Dectin-1 and TLRs Permit Macrophages to Distinguish between Different Aspergillus fumigatus Cellular States

摘要: Aspergillus fumigatus is a common cause of invasive and allergic pulmonary disease. Resting conidia the filamentous fungus are constantly inhaled, but infection only after initiating hyphal growth. In this study, we have explored whether macrophages can distinguish between resting spores maturing, potentially form fungus. Although bind ingest A. efficiently, there little inflammatory response; NF-κβ not activated, cytokines induced, reactive oxygen species produced. However, maturing germ tubes stimulate NF-κβ, secretion proinflammatory production by human monocyte-derived murine from multiple anatomical sites. These responses in part mediated dectin-1, which binds cell wall β-glucan that present on surface dormant conidia, cellular swelling loss hydrophobic proteinaceous wall. Dectin-1 binding to augments, required for, TLR2-mediated cytokine secretion. recognition also stimulates TNF-α absence both TLR2 MyD88 signaling. data demonstrate one mechanism response tailored toward metabolically active cells, thereby avoiding unnecessary tissue damage with frequent inhalation ubiquitous spores.