Abstract

Sepsis shock was associated with worse mortality than common sepsis caused by disseminated infection. The present study had shown that repression of adaptive immunity was a characteristic of sepsis shock rather than sepsis, but the mechanism in which it exerted the adverse reaction was still need to be studied. In this study, we first employed weighted gene co-expression network analysis for acquiring the key modules with sepsis shock. Then, the differentially expressed genes and transcription factors were screened in the module for further function analysis, protein-protein interaction network building and long noncoding ribonucleic acid-micro ribonucleic acid-transcription factor network study. The study strengthened the concept that adaptive immune repression typically featured the sepsis shock concerning antigen presentation via major histocompatibility complex class II, T-cell activation and T-cell depletion. Among which T-cell depletion ranked as an overwhelming contributor to sepsis shock outcome. The transcription factor tumor protein P53, forkhead box protein O1 and GATA binding protein 3 served as the master regulator for the T-cell depletion process mainly through driving hematopoietic stem cells out of quiescence to unrestrained hematopoietic stem cell expansion with detrimental deoxyribonucleic acid damage, which greatly decreased hematopoietic stem cells long-term differentiation potential into T lymphocyte hierarchy. The study enlightened that manipulating the expression level of tumor protein P53, forkhead box protein O1 and GATA binding protein 3 to an optimized state will guarantee the T cell replenishment for fighting sepsis shock, which might support a potential efficient therapeutic way for sepsis shock treatment.