Arup K Indra
Oregon State University, USA
Title: Effects of Vitamin D containing nanofibers on wound healing in a humanized mouse model
Biography: Arup K Indra
Surgical site infections constitute nearly 25% of all healthcare-associated infections (HAIs) and are the most common cause of infections in patients undergoing surgery. Current treatment plan utilizes wound dressings that deliver antibiotics, but their use can lead to selection and survival of drug-resistant microorganisms. The increasing frequency of multidrug-resistant bacterial species highlights the need for new approaches with distinct modes of action in order to boost the antimicrobial treatment modules used for prevention of surgical site infections. In collaboration, we and others have demonstrated that 1,25-dihydroxy vitamin D3[(1,25(OH)2D3); an active and more potent form of vitamin D] induces expression of cathelicidin antimicrobial peptide (CAMP) gene, the encoded hCAP18 protein and secretion of the antimicrobial peptide LL-37 that is cleaved from the C-terminal end of hCAP18 in human immune cells, epithelial cells and skin keratinocytes. We recently demonstrated that local sustained delivery of 1,25(OH)2D3 by biocompatible and biodegradable, nanofibrous dressings can induce expression of endogenous antimicrobial peptide hCAP18/LL-37 in vitro in keratinocytes and immune cells, in vivo in skin wounds from a humanized transgenic mouse that expresses a human hCAMP gene, and in ex vivo human skin wounds. We also showed that nanofibers loaded with Calcipotriol, a low calcemic analog of 1,25(OH)2D3 can accelerate cutaneous wound healing and promote efficient wound closure in vivo in the humanized mouse model expressing the human CAMP gene (hCAMP) in place of the mouse counterpart. The cellular and the molecular mechanisms underlying efficient wound healing following treatment with Vitamin D3 loaded nanofibers is currently being investigated.