Human beta defensins (HBDs) are small cationic peptides with chemoattractant activities. HBD2 and HBD3 are generally expressed at low levels in physiologic conditions and are induced in response to microbial challenge (e.g. LPS), whereas HBD1 low expression is constitutive, with little regulation in response to infection or other stimuli. HBDs produced by HAEC co‐create an innate antimicrobial immune response in the materno‐placento‐fetal unit. PCD increases the risk of infection. According to recent studies, PCD activates the innate immune response through TLR5 or TLR1/2 on neonatal monocyte, but the data about HBDs are still lacking. The aim of this study was to examine comparatively the effect of resveratrol on SIRT1 level and HBD2 and HBD3 production in HAEC isolated after PCD (White’s class C) vs. NP. HAEC were isolated from the amnion immediately after cesarean section delivery terminating PCD (N = 24, group I) and NP (N = 24, group II) using trypsin‐based method and cultured in vitro under normoxia at 37 degrees C. Upon reaching confluence, HAEC were cultured in media supplemented with 0.5 μM resveratrol and SIRT1 levels were determined in HAEC culture lysates obtained once a day for 7 consecutive days. After pretreatment with LPS (1 μg/mL), HBD2 and HBD3 concentrations in the HAEC culture supernatant, obtained in the days 1,3 and 7 of the culture with resveratrol, were assessed in both goups using ELISA. Nonparametric Wilcoxon rank‐sum test was used and the differences between the groups were considered statistically significant if p < 0.05. In both groups resveratrol increased significantly SIRT1 levels in consecutive days. The response was stronger in PCD as compared to NP. Despite of this, observed increase in both HBD2 and HBD3 concentrations were significantly lower in PCD, amounting to 32.8 / 37.7, 45.5 / 42.9 and 55.3% / 49.5% (HBD2 / HBD3 days 1,3 and 7, respectively) of the values obtained in group II (NP). Importantly, the mean viability of cells in both groups did not differ significantly at the consecutive time points. Thus, susceptibility to infections in diabetes may be to some extent caused by compromised HBDs‐dependent antimicrobial immune respose. The nature of impaired SIRT1 – HBDs interaction is still under investigation.Support or Funding InformationWUM grant: 2M2‐W2‐18/2M2‐W1‐19