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

Abstract

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 ...

Impacts of Atmospheric Conditions on Influenza in Southern China. Part I. Taking Shenzhen City for Example

“…This is different from that of the results in temperate regions where ILI (%) is positively correlated to the PM 10 concentration [19,20], the underlying mechanism is such that the increases in PM 10 reduce ultraviolet radiation reaching the ground which helps to the development of flu virus, therefore, more PM 10 leads to the acceleration of development and transmission of influenza virus. However, our knowledge of how ultraviolet radiation influences human's immunity system is less certain.…”

Sequential Exposure to Carbon Nanotubes and Bacteria Enhances Pulmonary Inflammation and Infectivity

“…Using larger doses of LM in a rat model, Yin and colleagues attributed the immunosuppressive effects of acute exposure to diesel exhaust particles to attenuation of early macrophage activation and cytokine release (43). The cytokine profiles obtained in our study 3 days after infection (Experimental Day 6) appeared to be very similar between uninfected animals pre-treated with PBS or both doses of SWCNT.…”

Airway Inflammatory Responses to Oxidative Stress Induced by Prolonged Low-Dose Diesel Exhaust Particle Exposure From Birth Differ Between Mouse Balb/C and C57bl/6 Strains

“…DEP suppress alveolar macrophage function, as demonstrated by reduced production of the cytokines IL-1β and TNF-α, and this suppression could impair normal host defenses [32][33][34][35] with these reports: level of IL-1β and TNF-α in BAL fluid were significantly decreased in both the C57BL/6 and BALB/c strains, but C57BL/6 mice showed a more marked decreased than BALB/c mice. This difference in reduction in macrophage function was also a mechanism of defense against DEPs that differed between hosts.…”

“…In contrast, our present results showed that after prolonged low-dose DEP exposure, the expression of GST in lung tissues decreased and the expression of HO-1 was unchanged. On the one hand, DEP exposure induces the expression of antioxidative stress enzymes via the antioxidant-responsive element in macrophages [11][12][13]; on the other, DEP exposure impairs macrophage function [32][33][34][35]. Therefore, we think that the decrease in GST expression in C57BL/6 mice may be involved in the impairment of macrophage function after prolonged DEP exposure, and that HO-1 expression contributed only in the early stages of DEP exposure.…”