Mast cells are required for normal healing of skin wounds in mice.

TY - JOUR

T1 - Mast cells are required for normal healing of skin wounds in mice.

AU - Weller, Karsten

AU - Foitzik, Kerstin

AU - Paus, Ralf

AU - Syska, Wolfgang

AU - Maurer, Marcus

PY - 2006

Y1 - 2006

N2 - Mast cells (MCs) have recently been reported to play a pivotal role in the elicitation of inflammatory reactions that are beneficial to the host, e.g., during innate immune responses to bacteria. To explore whether MCs also contribute to wound repair, we studied experimentally induced skin wounds in MC-deficient Kit(W)/Kit(W-v) mice, normal Kit+/+ mice, and MC-reconstituted Kit(W)/Kit(W-v) mice. Wound closure was significantly impaired in the absence of MCs during the first 6 days of wound healing and histomorphometric analyses of MC degranulation at the wound edges revealed distance-dependent MC activation, i.e., MC degranulation was most prominent directly adjacent to the wound. In addition, Kit(W)/Kit(W-v) mice showed impaired extravasation and recruitment of neutrophils to the wounded areas. Notably, wound closure, extravasation, and neutrophil recruitment were found to be normal in MC-reconstituted Kit(W)/Kit(W-v) mice. Therefore, we examined whether MCs promote wound healing by releasing histamine or TNF-alpha. Interestingly, wound closure was reduced in mice treated with an H1-receptor antagonist but not after treatment with an H2-receptor antagonist or in the absence of TNF-alpha. Taken together, our findings indicate that MC activation and histamine release are required for normal cutaneous wound healing.

AB - Mast cells (MCs) have recently been reported to play a pivotal role in the elicitation of inflammatory reactions that are beneficial to the host, e.g., during innate immune responses to bacteria. To explore whether MCs also contribute to wound repair, we studied experimentally induced skin wounds in MC-deficient Kit(W)/Kit(W-v) mice, normal Kit+/+ mice, and MC-reconstituted Kit(W)/Kit(W-v) mice. Wound closure was significantly impaired in the absence of MCs during the first 6 days of wound healing and histomorphometric analyses of MC degranulation at the wound edges revealed distance-dependent MC activation, i.e., MC degranulation was most prominent directly adjacent to the wound. In addition, Kit(W)/Kit(W-v) mice showed impaired extravasation and recruitment of neutrophils to the wounded areas. Notably, wound closure, extravasation, and neutrophil recruitment were found to be normal in MC-reconstituted Kit(W)/Kit(W-v) mice. Therefore, we examined whether MCs promote wound healing by releasing histamine or TNF-alpha. Interestingly, wound closure was reduced in mice treated with an H1-receptor antagonist but not after treatment with an H2-receptor antagonist or in the absence of TNF-alpha. Taken together, our findings indicate that MC activation and histamine release are required for normal cutaneous wound healing.

M3 - SCORING: Zeitschriftenaufsatz

VL - 20

SP - 2366

EP - 2368

JO - FASEB J

JF - FASEB J

SN - 0892-6638

IS - 13

M1 - 13

ER -