critical role of macrophages and their activation via myd88-nfκb signaling in lung innate immunity to mycoplasma pneumoniae关键作用的巨噬细胞及其在肺通过myd88-nfκb信号激活先天免疫肺炎支原体.pdf

Critical Role of Macrophages and Their Activation via MyD88-NFkB Signaling in Lung Innate Immunity to Mycoplasma pneumoniae 1 1,2 2 3 2¤ Jen-Feng Lai , Carlene L. Zindl , Lynn B. Duffy , T. Prescott Atkinson , Yong Woo Jung , Nico van 4 2 5 1 Rooijen , Ken B. Waites , Duncan C. Krause , David D. Chaplin * 1 Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America, 2 Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America, 3 Department of Pediatrics, University of Alabama at Birmingham, Birmingham, Alabama, United States of America, 4 Department of Molecular Cell Biology, Vrije University Medical Center, Amsterdam, The Netherlands, 5 Department of Microbiology, University of Georgia, Athens, Georgia, United States of America Abstract Mycoplasma pneumoniae (Mp), a common cause of pneumonia, is associated with asthma; however, the mechanisms underlying this association remain unclear. We investigated the cellular immune response to Mp in mice. Intranasal inoculation with Mp elicited infiltration of the lungs with neutrophils, monocytes and macrophages. Systemic depletion of macrophages, but not neutrophils, resulted in impaired clearance of Mp from the lungs. Accumulation and activation of macrophages were decreased in the lungs of MyD882/ 2 mice and clearance of Mp was impaired, indicating that MyD88 is a key signaling protein in the anti-Mp response. MyD88-dependent signaling was also required for the Mp-induced activation of NFkB, which was essential