A recent study on distinct inflammasomes NLRC4 and NLRP3 in cystic fibrosis (CF)-associated lung infections showed that NLRP3 activity can be impaired by Kineret.
The study, “IL-1 receptor antagonist ameliorates inflammasome-dependent inflammation in murine and human cystic fibrosis,” published in the journal Nature Communications, also found that NLRP3 activity can be impaired by Kineret (anakinra), an approved rheumatoid arthritis treatment, revealing a promising therapy approach for CF patients.
In CF patients, a continuous cycle of infection, inflammation, and tissue damage is responsible for the progressive decline of pulmonary function. When an infection takes place, the innate immune system is the first to be activated. This immune response relies mainly on cells that are always present, and ready to mobilize and fight microbes at the site of infection.
But the pulmonary innate immune response in CF is dysregulated at several levels, resulting in inefficient bacterial clearance and, ultimately, contributing to lung diseases associated with CF. Inflammasome activation is critical to fight infection, leading to the production of Interleukin (IL)-1? and IL-18 that recruit T-cells to kill the pathogens. But excessive activation of these complexes can result in an extreme inflammatory response that compromises the host’s ability to control infection.
Several different inflammasome complexes have been described to date. All of them recognize specific danger signals, and subsequently instruct immune cells to act against harmful pathogens.
