Type I interferon is a key player in the host response to viruses, but its role during extracellular bacterial infections is less clear. LeMessurier et al. now report that type 1 interferon prevents the translocation of Streptococcus pneumoniae from the lung into the bloodstream, limiting systemic bacterial infections (PLoS Pathog. 9, e1003727, 2013).
Intranasal infection with S. pneumoniae upregulated the expression of interferon-b1 (Ifnb1) mRNA in the lungs before bacteria were detected in the blood. Blockade of IFN-b signaling in mice resulted in earlier and more pronounced bacteremia following intranasal infection without affecting bacterial titers in the lungs. Pretreating mice with IFN-b reduced the titer of bacteria in the blood of wild-type mice infected with S. pneumoniae.
The effects of type I interferons may be attributable to two mechanisms. The expression of certain tight junction proteins in the lung was lower in S. pneumoniae–infected Ifnar1−/− mice (which lack the type 1 IFN receptor) as compared with wild-type mice, whereas treatment of mice with IFN-b increased the expression of these proteins. IFN-b also reduced epithelial cell expression of platelet-activating factor receptor, which is known to participate in receptor-mediated transmigration of S. pneumoniae across cell layers. Thus, the induction of Ifnb1 expression in the lung during S. pneumoniae infection helps prevent systemic dissemination of bacteria by reducing their ability to migrate through or between alveolar cells and enter the vasculature. Taken together, these findings suggest that type 1 interferons may be used therapeutically to limit the development of invasive bacterial disease.
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Farrell, A. Blocking bacteria. Nat Med 19, 1582 (2013). https://doi.org/10.1038/nm.3429