Review Article

Cigarette Smoke, Bacteria, Mold, Microbial Toxins, and Chronic Lung Inflammation

Figure 1

A schematic view of an alveolus that depicts the effect of inhaled tobacco smoke on the terminal (respiratory) structure of the lung. Particulate matter “Tar” in tobacco smoke is inhaled deep into the lung where it is recognized by macrophages. The macrophages arise from the blood monocytes that migrate into the lung where they undergo differentiation and maturation. Macrophage phagocytosis of the chemical-rich “Tar” evokes the production of diverse proinflammatory mediators (for details, see Figure 1). Macrophages have toll-like receptors (TLR) that recognize diverse microbes and toxins (LPS is recognized by TLR-4). Shown in this illustration is the production of five proinflammatory cytokines: tumor necrosis factor, type alpha (TNFα), interleukin 1-beta (IL-1β), leukemia inhibitory factor (LIF), oncostatin M (OSM), and Interleukin-4 (IL-4). These soluble factors interact with other cells of the lung, and the response of these cells is thought to accelerate, amplify, and prolong pulmonary inflammation. The target cells may include T cells. The T cell that is depicted herein is representative of many different T cell subsets, including T helper cell subsets Th1, Th2, and Th17. Type I epithelial cells are the major cells lining the alveolar space, and facilitating O2/CO2. The type I cells are spread out and cover about 90 to 95% of the alveolar surface. The type II cells form only 5 to 10% of the surface but produce surfactant proteins. Polymorphonuclear leukocytes (PMN) mediate inflammation in multiple ways, including the production of an oxidative burst. Dendritic cells (DC) are professional antigen-presenting cells; they also mediate inflammation.
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