Inhalation of diesel exhaust enhances antigen-specific IgE antibody production in mice

Fujimaki, Hidekazu; Saneyoshi, Kensaku; Shiraishi, Fujio; Imai, Toru; Endo, Takuro

doi:10.1016/s0300-483x(96)03539-1

Cited by 84 publications

(37 citation statements)

References 23 publications

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“…24 Draining thoracic lymph nodes from mice exposed to DEPs harbor T cells with higher IL-4 secretory capacity in mice exposed to both ovalbumin and DEPs. 25 Similar to what was found in this study, the propensity of the data support a synergistic effect when allergens and DEPs are given together. 26,27 When given serially or alternately, however, the effect of the particulates is diminished or vanishes completely.…”

Section: Synergistic Response In Simultaneous Administration Of Deps supporting

confidence: 85%

Pulmonary Effects of Diesel Exhaust

Kenyon

Liu

2011

The American Journal of Pathology

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Diesel exhaust particulates (DEPs) have the capacity to affect lung growth and cause systemic health effects. Recent epidemiologic studies have highlighted the difficulties in understanding the contribution of traffic-related DEPs to allergy and asthma. In this issue of The American Journal of Pathology, Kim et al 1 investigated the effect of DEPs on the inflammatory response and airway hyperresponsiveness induced by allergens in a mouse model of asthma. The investigators found that mice exposed to house dust mite extract (HDE) in combination with DEP (HDE/DEP) showed a marked increase in mucus production and greater airway resistance compared with those receiving only HDE. This effect was partly mediated by the neutrophil chemokines KC and macrophage inflammatory protein (MIP)-2. These interesting findings further illustrate the important interaction between DEP exposure and asthma. We discuss the investigators' findings in light of other recent research efforts in ambient pollution, DEP, and lung health. Multiple Causes of AsthmaAsthma increasingly is described as a syndrome rather than a single disease. Indeed, numerous exposuresviral infections, indoor as well as outdoor aeroallergens, and ambient pollution-contribute to the development of asthma in childhood and the persistence of asthma in adulthood. Environmental influences weigh heavily on early lung growth, particularly traffic-related pollution, including DEPs. DEPs are primarily ultrafine (0.1 m diameter) particulates that have the capacity to penetrate the lung down to the alveoli and cause systemic effects. Diesel truck engines are reported to be the primary producers of DEPs and account for the majority of the ambient particulate matter (PM) in urban environments. 2Many epidemiologic studies have reported correlations between asthma (prevalence or symptoms) and exposure to either traffic pollution or DEPs specifically. A few have commented on correlations with allergic inflammation and increased serum IgE levels and suggested a dose-and time-dependent sensitization effect also. Taken together, however, the results of these epidemiologic studies have been maddeningly inconsistent. In 2005, the World Health Organization wrote that although there were good data to suggest a correlation between traffic pollution and respiratory symptoms, there was no correlation with atopic asthma. Increased Risk for Asthma in ChildhoodChildren appear to be at increased risk of lung toxicity from traffic-related pollution because their lungs are not fully developed and because of pollution dose.4,5 Children exercise outside and their exposure to PM is increased compared with adults in the same environment. Alveolar number increases at least 10-fold in the first 4 years of life (from approximately 20 million to 260 million), and increased exposure to polluted air at a young age could adversely affect alveolar budding, lung growth, and airway epithelial development. 6 In addition, children have imperfect airway epithelial barriers and immature immune systems, and it is ...

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Section: Synergistic Response In Simultaneous Administration Of Deps supporting

confidence: 85%

Pulmonary Effects of Diesel Exhaust

Kenyon

Liu

2011

The American Journal of Pathology

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“…In addition, DEPs were also shown to be capable of potentiating antigen sensitization with increased production of antigen-specific immunoglobulin E (17)(18)(19). In a recent study, we further demonstrated that exposure to DEPs, but not to carbon black, decreased pulmonary bacterial clearance in rats, suggesting that DEPs may have an adverse influence on both the innate and the T-cell-mediated immune responses (20).…”

mentioning

confidence: 71%

Alteration of pulmonary immunity to Listeria monocytogenes by diesel exhaust particles (DEPs). I. Effects of DEPs on early pulmonary responses.

Yin

Schafer

Jane

et al. 2002

Environ Health Perspect

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Diesel exhaust particles (DEPs), generated by heavy-duty diesel engines in various industries, can adsorb over 450 different organic compounds, including mutagenic and carcinogenic polycyclic aromatic hydrocarbons (1). With diameters < 2 µm, these fine respirable particles can remain airborne for long periods of time and deposit in great numbers deeply in the lungs. For these reasons, exposure of truckers, railroad and construction workers, and engine mechanics to DEPs is an occupational health concern. A report from the U.S. Department of Labor showed that the worst-case mean exposures to DEPs in underground metal and nonmetal mines are about 2,000 µg/m 3 , with maximum measurements as high as 3,650 µg/m 3 (2). Epidemiologic studies have also shown a consistent association between elevated levels of particulate matter in ambient air and increased incidence of pulmonary infections (3) or increased respiratory mortality and morbidity in high-risk groups (4,5). Because DEPs are a major component of particulate air pollution in most industrialized urban areas, their effect on pulmonary infections is of great environmental and occupational concern.The principal function of pulmonary host defense mechanisms is to clear inhaled particles or microorganisms from the lungs and prevent infections. Among the various cell types involved in the innate immune system, alveolar macrophages (AMs) are responsible for the clearance of inhaled particles and/or microorganisms from the distal airways and alveolar spaces. These cells engulf inhaled particles or microorganisms and become activated to release reactive oxygen species (ROS), cytokines, and a variety of mediators that are capable of killing microorganisms (6,7). It has been well documented that AM-derived proinflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α), provide innate resistance to bacterial infection, promote the inflammatory process by recruiting neutrophils into the air spaces, and stimulate these phagocytes to release ROS and enzymes (7,8). A successful pulmonary host defense, on the other hand, also needs specific cell-mediated immunity (9). In this aspect, studies have already shown that AMs, through their secretion of cytokines in response to specific antigen exposure, provide a critical link between these two systems. For example, Hsieh et al. (10) showed that the production of IL-12 by macrophages is a key process for the development of the appropriate CD4 + T helper (Th) subset during the immune response to Listeria monocytogenes infection. IL-12, in fact, not only initiates but also plays an important role in maintaining the Th1 response (11). This cytokine is produced very rapidly after infection, thus serving as an early marker for the study of DEP effect(s) on cell-mediated immunity.Studies from our laboratory as well as from others have suggested that DEPs may suppress host immunity by suppressing mucociliary clearance and the phagocytic activity of AMs (12,13), reducing interferon production in response to viral ...

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“…This enhancement in IL-4 production increased to an 8-fold level in mice injected with OVA and DEPs compared with mice receiving only OVA. A later study examining cytokine production in DEPexposed and control mice sensitized with OVA found that IL-4 and IL-10 production in spleen cells was significantly increased in the group of DEP-exposed mice (69). In addition, humans challenged with DEPs plus ragweed antigen had enhanced local IgE, IL-4, and IL-13 production accompanied by isotype switching from IgM or IgD to IgE antibody in nasal lavage cells (71).…”

Section: Influence On Cytokine Expressionmentioning

confidence: 99%

“…The IgE stimulation by phenanthrene was accompanied by an increased expression of total IgE mRNA. In addition, several studies have found that the DEP-mediated increase in IgE synthesis may be amplified when DEPs act as an adjuvant to environmental allergens (68)(69)(70)(71)(72)(73).…”

Section: Direct Immunologic Effects Of Deps Enhanced Ige Production Bmentioning

confidence: 99%

Diesel exhaust and asthma: hypotheses and molecular mechanisms of action.

Pandya

Solomon

Kinner

et al. 2002

Environ Health Perspect

205

126

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Several components of air pollution have been linked to asthma. In addition to the well-studied critera air pollutants, such as nitrogen dioxide, sulfur dioxide, and ozone, diesel exhaust and diesel exhaust particles (DEPs) also appear to play a role in respiratory and allergic diseases. Diesel exhaust is composed of vapors, gases, and fine particles emitted by diesel-fueled compressionignition engines. DEPs can act as nonspecific airway irritants at relatively high levels. At lower levels, DEPs promote release of specific cytokines, chemokines, immunoglobulins, and oxidants in the upper and lower airway. Release of these mediators of the allergic and inflammatory response initiates a cascade that can culminate in airway inflammation, mucus secretion, serum leakage into the airways, and bronchial smooth muscle contraction. DEPs also may promote expression of the T H 2 immunologic response phenotype that has been associated with asthma and allergic disease. DEPs appear to have greater immunologic effects in the presence of environmental allergens than they do alone. This immunologic evidence may help explain the epidemiologic studies indicating that children living along major trucking thoroughfares are at increased risk for asthmatic and allergic symptoms and are more likely to have objective evidence of respiratory dysfunction.

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Inhalation of diesel exhaust enhances antigen-specific IgE antibody production in mice

Cited by 84 publications

References 23 publications

Pulmonary Effects of Diesel Exhaust

Pulmonary Effects of Diesel Exhaust

Alteration of pulmonary immunity to Listeria monocytogenes by diesel exhaust particles (DEPs). I. Effects of DEPs on early pulmonary responses.

Diesel exhaust and asthma: hypotheses and molecular mechanisms of action.

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