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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: Staphylococcus aureus vesicles impair cutaneous wound healing through p38 MAPK-MerTK cleavage-mediated inhibition of macrophage efferocytosis

Fig. 1

The presence of S. aureus vesicles in the wounds of trauma patients. A Distribution of isolated pathogenic bacteria and the proportion of Gram-positive or -negative bacteria at the wound sites of 33 patients. B A schematic diagram depicting vesicle purification protocol from the wound tissue. Wound bacterial extracellular vesicles (wBEVs) fractionated by OptiPrep density-gradient centrifugation. Representative (C) pictures, (D) size, and (E) TEM images of precipitated rough EVs (upper) and wBEVs (lower) collected from 30 − 45% layer (scale bar = 50 − 100 nm). Rough EV pellets contained a mixture of vesicles and non-vesicular components. Black arrows point to heterogeneous EVs. Box showed vesicles with a typical round double layer. F TLR2 (left) and TLR4 (right) activation levels from wBEVs extracted from rough EVs. G Coomassie staining of total wBEVs separated by SDS-PAGE (H) WB analysis of ScpA, staphylococcal protein A, OmpA, and LPS in wBEVs and bacterial lysates. S. aureus and E. coli cell lysates served as positive controls. I Images of skin wound and overlay of representative profile plots. J Wound healing dynamics in WT mice after PBS or wBEVs treatment. K Red brackets in the representative histology images show the size of the wound bed in PBS or wBEVs-treated groups. Scale bar = 2.0 mm. Unpaired two-tailed t-test. **, p < 0.01; ***, p < 0.001

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