Case Western Reserve Logo Sepsis appears as a major killer in hospital intensive care units. In a major breakthrough experts from the Case Western Reserve University School of Medicine found that manipulating a genetic factor that can launch or throttle the body’s defenses can boost survival rates in bacterial infection. The research findings supposedly have major implications in the health world.

Indiscriminately boosting immune cells apparently causes harm and even death. When a patient is suffering from the end-stage of sepsis, the defense system allegedly needs to be curbed to prevent the body’s own immune cells from contributing to shock and death. The key to better sepsis therapies may be understanding when to turn up or turn down the factor, called Kruppel-like transcription factor 2 (KLF2). Reportedly, KLF2 acts like a concert mix-master within immune cells known as macrophages.

Instead of adjusting the base and feedback, the factor seemingly adjusts cell activities in accordance to signals from the internal environment. Hence, the factor may maintain immune cells in a quiet state. During the first phase of sepsis, when bacteria begin to attack, the resulting low oxygen levels and high amounts of bacterial products supposedly diminish the level of KLF2. This reduction in the level of KLF2 purportedly enables macrophages to release noxious products that kill bacteria.

Mukesh K. Jain, MD, Ellery Sedgwick Jr. Chair, director of the Case Cardiovascular Research Institute, and colleagues found that when sepsis moves into the second phase, the body’s own defenses do harm by promoting inflammation that can cause shock and death. It is predicted that hypoxia and leaching of bacterial products into circulation keep KLF2 levels low. While conducting the research, it was affirmed that mouse models deficient in KLF2 were effective in defeating polymicrobial infections in the early stage of infection. When testing the late-stage of sepsis, mouse models lacking KLF2 were possibly more likely to die and die sooner.

The research is published in the May 27 edition of the journal Immunity.