Abstract Inflammation plays a crucial role in the control of Mycobacterium tuberculosis ( M . tb ) infection. In this study, we demonstrate that an inflammatory pulmonary environment at the time of infection mediated by liposaccharide (LPS) treatment in mice confers enhanced protection against M . tb for up to 6 months post infection. This transient protective inflammatory environment was associated with a neutrophil and monocyte/macrophage influx as well as increased inflammatory cytokines. In vitro infection of neutrophils from LPS treated mice demonstrated that LPS neutrophils exhibited increased recognition of M . tb , and had a greater innate capacity for killing M . tb . Finally, partial depletion of neutrophils in LPS treated mice showed an increase in M . tb burden, suggesting neutrophils conferred the enhanced protection observed in LPS treated mice. These results indicate a positive role of an inflammatory environment during initial M . tb infection, and suggests that acute inflammation at the time of M . tb infection can positively alter disease outcome.

Acute inflammation, mediated by lung neutrophils, confers enhanced protection againstMycobacterium tuberculosisinfection in mice