[PDF][PDF] Innate lymphocyte/Ly6Chi monocyte crosstalk promotes Klebsiella pneumoniae clearance

H Xiong, JW Keith, DW Samilo, RA Carter, IM Leiner… - Cell, 2016 - cell.com
H Xiong, JW Keith, DW Samilo, RA Carter, IM Leiner, EG Pamer
Cell, 2016cell.com
Increasing antibiotic resistance among bacterial pathogens has rendered some infections
untreatable with available antibiotics. Klebsiella pneumoniae, a bacterial pathogen that has
acquired high-level antibiotic resistance, is a common cause of pulmonary infections.
Optimal clearance of K. pneumoniae from the host lung requires TNF and IL-17A. Herein, we
demonstrate that inflammatory monocytes are rapidly recruited to the lungs of K.
pneumoniae-infected mice and produce TNF, which markedly increases the frequency of IL …
Summary
Increasing antibiotic resistance among bacterial pathogens has rendered some infections untreatable with available antibiotics. Klebsiella pneumoniae, a bacterial pathogen that has acquired high-level antibiotic resistance, is a common cause of pulmonary infections. Optimal clearance of K. pneumoniae from the host lung requires TNF and IL-17A. Herein, we demonstrate that inflammatory monocytes are rapidly recruited to the lungs of K. pneumoniae-infected mice and produce TNF, which markedly increases the frequency of IL-17-producing innate lymphoid cells. While pulmonary clearance of K. pneumoniae is preserved in neutrophil-depleted mice, monocyte depletion or TNF deficiency impairs IL-17A-dependent resolution of pneumonia. Monocyte-mediated bacterial uptake and killing is enhanced by ILC production of IL-17A, indicating that innate lymphocytes engage in a positive-feedback loop with monocytes that promotes clearance of pneumonia. Innate immune defense against a highly antibiotic-resistant bacterial pathogen depends on crosstalk between inflammatory monocytes and innate lymphocytes that is mediated by TNF and IL-17A.
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