Why SP-D levels would relate to bronchial dysplasia is uncertain. SP-D is a large, multimeric, calcium-dependent, collagenous glycoprotein (ie, lectin) that is part of the collectin family of carbohydrate-binding proteins. SP-D is found predominantly in the endoplasmic reticulum of type 2 pneumocytes and in the secretory granules of Clara or nonciliated bronchiolar cells.22 Its primary functions are to regulate antibody-independent immune responses (ie, innate immunity) against invading microorganisms as part of the first-line defense against lung infections,23 to modulate lung inflammation, and to attenuate oxidative stress in the lungs. In animal models, intratracheal instillation of bleomycin leads to a higher risk of weight loss, respiratory distress, and death in SP-D-deficient mice than in wild-type mice. SP-D-deficient mice have also demonstrated24 increased oxidant stress in the lungs and more airway inflammation compared to wild-type mice. Mice that overexpress SP-D, on the other hand, are protected from lung injury.25 SP-D, in general, plays an important role in maintaining lung homeostasis and in preventing lung damage from excess inflammation or oxidative stress in response to pathogens or toxins.26 Consistent with this notion, we found in the present study that 37% of the variation in SP-D levels in BAL fluid could be explained by CRP levels in plasma (a measure of inflammation), smoking history, and the subject's lung function. By causing excess inflammation and oxidative stress, it is possible that SP-D deficiency in the lungs could contribute to the progression of dysplastic lesions in the airways. An alternate possibility is that SP-D levels in the BAL fluid may simply reflect the general health of the lungs. SP-D deficiency may thus indicate poor health status of airway epithelial cells. Whatever the mechanism, our study findings suggest that SP-D levels in BAL fluid “predict” the progression of dysplastic lesions in the airway and may serve as potential biomarkers for early lung cancer.