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Leukotriene B 4  (LTB 4 ) is essential for host immune defence. It increases neutrophil recruitment, phagocytosis and pathogen clearance, and decreases oedema and inflammasome activation. The host response and the role of LTB 4  during  Achromobacter xylosoxidans  infection remain unexplored. Wild-type (129 sv ) and LTB 4  deficient ( Alox5   −/− ) mice were intratracheally infected with  A. xylosoxidans . Wild-type 129 sv  infected mice survived beyond the 8 th  day post-infection, exhibited increased levels of LTB 4  in the lung on the 1 st  day, while levels of PGE 2  increased on the 7 th  day post-infection. Infected  Alox5   −/−  mice showed impaired bacterial clearance, increased lung inflammation, and succumbed to the infection by the 7 th  day. We found that exogenous LTB 4  does not affect the phagocytosis of  A. xylosoxidans  by alveolar macrophages  in vitro . However, treatment of infected animals with LTB 4  protected from mortality, by reducing the bacterial load and inflammation via BLT 1  signalling, the high affinity receptor for LTB 4 . Of importance, we uncovered that LTB 4  induces gene and protein expression of α-defensin-1 during the infection. This molecule is essential for bacterial clearance and exhibits potent antimicrobial activity by disrupting  A. xylosoxidans  cell wall. Taken together, our data demonstrate a major role for LTB 4  on the control of  A. xylosoxidans  infection.

Leukotriene B4 is essential for lung host defence and alpha-defensin-1 production during Achromobacter xylosoxidans infection