NK1.1+ cells regulate neutrophil migration in mice with Acinetobacter baumannii pneumonia


Hiroshi Tsujibo, Department of Microbiology, Osaka University of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki, Osaka 569-1094, Japan.
Tel: +81 72 690 1057; fax: +81 72 690 1057; email: tsujibo@gly.oups.ac.jp


Acinetobacter baumannii is a major cause of both community-associated and nosocomial infections worldwide. These infections are difficult to treat because the bacterium rapidly develops resistance to multiple antibiotics. However, little is known about the nature of the innate cellular response to A. baumannii infection. In the present study, we identified the cells infiltrating the lungs of mice with Acinetobacter pneumonia and analyzed their response to infection. Normal mice eradicated the A. baumannii infection within 3 days of inoculation. Neutrophils were rapidly recruited to the lungs, followed by macrophages and NK1.1+ cells. Neutrophil-depleted mice showed acute and severe symptoms, and all of the mice died within 3 days of inoculation. The majority of macrophage-depleted mice responded in a similar manner to the control mice. These results indicate that neutrophils are essential for the elimination of A. baumannii. Half of NK1.1+ cell-depleted mice died within 1 day of inoculation and the number of infiltrating neutrophils was lower than that in control mice up until 3 days post-inoculation. Moreover, the expression levels of keratinocyte chemoattractant protein (KC) decreased in NK1.1+ cell-depleted mice. These results indicate that NK1.1+ cells recruit neutrophils during the early phase of Acinetobacter infection by increasing KC expression.