Abstract
Despite the advancement in the treatment, nonhealing diabetic foot ulcers (DFUs) are an important clinical issue accounting for increased morbidity and risk of amputation. Persistent inflammation, decreased granulation tissue formation, decreased neo-angiogenesis, and infections are common underlying causes of the nonhealing pattern. Fibroblasts play a critical role in granulation tissue formation and angiogenesis and mediate wound healing how fibroblasts regulate inflammation in nonhealing DFUs is a question to ponder. This study aims to investigate the expression of a de-differentiated subpopulation of fibroblasts which are CD40+ (secretory fibroblasts) and increased secretion of IL-6 and IL-8 but have never been reported in DFUs. We characterized 11 DFU tissues and nearby clean tissues histologically and for the presence of inflammation and CD40+ fibroblasts using immunohistochemistry and RT-PCR. The results revealed significantly increased density of CD40+ fibroblasts and differential expression of mediators of inflammation in DFU tissues compared to clean tissue. Increased expression of IL-6, IL-1β, and TNF-α in DFU tissues along with CD40+ fibroblast suggest that CD40+ fibroblasts in DFUs contribute to the chronicity of inflammation and targeting fibroblasts phenotypic switch to decrease secretory fibroblasts may have therapeutic significance to promote healing.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
