Researchers at Purdue University have made a promising discovery that could lead to new treatments for inflammation without compromising the immune system.
Led by Assistant Professor Qing Deng from the Department of Biological Sciences, the study focuses on a specific type of white blood cell known as neutrophils, which play a critical role in the body’s defense against infections.
Neutrophils are essential for killing pathogens, but their migration into tissues can also cause excessive inflammation, resulting in tissue damage and other negative effects.
To address this issue, the Purdue team explored the role of microRNAs, small genetic molecules that regulate various cellular processes.
The study, published in the Proceedings of the National Academy of Sciences, highlights the potential of a particular microRNA, miR-199, to reduce the migration of neutrophils and thereby alleviate inflammation.
MicroRNAs have recently gained attention in the medical field for their roles in treating diseases such as cancer and infections and as tools in disease mechanism identification.
However, their function in controlling neutrophil migration has not been well understood until now. Through genetic screening, the researchers identified eight microRNAs that can suppress neutrophil migration, with miR-199 being particularly effective.
Further investigation revealed that miR-199 directly targets an enzyme called cyclin-dependent kinase 2 (CDK2), known for its role in cell cycle regulation.
This interaction between miR-199 and CDK2 reduces the activity of CDK2, which in turn dampens the migration of neutrophils.
This discovery not only offers new insights into the control of neutrophil-induced inflammation but also suggests a previously unknown function of CDK2 outside of cell cycle regulation.
This breakthrough provides a foundation for developing new therapeutic strategies that target the migration of neutrophils to manage inflammation effectively without negatively affecting the immune system.
The findings expand current understanding of neutrophil behavior and open up novel avenues for research into inflammatory diseases.
As the study progresses, the next steps include delving deeper into the molecular mechanisms by which CDK2 influences neutrophil migration and exploring the broader implications of this pathway in treating inflammatory conditions.
This innovative approach holds potential for significant advancements in the treatment of diseases characterized by excessive inflammation, such as rheumatic arthritis, offering hope for safer and more effective management options.
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.
For more information about nutrition, please see recent studies about new way to halt excessive inflammation, and results showing foods that could cause inflammation.
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