Figure 1.
Figure 1. Detection of Eap in wounds and effect of Eap on wound healing. (A) Eap detection in S aureus–infected wounds. (B) Eap was detected by Western blot analysis in extracts of noninfected (lane 1) or S aureus–infected (lane 2) wounds. Molecular mass markers are indicated along the right margin. (C) The course of wound closure is shown in the absence (buffer; •), or in the presence of wild-type S aureus (▪) or the Eap-deficient strain (□). *P < .05 compared with buffer-treated wounds; #P < .05 compared with wounds that received the Eap-deficient strain; **P < .05 compared with buffer-treated wounds. (D) The course of wound closure is shown in the absence (•) or presence of 20 μg Eap (▪) or protein A (▵). *P < .05 compared with buffer-treated wounds. Wound closure is expressed relative to the wound size of each wound at day 0 that represents 100%. Data are expressed as mean ± SD (n = 8).

Detection of Eap in wounds and effect of Eap on wound healing. (A) Eap detection in S aureus–infected wounds. (B) Eap was detected by Western blot analysis in extracts of noninfected (lane 1) or S aureus–infected (lane 2) wounds. Molecular mass markers are indicated along the right margin. (C) The course of wound closure is shown in the absence (buffer; •), or in the presence of wild-type S aureus (▪) or the Eap-deficient strain (□). *P < .05 compared with buffer-treated wounds; #P < .05 compared with wounds that received the Eap-deficient strain; **P < .05 compared with buffer-treated wounds. (D) The course of wound closure is shown in the absence (•) or presence of 20 μg Eap (▪) or protein A (▵). *P < .05 compared with buffer-treated wounds. Wound closure is expressed relative to the wound size of each wound at day 0 that represents 100%. Data are expressed as mean ± SD (n = 8).

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