| First Author | Livraghi-Butrico A | Year | 2012 |
| Journal | Mucosal Immunol | Volume | 5 |
| Issue | 4 | Pages | 397-408 |
| PubMed ID | 22419116 | Mgi Jnum | J:297349 |
| Mgi Id | MGI:6478086 | Doi | 10.1038/mi.2012.17 |
| Citation | Livraghi-Butrico A, et al. (2012) Mucus clearance, MyD88-dependent and MyD88-independent immunity modulate lung susceptibility to spontaneous bacterial infection and inflammation. Mucosal Immunol 5(4):397-408 |
| abstractText | It has been postulated that mucus stasis is central to the pathogenesis of obstructive lung diseases. In Scnn1b-transgenic (Scnn1b-Tg(+) mice, airway-targeted overexpression of the epithelial Na(+) channel beta subunit causes airway surface dehydration, which results in mucus stasis and inflammation. Bronchoalveolar lavage from neonatal Scnn1b-Tg(+) mice, but not wild-type littermates, contained increased mucus, bacteria, and neutrophils, which declined with age. Scnn1b-Tg(+) mice lung bacterial flora included environmental and oropharyngeal species, suggesting inhalation and/or aspiration as routes of entry. Genetic deletion of the Toll-interleukin-1 receptor adapter molecule MyD88 in Scnn1b-Tg(+) mice did not modify airway mucus obstruction, but caused defective neutrophil recruitment and increased bacterial infection, which persisted into adulthood. Scnn1b-Tg(+) mice derived into germ-free conditions exhibited mucus obstruction similar to conventional Scnn1b-Tg(+) mice and sterile inflammation. Collectively, these data suggest that dehydration-induced mucus stasis promotes infection, compounds defects in other immune mechanisms, and alone is sufficient to trigger airway inflammation. |
