The team previously showed that mice that had just recovered from the flu had a weak inflammatory response that made them more susceptible to other pathogens over the next six months. The group now finds that post-flu inflammation in these mice is tempered by a dampened innate immune system.

The innate system usually responds to ligands that activate Toll-like receptors (TLRs). But in mice recovering from the flu, these ligands did not activate TLRs on lung macrophages. The cells therefore did not produce the chemokines necessary to attract neutrophils—the main instigators of lung inflammation.

Although the blunted TLR response might protect the lungs against inflammation-induced damage, it made them vulnerable to bacterial infection. After beating influenza, the mice were killed by pneumonia-causing bacteria that are normally held at bay in the airways.

Influenza and other respiratory viruses are not known to encode TLR-suppressing proteins. This suppression may thus represent the lung's attempts to protect itself from damaging levels of inflammation. The authors suspect that the lungs might suppress TLR expression in response to any insult that causes a massive inflammatory response, including pathogens, injury, or environmental allergens. Their theory is bolstered by the fact that another respiratory pathogen, respiratory syncytial virus, also suppressed macrophage TLR signaling.

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