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Accumulation of neutrophils in the site of inflammation is atypical mechanism of innate immunity. The accumulated neutrophilsare exposed to stressogenic factors usually associated withinflammation. Here, we studied response of human peripheral bloodneutrophils  subjected to short, febrile-range heat stress. Weshow that 90 min heat stress slowed down the spontaneous apoptosisof neutrophils. In the absence of typical markers of apoptosis theheat-shocked neutrophils induced antiinflammatory effect in humanmonocyte-derived macrophages (hMDMs), yet without being engulfed.Importantly, the expression of FcγRIII (CD16) was sharply reduced.Surprisingly, concentration of the soluble CD16 did not change inheat-shocked neutrophil supernates indicating that the reductionof the cell surface CD16 was achieved mainly by inhibition offresh CD16 delivery. Inhibitors of 90 kDa heat shock protein(HSP90), a molecular chaperone found in membrane platformstogether with CD16 and CD11b, significantly increased the observedeffects caused by heat shock. The presented data suggest a novelsystemic aspect of increased temperature which relies on immediatemodification by heat of a neutrophil molecular pattern. Thiseffect precedes cell death and may be beneficial in the initialphase of inflammation providing a nonphlogistic signal tomacrophages before it comes from apoptotic cells

Rapid Decrease of CD16 (FcγRIII) Expression on Heat-Shocked Neutrophils and Their Recognition by Macrophages