期刊
JOURNAL OF INFECTIOUS DISEASES
卷 217, 期 9, 页码 1481-1490出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiy049
关键词
Acute lung infection; Francisella tularensis; immature myeloid cells; MDSC; macrophages; neutrophils; pneumonia
资金
- National Institute of Allergy and Infectious Diseases, National Institutes of Health [P01AI056320]
Bacterial pneumonia is a common risk factor for acute lung injury and sepsis-mediated death, but the mechanisms underlying the overt inflammation and accompanying pathology are unclear. Infiltration of immature myeloid cells and necrotizing inflammation mediate severe pathology and death during pulmonary infection with Francisella tularensis. However, eliciting mature myeloid cells provides protection. Yet, the host factors responsible for this pathologic immature myeloid cell response are unknown. Here, we report that while the influx of both mature and immature myeloid cells is strictly MyD88 dependent, the interleukin 1 (IL-1) receptor mediates an important dual function via its ligands IL-1 alpha and IL-1 beta. Although IL-1 beta favors the appearance of bacteria-clearing mature myeloid cells, IL-1 alpha contributes to lung infiltration by ineffective and pathologic immature myeloid cells. Finally, IL-1 alpha and IL-1 beta are not the sole factors involved, but myeloid cell responses during acute pneumonia were largely unaffected by lung levels of interleukin 10, interleukin 17, CXCL1, granulocyte colony-stimulating factor, and granulocyte-macrophage colony-stimulating factor.
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