Discovery of alarmin release mechanisms in immune system

E-selectin triggers quick NLRP3 inflammasome activation in neutrophils.

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The study “Immune System: Mechanisms of Alarmin Release Discovered” delves into the fascinating realm of alarmins and the mechanisms by which the immune system releases them. Alarmins are molecules released by damaged or stressed cells that serve as danger signals, alerting the immune system to potential threats. Understanding the mechanisms behind alarmin release is crucial for elucidating the immune system’s response to various threats and conditions.

Inflammation is linked to various common illnesses like arteriosclerosis and diabetes, as well as neurodegenerative diseases such as Alzheimer’s. Understanding these processes is crucial for developing new treatments. Neutrophils, a type of immune cell, play a vital role in starting and maintaining inflammation in our blood and tissues. 

When they become active, neutrophils release pro-inflammatory signals to alert the body’s immune system. Professor Markus Sperandio’s team at Ludwig Maximilians Universitat Munchen discovered how neutrophils release these signals, called alarmins, very early in the immune response.

Their research, published in Nature Immunology, shows that alarmins are released through pores in the neutrophil cell membrane formed by the NLRP3 inflammasome. While it was known that immune cells could form these pores after prolonged activation, this team, with the support of collaborators in Germany and Switzerland, revealed that this process occurs in the bloodstream, not just in the tissues.

In this study, researchers found that neutrophil immune cells can quickly create pores in their cell membranes using a process linked to the NLRP3 inflammasome. Even more surprising is that these pores can be removed in just a few minutes. This rapid and reversible pore formation helps prevent cell death, which is usually a result of NLRP3 inflammasome activation and pore creation.

This discovery not only advances our understanding of how the NLRP3 inflammasome functions but also opens the door to potential treatments that can influence and control inflammation very early on by adjusting the way alarmins are released. It’s a promising development for managing inflammatory conditions like arteriosclerosis, diabetes, and neurodegenerative diseases.

In conclusion, the study on the mechanisms of alarmin release in the immune system provides a deeper understanding of the immune response to cellular distress. These findings have the potential to revolutionize the way we approach the treatment of immune-related diseases and conditions by targeting the release of these critical alarm signals.

Journal reference:

  1. Pruenster, M., Immler, R., Roth, J. et al. E-selectin-mediated rapid NLRP3 inflammasome activation regulates S100A8/S100A9 release from neutrophils via transient gasdermin D pore formation. Nature Immunology. DOI: 10.1038/s41590-023-01656-1.
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