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Genetic deficiency of ₁-PI in mice influences lung responses to bleomycin

¹ Dept of Physiopathology and Experimental Medicine, University of Siena, Via Aldo Moro, I-53100, Siena, Italy and ² Tulane University, Medical Center, New Orleans, LA, USA

CORRESPONDENCE: G. Lungarella, Dept of Physiopathology and Experimental Medicine, University of Siena, Via Aldo Moro, I-53100, Siena, Italy. Fax: 39 0577234 019

Keywords: antiproteases, collagen, cytokines, elastin, mouse intrastrain variability

Received: February 2, 2000
Accepted September 25, 2000

This work was supported by a grant from Ministero dell'Universita' e della Ricerca Scientifica e Tecnologica.

It has recently been suggested that proteinase inhibitors modulate the fibrotic response in the lung. This study investigated the development of bleomycin-induced pulmonary changes in pallid mice, deficient in serum ₁-proteinase inhibitor, and with a lower elastase inhibitory capacity, and in congenic C57Bl/6J mice.

Male pallid and C57Bl/6J mice received a single intratracheal instillation of either saline or bleomycin. The investigation was carried out by means of biochemical, morphological and morphometrical methods.

In both strains, 21 and 72 h after bleomycin, the lungs showed foci of inflammatory cell infiltration associated with emphysema. Fibrosis developed with time after bleomycin. At 14 days fibrosis affected 23.46±9.48% (mean± sd) and 40.62±13.34% (p<0.01) of the lungs of C57Bl/6J and pallid mice, respectively. Emphysema affected 3.68±3.11% and 12.57±4.13% (p<0.01) of lung in C57Bl/6J and pallid mice, respectively. In C57Bl/6J mice bleomycin increased lung hydroxyproline content by 34% and desmosine content by 44% (p<0.01 for both). In pallid mice these increases were only 21% (p<0.01) and 6%, which may reflect parenchymal loss.

Thus, the lung destructive response (emphysema) and the subsequent proliferative reaction (fibrosis) to bleomycin are potentiated in ₁-proteinase inhibitor deficiency.

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