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Am. J. Respir. Crit. Care Med., Volume 157, Number 4, April 1998, 1253-1262

Impaired Ability of Cftr Knockout Mice to Control Lung Infection with Pseudomonas aeruginosa

DIANE GOSSELIN, MARY M. STEVENSON, ELIZABETH A. COWLEY, UTA GRIESENBACH, DAVID H. EIDELMAN, MARIE BOULÉ, MI-FONG TAM, GERALDINE KENT, EMIL SKAMENE, LAP-CHEE TSUI, and DANUTA RADZIOCH

Centre for the Study of Host Resistance, McGill University, Montreal, Quebec; Meakins-Christies Laboratories, McGill University, Montreal, Quebec; and Research Institute, Hospital for Sick Children, Toronto, Ontario, Canada

The present study was aimed at investigating the innate susceptibility of C57BL/6-Cftr unc/Cftr unc knockout [B6-Cftr (-/-)] mice to pulmonary infection with Pseudomonas aeruginosa. Our results indicate that 58.4% of B6-Cftr (-/-) mice died within 6 d following lung infection with 105 P. aeruginosa entrapped in agar beads, whereas only 12.1% of B6-Cftr (+/+) mice died over the same period of time. Moreover, the number of bacteria recovered from the lungs of B6-Cftr (-/-) mice 3 and 6 d after infection was significantly higher than that observed in their littermate controls. No correlation was found between the weight or age of the animals and the number of viable bacteria recovered from the lungs of mice. Histopathological examination of lung sections from P. aeruginosa-infected mice revealed that the infection results in a severe bronchopneumonia. Both B6-Cftr (-/-) knockout mice and their littermate controls developed similar lung pathology during the course of infection. Overall, results reported in the present study suggest that a defect at the Cftr locus leads to an exacerbation of P. aeruginosa lung infection resulting in a dramatically increased mortality rate and higher bacterial load.




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