Abstract
BackgroundThe delayed repair process in the aging diabetic population is becoming an alarming public health concern. ICAM-1 plays an important role in orchestrating the repair process by mediating neutrophil recruitment and phagocytosis. However, little is known about the role of ICAM-1 in aging diabetic repair. MethodsBy causing injury in aging diabetic mice with ICAM-1 deletion (AD-ICAM-1−/−), we found that AD-ICAM-1−/− mice exhibited a delayed repair process with incomplete re-epithelialization and reduced angiogenesis. Additionally, high-throughput Illumina sequencing was performed to evaluate the microbiota of such mice. ResultsThe results indicate that the microbiota of the AD-ICAM-1−/− injury site differed taxonomically at both the phylum and genus levels. Neutrophil recruitment and phagocytic function were also reduced in the AD-ICAM-1−/− group. Notably, major inflammatory biomarker expression was also detected in AD-ICAM-1−/− injured tissue. ConclusionsOverall, this study demonstrated that AD-ICAM-1−/− mice exhibit delayed repair. In addition, neutrophil recruitment and phagocytic activity were impaired in the AD-ICAM-1−/− group, which may have allowed microbes to colonize the injury site.
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