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2 October 2018 A Chromosome 6, not Natural Killer Cell, Contribution to Radiation- and Bleomycin-Induced Lung Disease in Mice
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Abstract

Inbred strains of mice differ in susceptibility to both radiation-induced and bleomycin-induced pulmonary fibrosis and these traits have been mapped to a common locus on chromosome 6 which harbors genes of natural killer cell function. To investigate this putative locus of fibrosis susceptibility we assessed the fibrotic response of chromosome-6 consomic mice (B6.6A), and of mice deficient for natural killer cells, C57BL/6J Ly49A transgenic mice, after each of thoracic irradiation and bleomycin treatment via osmotic minipump. Thoracic irradiation resulted in less than 15% survival at 26 weeks in parental strain C57BL/6J and A/J mice, due to the development of pneumonitis with fibrosis in C57BL/6J (B6) mice, and pneumonitis in A/J mice. One hundred percent of consomic B6.6A mice survived at 26 weeks after thoracic irradiation, and developed a fibrosis level similar to that of fibrosis-resistant A/J mice, after irradiation (P = 0.38) or bleomycin challenge (P = 0.32). C57BL/6J Ly49A transgenic mice were confirmed through flow cytometric analysis to be deficient in NK cells, but the post-irradiation survival of these mice was not significantly different from that of wild-type littermate mice (P = 0.64). Extent of pulmonary fibrosis by histological examination did not differ between C57BL/6J Ly49A transgenic mice and wild-type littermate mice in response to either irradiation (P = 0.14) or bleomycin treatment (P = 0.62). We conclude that chromosome 6 genes, but not NK cells, contribute to the susceptibility to both radiation-induced and bleomycin-induced pulmonary fibrosis of C57BL/6J mice.

©2018 by Radiation Research Society
Anne-Marie Lemay and Christina K. Haston "A Chromosome 6, not Natural Killer Cell, Contribution to Radiation- and Bleomycin-Induced Lung Disease in Mice," Radiation Research 190(6), 605-611, (2 October 2018). https://doi.org/10.1667/RR15144.1
Received: 24 May 2018; Accepted: 21 August 2018; Published: 2 October 2018
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