One manner in which the host response to NTHi lysate differs from reported pandemic virus-induced inflammation [11] is in its restriction to the lung. While documenting massive increases in indicators of lung inflammation following treatment, there is virtually no systemic inflammation noted (Fig 3c) . Similarly, treatment with NTHi lysate induces no systemic leukocytosis (data not shown), despite the profound cellular infiltration induced in the lungs. We presume this confinement of the response to the lungs explains the lack of morbidity we have observed when mice are treated acutely even with very high doses of NTHi lysate [16] . Based on these observations, we conclude that influenza pneumonia does not kill via excessive pulmonary inflammation, but progresses through a deficit of effective inflammation.