Background: Diesel exhaust particles (DEPs) have been implicated in the worldwide increased incidence of allergic airway disorders over the past century. They can enhance in vivo IgE production in the human upper respiratory mucosa. Objective: The study was carried out to determine whether DEPs can alter the production of cytokines by cells residing in the nasal mucosa. Methods: Eighteen hours after intranasal challenge with saline solution or DEPs, we studied the levels of messenger RNA for cytokines in nasal lavage cells and the number of subjects in whom cytokine mRNA could be detected. Results: Before challenge, most subjects’ nasal lavage cells had detectable levels of only interferon-γ, IL-2, and IL-13 mRNA. After challenge, the cells produced readily detectable mRNA for IL-2, IL-4, IL-5, IL-6, IL-10, IL-13, and interferon-γ. In addition, the levels of all cytokine mRNA increased. Enhanced IL-4 protein was also present in the postchallenge lavage fluid. Although the cells in nasal lavage before and after challenge do not necessarily represent the same cells either in number or type, the broad increase in cytokine production was not simply the result of an increase in T cells recovered in the lavage fluid. Conclusion: An increase in nasal cytokine expression after exposure to DEPs can be predicted to contribute to enhanced local IgE production and thus play a role in the increased incidence of respiratory allergic disease. (J ALLERGY CLIN IMMUNOL 1996;98:114-23.)

Section snippets

Subjects

Fourteen healthy, nonsmoking volunteers (eight men and six women), ranging in age from 23 to 48 years, were recruited for this study. Eight had no history of asthma, allergic rhinitis, or any allergic or chronic respiratory illness. Six had a history of seasonal allergies but were free of symptoms and did not take any medication 3 days before or at any time during the study. All atopic subjects were outside their allergy season. None of the volunteers had previously had any known extensive or

DEPs enhance nasal IgE levels

The IgE levels in the nasal washes of 14 subjects, which were performed immediately before or 4 days after nasal challenge with DEPs, were measured to confirm that DEPs enhanced IgE production as previously reported. Fig. 1 shows that IgE levels rose after challenge, so that by day 4 they were significantly higher than prechallenge levels. No IgE enhancement was observed after saline challenge. The cDNAs from these challenges were used for the measurement of cytokine mRNAs.

. An IgE response

DISCUSSION

We have previously shown that DEPs can enhance human IgE responses in vivo and that this increase is due to the expansion of the local population of IgE-secreting cells.⁷ Our results showed that DEPs in vivo and PAH-DEP in vitro⁶ can affect B-cell IgE production both quantitatively and qualitatively. In this report we extend these findings to provide a further mechanism by demonstrating that DEP can act in vivo to potentiate cytokine production at the human upper respiratory mucosal surface. An

Acknowledgements

We thank Dr. Shigeru Takafuji (Department of Medicine and Physical Therapy, Faculty of Medicine, University of Tokyo) and Dr. Hiroshi Takenaka (Department of Otorhinolaryngology, Kyoto Prefectural University of Medicine) for their kind gift of diesel exhaust particles. We also thank Dr. Robert Modlin (Department of Dermatology, University of California, Los Angeles) for his advice and kind gift of the cytokine mRNA primer sequences.

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^☆: From The Hart and Louise Lyon Laboratory; Division of Clinical Immunology/Allergy, Department of Medicine, University of California, Los Angeles, School of Medicine.

^☆☆: Supported by United States Public Health Service grants AI-15251 and the University of California, Los Angeles Asthma, Allergy and Immunologic Disease Center (AI-34567 funded by the National Institute of Allergy and Infectious Diseases and National Institute of Environmental Health Sciences) and by gifts from the Dorothy Fund and the Asthma Research Foundation. Dr. Diaz-Sanchez was the recipient of the McClure Foundation Fellowship from the Los Angeles Chapter of the Asthma and Allergy Foundation, and Dr. Casillas was the recipient of a Robert Woods Johnson Fellowship. Dr. Tsien was supported by National Institutes of Health training grant AI-07126.

^★: Reprint requests: David Diaz-Sanchez, PhD, Division of Clinical Immunology/Allergy, Department of Medicine, 52-175 Center for Health Sciences, UCLA School of Medicine, Los Angeles, CA 90024-1680.

^★★: 1/1/69612

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Enhanced nasal cytokine production in human beings after in vivo challenge with diesel exhaust particles☆,☆☆,★,★★

Abstract

Section snippets

Subjects

DEPs enhance nasal IgE levels

DISCUSSION

Acknowledgements

J ALLERGY CLIN IMMUNOL

J ALLERGY CLIN IMMUNOL

Toxicol Appl Pharmacol

Biochem Biophys Res Commun

J ALLERGY CLIN IMMUNOL

Immunol Today

J ALLERGY CLIN IMMUNOL

J ALLERGY CLIN IMMUNOL

J Biol Chem

J ALLERGY CLIN IMMUNOL

Hay fever, a post industrial revolution epidemic: a history of its growth during the 19th century

Clin Allergy

Upper respiratory tract environmental tobacco smoke sensitivity

Am Rev Respir Dis

Influence of environmental factors on IgE production. IgE, mast cells and the allergic response

Ciba Found Symp

Nasal allergy and air pollution

Otorhinolaryngol Tokyo

Particulate air quality: the 1994 air quality management plan

Topical glucocorticosteroid (fluticasone propionate) inhibits cells expressing cytokine mRNA for interleukin-4 in the nasal mucosa in allergen-induced rhinitis

Immunology

Cytokine messenger RNA expression for IL-3, IL-4, IL-5 and granulocyte/macrophage-colony-stimulating factor in the nasal mucosa after local allergen provocation: relationship to tissue eosnophilia

J Immunol

In vitro acute effects of tobacco smoke on tumour necrosis factor and interleukin-6 production by alveolar macrophages

Exp Lung Res