Clinical efficacy of dialkylcarbamoylchloride‐coated cotton acetate dressing versus combination of normal saline dressing and 2% mupirocin ointment in infected wounds of epidermolysis bullosa

Dialkylcarbamoylchloride (DACC)‐coated cotton acetate dressing works directly through hydrophobic interaction to reduce the number of bacteria without the risk of resistance. It is easy to use and therefore expected to improve patient's compliance. This study aimed to assess the clinical efficacy of DACC‐coated cotton acetate dressing compared to a combination of normal saline dressing and 2% mupirocin ointment. A single‐blind controlled trial was conducted and included 14 infected epidermolysis bullosa (EB) wounds which were divided into two groups. Group I received DACC‐coated cotton acetate dressing, and Group II received the combination of normal saline dressing and 2% mupirocin ointment. Study results showed that the average time required for complete wound closure was 8.6 and 11.1 days in Groups I and II, respectively (p = .014), which was statistically significant. Both groups showed complete bacterial elimination on Day 3 based on negative Gram stain results and on Day 6 based on clearance of clinical manifestations (p = 1.000). This is a novel study in EB‐infected wounds, which shows that DACC‐coated cotton acetate dressing promotes faster wound closure and is as effective as the combination of normal saline dressing and 2% mupirocin ointment in eliminating bacterial infection.     

The extra domain A of fibronectin stimulates murine mast cells via toll-like receptor 4

The activation of mast cells by extra domain A of fibronectin (FN-EDA), an endogenous ligand of TLR4, and its contribution to the pathogenesis of rheumatoid arthritis (RA) in vivo were examined. FN-EDA, but no other domain of the fibronectin fragment, III(11) (FN-III(11)) and III(12) (FN-III(12)), stimulated bone marrow-derived murine mast cells (BMMCs) dose-dependently to secret cytokines (TNF-alpha, IL-6, and IL-1beta), similar to the pattern produced by LPS. FN-EDA-induced cytokine production was mediated by TLR4, as cytokine production by FN-EDA was absent in TLR4-deficient (TLR4-/-) BMMCs. We examined the roles of TLR4-mediated mast cell activation by this form of fibronectin fragment in the pathogenesis of RA in vivo. The injection of FN-EDA, but not FN-III(11)and FN-III(12), to joints resulted in joint swelling of mice in vivo. Genetically mast cell-deficient WBB6F(1)-W/W(v) mice exhibited significantly less swelling and cytokine production compared with mast cell-sufficient +/+ mice, suggesting that swelling and inflammatory cytokine production were partially dependent on tissue mast cells. Reduced swelling and cytokine production were recovered by the reconstitution of tissue mast cells by the injection of BMMCs from wild-type mice but not from TLR4-/- mice. Altogether, these results suggest that the TLR4-mediated activation of mast cells by endogenous ligand FN-EDA might contribute to the pathogenesis of RA through proinflammatory cytokine production.