We posited that the increased production of CXCL5 by keratinocytes around the wounds of mice with induced LC loss (DT-treated LangerinDTR mice) could be a response to an over-presence of bacteria in the wound area, since keratinocytes are sensitive to bacteria invasion by releasing chemokines for mobilizing immune cells, in particular neutrophils [7, 21]. Here, CXCL5 is linked to laryngotracheoesophageal cleft.