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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
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, and with a lower elastase inhibitory
capacity, and in congenic C57Bl/6J mice. 1-proteinase inhibitor deficiency.
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