Interactions between Cigarette Smoking and the Natural History of Idiopathic Pulmonary Fibrosis: Discussion (Part 3)
In addition, animal as well as human data have demonstrated that the number of accessory cells can dramatically alter the T-cell proliferative responses to mitogens or antigens: in the case of a high macrophage-lymphocyte ratio, the whole result is a lymphocyte proliferation suppressive effect.’ In the present study, the high macrophage count in BAL fluid from smokers could promote such a lymphoproliferative down-regulation and may explain the low grade of lymphocytic alveolitis associated with an insidious dyspnea onset observed in our smoking patients. The increase of eosinophils (expressed in number per milliliter) observed in smokers may be related to cigarette smoke, as suggested in healthy subjects. However, it also could reflect another stage of the disease as previously demonstrated in patients with IPF. buy diabetes drugs
Cigarette Smoking, and Prednisolone Response
After prednisolone therapy, there was a striking contrast between nonsmokers who fairly often showed a high lymphocyte count in BAL with a substantial prednisolone response and smokers with nearly normal lymphocyte count and no PFT improvement. The observation of such a relationship between lymphocyte count in BAL and prednisolone responsiveness already has been reported. Similarly, a subacute onset with low PFT results despite dyspnea of short duration has been shown to be associated with a high rate of glucosteroid response. Taken together, those observations corroborate that a subacute onset and a high lymphocyte count in BAL fluid are closely linked features of IPF which point to improvement after therapy.