Characterization of Krüppel-like factor 3 expression in T lymphocytes in septic mice

Background Krüppel-like factor 3 (KLF3) may be involved in the regulation of inflammatory responses and lymphocyte function. Moreover, immune dysfunction in sepsis involves both hyperinflammatory responses and immunosuppression. However, studies on T-lymphocyte KLF3 expression characteristics in sepsis are lacking. Methods We induced sepsis in mice through cecal ligation and puncture (CLP) and evaluated their survival rate over 7 days. To identify the immune status of the septic mice, we assessed their cytokine levels, organ damage scores, and splenic T-lymphocyte phenotype. Finally, KLF3 expression in T lymphocytes was detected through flow cytometry. Results Over the 7 days of observation, septic mice demonstrated 64.7% mortality. In the early stages after CLP, the proinflammatory and anti-inflammatory cytokine levels increased rapidly, multiple organ damage occurred, and splenic T lymphocytes became activated (with an increase in the proportions of CD69 ⁺ cells and mean fluorescence intensity for CD71). However, the proportion of KLF3 ⁺ T lymphocytes decreased. Subsequently, cytokine levels and lymphocyte activation decreased. An increase in cell apoptosis led to a substantial loss of T lymphocytes. Considering the continual elevations in serum interleukin 10 and interleukin 6 levels and worsening severe organ damage, the septic mice may have entered a state of chronic inflammation and immunosuppression, with a simultaneous increase in KLF3 expression in T lymphocytes, in the later stages after CLP. Conclusions In septic mice, T-lymphocyte KLF3 expression decreased in the early stage after CLP (i.e., systemic inflammatory response and T-lymphocyte activation stage) but increased in the later stage (i.e., chronic inflammation and immunosuppression stage). As such, KLF3 may be a promising target for dynamic immune monitoring and immunomodulatory therapy for sepsis.