The study of the mechanism of reversible thymic atrophy caused by sepsis.

Sepsis is a life-threatening host inflammatory response caused by infection, accompanied by severe organ dysfunction and failure, with a mortality rate of 35.5%, making it the main cause of death in intensive care patients. As a systemic inflammatory response to infection, sepsis simultaneously triggers both pro-inflammatory and anti-inflammatory reactions. After a brief pro-inflammatory phase, the immune status of sepsis patients gradually enters a period dominated by anti-inflammatory responses, and the increased susceptibility to secondary infections due to the latter is the main cause of death for patients in the later stages of sepsis. Some studies have found that sepsis can cause reversible atrophy of the thymus, and it is believed that this atrophy is related to the long-term suppression of the adaptive immune system caused by sepsis, but there is still a lack of in-depth mechanism research. On the other hand, although this reversible atrophy will have significant morphological recovery after a period of recovery, there is still a lack of systematic research on the recovery of thymic function. In response to the above situation, we used cecal ligation and puncture (CLP) surgery to establish a sepsis mouse model, collected thymus from control group, atrophy phase, and after recovery, and conducted single-cell and spatiotemporal transcriptome sequencing to systematically describe the distribution, proliferation, differentiation, and apoptosis dynamics of thymic T cells during thymic atrophy and recovery. This helps us to further understand the mechanism of thymic atrophy and recovery caused by sepsis, and lays a certain foundation for the development of new immunotherapeutic tools targeting the recovery of thymic T cell function.