Original articleMechanisms of allergic and immune diseaseEffects of diesel exhaust particles on primary cultured healthy human conjunctival epithelium
Introduction
Allergic conjunctivitis is the most common ocular surface allergic disease and affects more than 20% of the population.[1], [2], [3] As a result of changes in the living environment and other factors, the incidence of allergic diseases, including atopic dermatitis and pollinosis, is progressively increasing. The medical community has been challenged to develop effective therapies for these allergic diseases.4 To better understand the pathogenesis of allergic disease, researchers are increasingly focusing on the effects of environmental factors, such as exposure to atmospheric pollutants, UV light, and viral infection. Epidemiologic studies have found that the increased incidence of allergic diseases is at least partly due to increased exposure to atmospheric pollutants.
The effects of diesel exhaust on the pathophysiology of allergic airway disease have been analyzed in animals and humans using in vitro and in vivo models. The components of diesel exhaust as environmental factors have received much attention in these studies. In fact, it was reported that diesel exhaust particles and carbon black can induce dust mite allergy in rats.5 Exposure to diesel exhaust also enhances ozone-induced airway inflammation in healthy humans6 and in people with asthma.7 In the bronchial epithelium, diesel exhaust increases interleukin (IL) 8, growth-regulated oncogene (GRO) α, and IL-13 and activates several transcription factors (eg, nuclear factor–κB and activator protein 1) and mitogen-activated protein kinases (eg, p38 and c-Jun N-terminal kinase).[8], [9] Holgate et al[10], [11] exposed healthy and asthmatic individuals to diesel exhaust for 2 hours and determined messenger RNA expression in bronchial wash fluid. Stenfors et al12 determined cytokine production in lavage fluid after exposing asthmatic and healthy individuals to diesel exhaust for 6 hours. These findings suggest that oxidant pollutants, including diesel exhaust particles, cause allergic inflammation by activating allergic inflammatory response elements.
In this study, we hypothesized that the ocular surface is exposed to diesel exhaust particles, which enhance the expression of cytokines and growth factors, leading to allergic conjunctival inflammation. Using a GeneChip array, we first investigated the effects of exposure to diesel exhaust in vitro.
Section snippets
Culture of human conjunctival epithelial cells
This study was approved by the Ethics Committee of Tokyo Dental College (Chiba, Japan). All experiments were conducted in accordance with principles of the Declaration of Helsinki. Written informed consent was obtained from all volunteers before participation. Human conjunctival samples were collected from 7 healthy volunteers using scissors under 2% Xylocaine anesthesia. To establish primary conjunctival epithelial cells, samples were cultured in supplemented hormonal epithelial medium
Elevated transcripts in deactivated conjunctival cells
The optimal incubation time to measure the apparent increase of the mRNAs in the model was revealed as 6 hours after exposure among 1, 3, and 6 hours. In addition, 24 hours after exposure among 8, 24, and 48 hours was the optimal time to determine protein production.
We used a GeneChip array to examine the expression levels of approximately 12,000 genes in conjunctival cells exposed to diesel exhaust particles. The fold-increase in expression was determined by calculating the mean difference in
Discussion
There is growing evidence that particulate air pollution increases the incidence of allergy and asthma, in addition to augmenting the severity of asthma and allergic diseases.[14], [15], [16], [17] For example, diesel exhaust was reported to increase histamine-induced IL-8 and granulocyte-macrophage colony-stimulating factor production in nasal epithelial cells and endothelial cells.18 Diesel exhaust was also reported to induce cytokine expression in human bronchial epithelial cells.19
Acknowledgments
We thank Ayako Igarashi and Akiko Kujira at the Tokyo Dental College for their technical assistance.
References (42)
Conjunctivitis of allergic origin: clinical presentation and differential diagnosis
Surv Ophthalmol
(1993)- et al.
Diesel exhaust exposure enhances the expression of IL-13 in the bronchial epithelium of healthy subjects
Respir Med
(2004) - et al.
Biology of diesel exhaust effects on respiratory function
J Allergy Clin Immunol
(2005) - et al.
Pulmonary effects of inhaled diesel exhaust in aged mice
Toxicol Appl Pharmacol
(2009) - et al.
Diesel exhaust exposure induces angiogenesis
Toxicol Lett
(2009) - et al.
Diesel exhaust exposure favors TH2 cell recruitment in nonatopic subjects by differentially regulating chemokine production
J Allergy Clin Immunol
(2006) - et al.
Diesel exhaust particles and allergenicity of pollen grains of Lilium martagon
Ecotoxicol Environ Saf
(2008) - et al.
Allergy adjuvant effect of particles from wood smoke and road traffic
Toxicology
(2008) - et al.
Diesel exhaust particulates exacerbate asthma-like inflammation by increasing CXC chemokines
Am J Pathol
(2011) - et al.
Olopatadine inhibits anti-immunoglobulin E-stimulated conjunctival mast cell upregulation of ICAM-1 expression on conjunctival epithelial cells
Ann Allergy Asthma Immunol
(2001)
Allergic conjunctivitis and dry eye syndrome
Ann Allergy Asthma Immunol
Managing eye conditions in general practice
BMJ
A review of olopatadine for the treatment of ocular allergy
Expert Opin Pharmacother
Comparison of the conjunctival allergen challenge model with the environmental model of allergic conjunctivitis
Acta Ophthalmol Scand Suppl
Effects of diesel exhaust particles and carbon black on induction of dust mite allergy in brown norway rats
J Immunotoxicol
Diesel exhaust exposure enhances the ozone-induced airway inflammation in healthy humans
Eur Respir J
Respiratory effects of exposure to diesel traffic in persons with asthma
N Engl J Med
Diesel exhaust increases EGFR and phosphorylated C-terminal Tyr 1173 in the bronchial epithelium
Part Fibre Toxicol
Health effects of acute exposure to air pollution, part II: Healthy subjects exposed to concentrated ambient particles
Res Rep Health Eff Inst
Health effects of acute exposure to air pollution, part I: healthy and asthmatic subjects exposed to diesel exhaust
Res Rep Health Eff Inst
Different airway inflammatory responses in asthmatic and healthy humans exposed to diesel
Eur Respir J
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Disclosures: Authors have nothing to disclose.
Funding Sources: This study was supported by a research grant from Santen Pharmaceutical Co, Ltd, Osaka, Japan.