Chest
Laboratory and Animal InvestigationsBacterial Endotoxin Is an Active Component of Cigarette Smoke
Section snippets
Reagents
Pyrogen-free water, chromogenic Limulus amebocyte lysate (LAL) assay reagents using the diazo-coupling method, LPS standard from Escherichia coli 0113:H10 (specific activity, 9.73 endotoxin units [EU])/ng), and pyrogen-free polystyrene microtiter plates were obtained from Associates of Cape Cod (Falmouth, MA). E coli 0111B4 LPS prepared by trichloroacetic acid precipitation was obtained from Sigma Chemical Co (St. Louis, MO); its specific activity was determined to be 1 EU/ng in our laboratory.
LPS Content in Unsmoked Cigarettes
We measured the levels of extractable LPS bioactivity in unsmoked 1R4F research cigarettes and commercially available light cigarettes. The tobacco and filter tip portions of the cigarettes were analyzed separately (Fig 1). Tobacco from 1R4F and light cigarettes contained LPS bioactivity equivalent to 17.8 ± 1.0 and 26.8 ± 7.3 μg LPS/cigarette (mean ± SE), respectively. The unsmoked filter tips from these cigarettes contained LPS bioactivity equivalent to 0.67 ± 0.55 and 0.70 ± 0.39 μg
Discussion
Based on the reported LPS content in other agricultural products, we reasoned that cigarette tobacco would contain biologically significant quantities of LPS, one of the most potent inflammatory stimuli known. We extracted 6 to 9 μg of biologically active LPS from each gram of tobacco in either research or commercially available cigarettes. This LPS level is similar to levels reported in other noncombusted agricultural products.2 Temperatures at the burning cigarette tip (880°F or 471°C)19
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2021, International ImmunopharmacologyCitation Excerpt :Cigarette smoke, for example, accelerates arthritis and citrullination in mice [72,73]. Notably, cigarettes contain not only LPS [74], but also acetaldehydes that, when coupled with alcohol (source of acetaldehyde generation), robustly increase MAA adduct formation as detected in bronchioalveolar lavage fluid of patients [75]. In addition, LPS has a short half-life, and it may not be the appropriate inflammatory agent to model former/past exposures, such as cigarette smoking, to the risk of RA-associated lung disease.
Presented in part at the Thomas L. Petty Aspen Lung Conference, Aspen, CO, June 7–10, 1995.
Supported by Public Health Service grant CA52741 and HL40945. Drs. Dubin and Costa were supported by Pulmonary Research Training Fellowships from the American Lung Association of Maryland.