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*
Department of Medicine, Division of Pulmonary and Critical Care Medicine,
Department of Pathology,
Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109; and
Department of Microbiology, Toho University School of Medicine, Tokyo, Japan
The contribution of neutrophils to lethal sensitivity and cytokine
balance governing T1 and T2 host responses was assessed in a murine
model of Legionella pneumophila pneumonia. Neutrophil
depletion by administration of granulocyte-specific mAb RB6-8C5 at 1
day before infection rendered mice 
100-fold more susceptible to
lethal pneumonia induced by L. pneumophila. However,
this treatment did not alter early bacterial clearance, despite a
substantial decrease in neutrophil influx at this time point. Cytokine
profiles in the lungs of control mice demonstrated strong T1 responses,
characterized by an increase of IFN-
and IL-12. In contrast,
neutrophil-depleted mice exhibited significantly lower levels of
IFN- and IL-12, and elevation of T2 cytokines, IL-4 and IL-10.
Immunohistochemistry of bronchoalveolar lavage cells demonstrated the
presence of IL-12 in neutrophils, but not alveolar macrophages.
Moreover, IL-12 was detected in lavage cell lysates by ELISA, which was
paralleled to neutrophil number. However, intratracheal administration
of recombinant murine IL-12 did not restore resistance, whereas
reconstitution of IFN- drastically improved bacterial clearance and
survival in neutrophil-depleted mice. Taken together, these data
demonstrated that neutrophils play crucial roles in primary L.
pneumophila infection, not via direct killing but more
immunomodulatory effects. Our results suggest that the early
recruitment of neutrophils may contribute to T1 polarization in a
murine model of L. pneumophila
pneumonia.
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