Researchers at Purdue University have discovered a promising new approach to managing inflammation without compromising the immune system, according to a recent study published in the Proceedings of the National Academy of Sciences.
The study, led by Assistant Professor Qing Deng from the Department of Biological Sciences, focuses on the behavior of neutrophils, a type of white blood cell essential for fighting infections but also a common cause of harmful inflammation.
Inflammation is a natural immune response but can lead to severe tissue damage and contribute to diseases like rheumatic arthritis when it becomes chronic or excessive. Typically, medications that reduce inflammation also suppress the immune system, posing a dilemma for treating such conditions effectively.
The Purdue team’s breakthrough involves a genetic molecule known as miR-199, classified as a “microRNA.” MicroRNAs are small non-coding RNA molecules found in plants, animals, and some viruses, which function in the regulation of gene expression.
The researchers identified miR-199’s capability to reduce the migration of neutrophils. By controlling how these cells move within tissues, miR-199 helps curb the excessive inflammatory responses they can provoke without stifling their pathogen-fighting capabilities.
During their research, the scientists employed a genetic screening method to pinpoint eight microRNAs that inhibit the migration of neutrophils, including miR-199. They discovered that miR-199 specifically suppresses the activity of an enzyme called cyclin-dependent kinase 2 (CDK2).
This enzyme is well-recognized for its role in regulating the cell cycle—particularly how a cell replicates its DNA and divides—but its involvement in controlling neutrophil migration had not been previously identified.
The suppression of CDK2 by miR-199 offers a dual benefit: it potentially reduces harmful inflammation while preserving the body’s ability to fight off infections, providing a balanced approach to treating inflammatory diseases.
This finding not only enhances the understanding of neutrophil behavior and its implications for inflammatory diseases but also positions miR-199 and CDK2 as promising targets for new anti-inflammatory treatments.
The implications of this research are significant, suggesting that manipulating microRNA levels could become a novel strategy for managing inflammation more effectively, particularly in conditions where immune suppression is a concern.
The research is ongoing, with the next steps focusing on detailing the molecular mechanisms by which CDK2 influences neutrophil migration and the resulting inflammation.
This could pave the way for developing targeted therapies that harness this pathway, potentially offering relief for millions suffering from inflammatory diseases without the side effects associated with current treatments.
If you care about inflammation, please read studies about the big cause of inflammation in common bowel disease, and vitamin B may help fight COVID-19 and reduce inflammation.
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