Abstract
Abstract Cigarette smoking is a risk factor for developing osteoporosis, and previous studies suggest lymphocytes are required for normal bone homeostasis and peak bone mass. We hypothesized that lymphocyte development is adversely affected by smoke exposure. If so, this outcome would provide a mechanism to partly explain how cigarette smoking promotes osteoporosis. To test this possibility, we investigated how the duration and cessation of cigarette smoke exposure affected the development, distribution, and function of lymphocytes normal mice. Consistent with the hypothesis, 3-12 weeks of smoke exposure significantly diminished bone marrow B220+CD43- B cell subsets, but, interestingly, did not significantly affect earlier progenitor B220+CD43+ B cells or thymic T cell subsets. In the spleen, by contrast, we find that individual splenic B cell populations, including transitional, marginal zone, and follicular mature B cell subsets, were largely unaffected by smoke exposure, but smoking did skew splenic CD4+:CD8+ T cell ratio to favor CD8+ T cells compared to sham controls. However, smoke exposure also had little or no effect on lymphocyte function ex vivo. Interestingly, smoking-induced alterations in lymphocyte populations observed at 12 weeks were lost when smoke exposure was stopped for six weeks. These data provide evidence that smoke exposure causes significant changes in lymphocyte populations that can largely be reversed after six weeks without smoking.