CD64 plays a key role in diabetic wound healing

Abstract

IntroductionWound healing poses a clinical challenge in diabetes mellitus (DM) due to compromised host immunity. CD64, an IgG-binding Fcgr1 receptor, acts as a pro-inflammatory mediator. While its presence has been identified in various inflammatory diseases, its specific role in wound healing, especially in DM, remains unclear.ObjectivesWe aimed to investigate the involvement of CD64 in diabetic wound healing using a DM animal model with CD64 KO mice.MethodsFirst, we compared CD64 expression in chronic skin ulcers from human DM and non-DM skin. Then, we monitored wound healing in a DM mouse model over 10 days, with or without CD64 KO, using macroscopic and microscopic observations, as well as immunohistochemistry.ResultsCD64 expression was significantly upregulated (1.25-fold) in chronic ulcerative skin from DM patients compared to non-DM individuals. Clinical observations were consistent with animal model findings, showing a significant delay in wound healing, particularly by day 7, in CD64 KO mice compared to WT mice. Additionally, infiltrating CD163+ M2 macrophages in the wounds of DM mice decreased significantly compared to non-DM mice over time. Delayed wound healing in DM CD64 KO mice correlated with the presence of inflammatory mediators.ConclusionCD64 seems to play a crucial role in wound healing, especially in DM conditions, where it is associated with CD163+ M2 macrophage infiltration. These data suggest that CD64 relies on host immunity during the wound healing process. Such data may provide useful information for both basic scientists and clinicians to deal with diabetic chronic wound healing.

Risk Factors Associated with Postoperative Cerebrospinal Fluid Leaks After Intrathecal Drug Delivery System and an External Pump Implantation in Cancer Patients: A Retrospective Study

“…The factors were analysed in the multivariable logistic model. According to the clinical experience and previous studies, we added BMI, albumin and diabetes as new variables, which is highly relevant to wound healing in clinic [15][16][17]. Hence, we conducted a cross-sectional study to collect data and explore the factors influencing CFSL, without conducting repeated measurements.…”

IL-38 promotes the development of prostate cancer

“…To confirm the source of IL-38 from the prostate cancer and the relationship between IL-38 and cell proliferation indices, immunofluorescent double staining was applied, as described previously ( 21 , 22 ). Briefly the sections were stained with anti-IL-38 and anti-P504S (RMA-0546, Fuzhou Maixin Biological Technology, China), anti-CD3, anti-CD68, anti-CD138, anti-CD20, and anti-Ki67 (ZM-0166, Beijing Sequoia Jinqiao Biological Technology), where IL-38 was used at a dilution of 1:400 (red fluorescence), anti-CD3, CD68, and CD138 were used at dilutions of 1:100, 1:1000, and 1:8000 respectively (green fluorescence), and anti-P504S and Ki67 were both used at a ready-to-use concentration (green fluorescence).…”

“…The numbers of IL-38 + cells were identified with containing CD138 + plasma cells, CD3 + pan-T cells, CD68 + macrophages, CD20 + B-lymphocyte, P504S + prostate tumour epithelial cells or Ki67 proliferative marker. These double staining sections were quantified, using the HALO Image analysis platform, as described previously ( 22 ) ( 21 ). The percentage of the double staining was calculated from the randomly selected 5 visual fields from each section, and quantified using Imagepro Plus V7 ( 23 ).…”