Sepsis, the body response to a life-threatening infection that causes damage to itself, is a leading cause of death around the globe, and failure of vital organs is one of the biggest contributors. Treatments of sepsis remain a serious concern and challenge in hospitals.
After More than 60 failed clinical studies and billions of dollars spent, barely any progress has been made. However, all the drugs and treatments available so far is mostly based on targeting the Gram-Negative bacteria LPS or using broad spectrum antibiotics which further worsen the conditions. The fact that sepsis is mostly a secondary form of problem which arises lately during an inflammatory disease treatment and mostly IL-1beta inhibitors are given to the patients for the treatment. Although these inhibitors give a temporarily ease but it further leads to the secondary infections which eventually leads to the sepsis.
We want to understand the complexities of sepsis majorly in the context of inflammasome regulation.
Inflammation plays a vital physiological role in maintaining homeostasis. Acute inflammation is the body’s initial response aimed at eliminating the underlying insult or threat. When this insult cannot be fully resolved, the body undergoes adaptive changes to coexist with it. However, this adaptation often comes at the expense of normal physiological functions, leading to a disruption in homeostasis. This state of dysregulation gives rise to chronic inflammation, whose primary purpose shifts from elimination to long-term adaptation. We are interested to understand how does the inflammasome regulation happens in chronic inflammation.
Inflammasomes in various cancers remains something of a mystery. It can either induce or inhibit tumor cell growth, depending on the cancer type and stage of the cancer. Inflammasome can manipulate immune recognition and many signaling pathways. We are interested to study how the inflammasome are dysregulated in cancer and how to utilize them against the cancer.