ABSTRACT
Fibrosis of organs and tissues are major causes of morbidity and mortality in human. The currently available pharmacologically based treatments are unsatisfactory. As an experimental animal model antitumor antibiotic drug bleomycin (BLM) is widely used to produce lung fibrosis. The present study has been undertaken to investigate the possible role of a potent immunomodulator Staphylococcus protein-A (SpA) in the modulation of lung lesions caused by treatment of BLM. In mice BLM, 0.5 mg in 200 microliters of normal saline and SpA, 6 micrograms in 200 microliters of normal saline was administered singly or in combination twice a week for 4 weeks. The fibrotic lesions in the lungs were observed after 4 weeks of BLM treatment. After 4 weeks treatment of SpA, the hyperreactive changes in bronchi and bronchioles were observed. In the co-treatment group of BLM and SpA, the effects observed were in the form of enhanced lesions in the lung parenchyma. Moreover, the pleural lesions were also observed in co-treatment group (BLM + SpA). Opposite to the assumption, SpA being a potent immunomodulator was not able to reduce the lung lesions produced by BLM.