Therefore it is likely that defects in the expression of SP-A may be important in the course of non infectious pulmo-RT-PCR: Transcription of SP-A1 and SP-A2 in NSCLC tumors (T) and corresponding tumor-free tissues (TF) from the same cases in comparison to GAPDH nary diseases of adult patients. In the case of idiopathic pulmonary fibrosis, for example, low levels of SP-A (measured by ELISA) have been reported in broncho alveolar lavages (BAL), but elevated levels were found in the sera [32] [33] [34] . Immunohistochemical examinations of the expression of SP-A in pulmonary fibrosis demonstrated evident defects by using specimens from different diseases displaying fibrotic changes in the lungs. In good agreement with the results in BAL reduced levels of SP-A have been observed in fibrotic lungs. This reduced SP-A-expression in fibrotic lungs may be caused by two reasons: a limited number of the SP-A producing type II pneumocytes and by a clearly reduced SP-A expression of the remaining cells [35] .