The mechanism of acute respiratory distress syndrome caused by new coronavirus infection revealed

The mechanism of acute respiratory distress syndrome caused by new coronavirus infection revealed

The mechanism of acute respiratory distress syndrome caused by new coronavirus infection has been revealed

Jinan University professor Wu Jianguo's team research revealed the molecular mechanism of the new coronavirus N protein to activate inflammasomes and cause organ damage
.

Related research was published in "Nature-Communication" on August 2

The new coronavirus mainly infects the human respiratory system.
An important feature of its infection is that viral infection can induce the body to produce a strong immune response and inflammatory response, resulting in the rapid and overexpression of a large number of cytokines.
This phenomenon is called "cytokine storm".
"
.

Cytokine storms can lead to uncontrolled inflammation, causing acute respiratory distress syndrome, severe pneumonia, lung tissue damage and even multiple organ failure

Inflammasomes are an important part of the body's natural immune system.
They are named according to different sensor proteins.
There are four main types of inflammasomes: NLRP1, NLRP3, NLRC4 and AIM2
.

Among them, NLRP3 inflammasome plays an important role in RNA virus infection

However, excessive IL-1β can activate different signal pathways, induce systemic inflammation, and promote the release of a large number of cytokines (including IL-6, TNF, IFN-α and IFN-β, etc.
), resulting in a cytokine storm.
Lead to acute inflammatory diseases
.

The study revealed the molecular mechanism that the new coronavirus N protein directly interacts with the NLRP3 protein to promote the assembly and activation of NLRP3 inflammasomes and induce the overexpression of cellular inflammatory factors, leading to acute inflammation and organ damage
.

Through in-depth research, it is found that in the acute inflammation mouse model, the new coronavirus N protein can promote the activation of NLRP3 inflammasomes, aggravate lung tissue damage, and accelerate the death of mice

Compared with NLRP3 wild-type (NLRP3+/+) mice, in NLRP3-deficient (NLRP3-/-) mice, the overexpression of cytokines and lung tissue damage induced by the new coronavirus N protein were significantly suppressed
.

These findings prove that the new coronavirus N protein and NLRP3 inflammasome play a very important role in the inflammatory response and tissue damage caused by the new coronavirus infection

The research results revealed a unique molecular mechanism of acute respiratory distress syndrome caused by new coronavirus infection, and confirmed the important role of NLRP3 inflammasome in the excessive inflammatory response and lung injury caused by new coronavirus infection, and proposed the activation of new coronavirus N protein.
"Inflammatory factor storm" may be a key factor in viral infections leading to acute pneumonia and lung injury, which has further deepened people's understanding of the pathogenic mechanism of new coronary pneumonia caused by new coronavirus infection
.

In addition, it is proposed that NLRP3 inhibitors and Caspase-1 inhibitors are expected to become potential drugs for the prevention and treatment of new coronavirus infections, and provide new ideas and theoretical basis for the prevention and treatment of new coronary pneumonia

It is worth mentioning that in recent years, Wu Jianguo's team has focused on the molecular mechanism of RNA virus infection regulating NLRP3 inflammasome leading to related diseases, and has achieved a series of research results
.

For example, it was discovered that Dengue virus regulates NLRP3 inflammasomes, promotes IL-1b activation, induces vascular leakage in mice, and causes tissue damage; it is determined that Zika virus infection promotes NLRP3 inflammasome assembly, induces IL-1β secretion, and activates the host Inflammatory response; it is proved that enterovirus 71 infection activates NLRP3 inflammasome and induces inflammatory response

Related paper information: https://doi.

https://doi.
org/10.
1038/s41467-021-25015-6