We have recently identified a CD11b+Gr1intF4/80+ (Gr1int) regulatory, non-migratory, cell type in the lung that is able to suppress a Th2 effector response via secretion of IL-10, arginase 1 and nitric oxide (NO). These regulatory cells also secrete IL-6 and GM-CSF, but low levels of IL-12. Our studies show that although Gr1int cells are present in the lung of naïve mice, their frequency increases following LPS exposure in a TLR4/MyD88 dependent fashion. The rapid appearance of these cells in response to a TLR ligand, combined with their non-migratory nature and their anatomical location in the lung interstitium, suggests a unique function during host defense against bacterial infections. Much is already known about the role of alveolar macrophages and neutrophils in host defense against Klebsiella Pneumoniae, however little is known about host defense mechanisms in the lung tissue/interstitium. For the first time, we have examined the role of Gr1int interstitial cells in defense against K. Pneumoniae. We show that the Gr1int cell population increases following exposure to K. Pneumoniae, are highly phagocytic, and co-localize with K. Pneumoniae, suggesting phagocytic uptake in vivo. Furthermore, Gr1int secrete high levels of NO, previously shown to be critical for effective innate immunity against K. Pneumoniae.
- Copyright © 2011 by The American Association of Immunologists, Inc.