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Alteration of pulmonary immunity to Listeria monocytogenes by diesel exhaust particles . I. Effects of DEPs on early pulmonary responses
Environmental Health Perspectives, Nov, 2002 by Xue-Jun Yin, Rosana Schafer, Jane Y.C. Ma, James M. Antonini, David D. Weissman, Paul D. Siegel, Mark W. Berger, Jenny R. Roberts, Joseph K.-H. Ma
Brown-Norway rats were used because of their applicability to investigations involving immunologic reactions such as pulmonary allergic sensitization. These rats exhibited high resistance to Listeria infection and survived at initial inoculation doses as high as 600,000 Listeria/rat (data not shown). In the present study, rats exposed to DEPs or dean air for 4 hr were inoculated with 100,000 bacteria and maintained for up to 7 days. All rats, including those exposed to the higher dose of DEPs, which resulted in the highest lung burden of bacteria (4.22 x [10.sup.6] Listeria/lung) at 3 days postinfection, survived without marked symptoms during the entire experimental period. The short-term DEP exposure via the nose-only inhalation system was shown to cause only a moderate inflammatory injury in the lung. In rats exposed to DEPs only, there was only a slight increase in LDH activity but with no significant change in albumin content in the BAL fluid. This short-term DEP exposure, however, dearly increased the susceptibility of rats to Listeria infection because rats exposed to DEPs and then inoculated with Listeria were less able to clear bacteria from the lungs than were rats exposed to dean air at 3 and 7 days postexposure. These results indicate that inhaled DEPs can result in cellular functional changes in rats at concentrations that do not cause substantial inflammatory injury in the alveolar space.
Listeria can live within a variety of host cells, including endothelial and epithelial cells, as well as some macrophages (32). Studies have shown that the initial host response to Listeria involves rapid recruitment of neutrophils and macrophages to the site of infection and the activation of natural killer (NK) cells (38). Activated macrophages have also been shown to play an important role in killing Listeria (27,39). Indeed, as a key cell type in the innate immune system, AMs serve to provide the primary and first line of defense against bacteria that reach the distal lung. These cells engulf and, through production of oxygen and nitrogen radicals and cytokines, kill the bacteria, thereby sequestering them from the vulnerable respiratory membrane (6,7,20). To study the underlying mechanism involved in the DEP-compromised defense against respiratory infection, we have investigated the potential. alteration of macrophage functions by DEPs in the presence and absence of Listeria infection. The phagocytic activity of AMs is directly linked to bacterial clearance. Van Loveren et al. (31) have shown that exposure to ozone slows the pulmonary clearance of Listeria in rats and decreases the number of the bacteria ingested and killed by AMs. In the present study, the effect of DEPs on the phagocytic activity of AMs was assessed, and the results demonstrate that AM phagocytosis was significantly suppressed by inhaled DEPs at 3 and 7 days postexposure (Figure 1). This effect may be attributed to direct interaction of DEPs with AMs, as demonstrated by the dose- and time-dependent inhibition of phagocytosis by DEPs in in vitro studies (Figure 2). Jakab et al. (40) have suggested that such an interaction may involve a suppression of macrophage membrane receptor-mediated phagocytic activity. The impairment of phagocytic activity of DEP-exposed AMs may at least partially account for the decreased pulmonary clearance of Listeria in the Brown-Norway rats.
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