Interactions between Cigarette Smoking and the Natural History of Idiopathic Pulmonary Fibrosis: Discussion (Part 2)
However, the hypothesis that an early aggressive course of IPF is more often observed in nonsmokers than in smokers seems to be more relevant. Indeed, first, in nonsmokers, in spite of a shorter duration of symptoms, functional impairment was similar or even greater than in cases of patients with smoking habits and long-standing dyspnea. Second, other mechanisms of dyspnea such as cardiac or obstructive lung diseases which could be more prevalent in smokers were excluded on the basis of PFTs, clinical examination and follow up. Finally, the clinical relevance of dyspnea duration assessment, in the setting of IPF, was also supported by the significant links observed between this subjective parameter and other measurable data such as lymphocyte counts in BAL or PFT changes after therapy. birth control pills
Cigarette Smoking and BAL Cell Populations
In the present series, a higher number of lymphocytes was observed in BAL fluids from nonsmokers than from smokers. Previous studies have reported a clear relationship between high lymphocyte counts in BAL fluid with clinical or pathologic evidence of IPF activity. In the pathogenesis of IPF, autoimmune reactions against the alveolar wall components are hypothesized to be the eliciting event leading to interstitial inflammation involving lymphocytes, mostly of the T subset. An inhibition of lung T cell blastogenesis related to cigarette smoking may be advocated as a possible explanation for the contrasted features of IPF observed between nonsmoking and smoking patients. Actually, cigarette smoke is known to affect accessory lung cells. For example, cigarette smoke reduces surface la antigens, and induces an expansion of accessory Langerhans’ cells; in similar concentrations, alveolar macrophages from heavy smokers mediate less of a lympho-proliferative response than macrophages from healthy nonsmokers.