Medications that mitigate inflammation caused by a variety of diseases including rheumatic arthritis may also compromise a person’s immune system.
In a Purdue University study, researchers found a new approach that provides a possible solution to this problem.
The team found a mechanism that might alleviate inflammation by suppressing the migration of a type of white blood cell called neutrophils.
The cells migrate within tissues in order to kill pathogens but may also cause excessive inflammation, resulting in tissue injury and other adverse effects.
The scientists identified a genetic molecule called miR-199, a type of “microRNA,” which reduces the migration of neutrophils, therefore potentially relieving inflammation without compromising the immune system.
Recently, microRNAs have been used in clinical trials to treat cancer and infection.
They also are used as screening tools to identify the underlying mechanisms of diseases and cell behavior.
However, the role of microRNAs in regulating neutrophil migration is largely unknown.
The researchers used a genetic-screening method to identify eight microRNAs that suppress neutrophilic migration, including miR-199.
They found that miR-199 directly suppresses the action of an enzyme called cyclin-dependent kinase 2, or CDK2, in turn dampening the migration of neutrophils.
Although CDK2 is well known for its role in regulating a cell’s life cycle—the process of a cell replicating its DNA and dividing to generate two cells—its link to neutrophil migration was previously unknown.
This work suggests miR-199 and CDK2 as new targets for treating inflammatory ailments and introduces an avenue of the function for CDK2 outside the cell cycle regulation.
The team says the research results expand the current understanding of neutrophil migration and suggest a novel strategy to manage neutrophilic inflammation.
The work is ongoing, and the next step is to understand the detailed molecular mechanisms for how CDK2 suppresses neutrophil migration and lethal inflammation.
The lead author of the study is Qing Deng, an assistant professor in the Department of Biological Sciences.
The study is published in Proceedings of the National Academy of Sciences.
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