Significant increases in IL-6, IL-17, and TNF-α confirmed the role of T-helper type 1 (Th1)- and Th17-related inflammation in NEC, with the former involved in intracellular pathogens and the latter in extracellular bacterial infections.17 The activation of Th1-mediated inflammation influences the severity of NEC,18 while the accumulation of CD4+ Th17 lymphocytes contributes directly to the development of NEC.19 Moreover, our study confirmed that an imbalance in regulatory (Tregs) and effector T cells was a key pathophysiological change in NEC, as indicated by reduced IL-10 production.20 This evidence concerns the gene TNF and bacterial infectious disease.