LAUSR

We read with much interest the research letter by Pantale on Garc ıa and colleagues regarding the response of lung microbiota to changes in pulmonary innate immunity (1). An important question that needs to be addressed is why the lungs of mice were harvested 6 days after exposure to Pam2-ODN, a Toll-like receptor agonist. Inhalation of Pam2-ODN has been shown to protect mice infected with a virus or bacteria a few hours after exposure to the Toll-like receptor agonist (2–4). Therefore, it is conceivable that earlier evaluation of lung microbiota would have provided different results. On the other hand, previous studies have shown that multisource reactive oxygen species generation is required to protect mice against viral or bacterial infection after exposure to Pam2-ODN (5). In addition, another study has shown that exposure to Pam2-ODN is associated with a dramatic increase in the expression of inflammatory cytokines (e.g., tumor necrosis factor-a) and chemokines (e.g., Cxcl1, Cxcl2, Cxcl13) in the lungs (6). These observations suggest that measuring reactive oxygen species, inflammatory cytokines, or chemokines in blood or lung homogenates may provide key information to determine the optimal time to assess changes in lung microbiota in response to an enhanced pulmonary innate immunity. We believe that addressing the above questions may further clarify whether changes in pulmonary innate immunity affect lung microbial communities.