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Cystic fibrosis transmembrane conductance regulator deficient mouse models develop phenotypes of relevance to clinical cystic fibrosis (CF) including airway hyperresponsiveness, small intestinal bacterial overgrowth and an altered intestinal microbiome. As dysbiosis of the intestinal microbiota has been recognized as an important contributor to many systemic diseases, herein we investigated whether altering the intestinal microbiome of BALB/c  Cftr  tm1UNC  mice and wild-type littermates, through treatment with the antibiotic streptomycin, affects the CF lung, intestinal and bone disease. We demonstrate that streptomycin treatment reduced the intestinal bacterial overgrowth in  Cftr  tm1UNC  mice and altered the intestinal microbiome similarly in  Cftr  tm1UNC  and wild-type mice, principally by affecting  Lactobacillus  levels. Airway hyperresponsiveness of  Cftr  tm1UNC  mice was ameliorated with streptomycin, and correlated with  Lactobacillus  abundance in the intestine. Additionally, streptomycin treated  Cftr  tm1UNC  and wild-type mice displayed an increased percentage of pulmonary and mesenteric lymph node Th17, CD8 + IL-17+ and CD8 + IFNγ+ lymphocytes, while the CF-specific increase in respiratory IL-17 producing γδ T cells was decreased in streptomycin treated  Cftr  tm1UNC  mice. Bone disease and intestinal phenotypes were not affected by streptomycin treatment. The airway hyperresponsiveness and lymphocyte profile of BALB/c  Cftr  tm1UNC  mice were affected by streptomycin treatment, revealing a potential intestinal microbiome influence on lung response in BALB/c  Cftr  tm1UNC  mice.

Streptomycin treatment alters the intestinal microbiome, pulmonary T cell profile and airway hyperresponsiveness in a cystic fibrosis mouse model