We've updated our Privacy Policy to make it clearer how we use your personal data.

We use cookies to provide you with a better experience. You can read our Cookie Policy here.

Advertisement
Heart Disease–Related Inflammation Prevented by Immune Cell Chemical Messages
News

Heart Disease–Related Inflammation Prevented by Immune Cell Chemical Messages

Heart Disease–Related Inflammation Prevented by Immune Cell Chemical Messages
News

Heart Disease–Related Inflammation Prevented by Immune Cell Chemical Messages

Credit: Pixabay.
Read time:
 

Want a FREE PDF version of This News Story?

Complete the form below and we will email you a PDF version of "Heart Disease–Related Inflammation Prevented by Immune Cell Chemical Messages"

First Name*
Last Name*
Email Address*
Country*
Company Type*
Job Function*
Would you like to receive further email communication from Technology Networks?

Technology Networks Ltd. needs the contact information you provide to us to contact you about our products and services. You may unsubscribe from these communications at any time. For information on how to unsubscribe, as well as our privacy practices and commitment to protecting your privacy, check out our Privacy Policy

The immune system’s white blood cells, which are produced in the bone marrow, mostly help to defend against bacteria and injury, but sometimes they can turn against the body—for example, in cardiovascular disease, their inflammatory aggression can harm arteries and the heart. New research in Nature Immunology that was led by investigators at Massachusetts General Hospital (MGH) provides insights into the pathways that increase or decrease the bone marrow’s output of these cells. The findings may lead to new treatments for conditions that arise when the balance of white blood cell production goes awry.


Senior author Matthias Nahrendorf, MD, PhD, an investigator in MGH’s Center for Systems Biology and The Richard Moerschner professor at the MGH Research Institute and Harvard Medical School, explains that the nervous system plays a role in controlling blood cell production through chemical messengers or neurotransmitters. “This is for instance important in people exposed to stress, where stress hormones—part of the ‘fight-or-flight’ response controlled by the sympathetic nervous system—may increase bone marrow activity and cardiovascular inflammation in response to the neurotransmitter noradrenaline,” he says. The sympathetic nerves have a counter player—the parasympathetic nerves, which slow down responses and bring about a state of calm to the body, mainly through the neurotransmitter acetylcholine.


Because acetylcholine can have a protective effect against inflammation and heart disease, the researchers studied this neurotransmitter in the bone marrow. “When we looked into how acetylcholine acts on the production of blood cells, we found that it does the expected—it reduces white blood cells, as opposed to noradrenaline, which increases them,” says Nahrendorf. “What was unexpected though was the source of the neurotransmitter acetylcholine.”


The team found no evidence in the bone marrow of the typical nerve fibers that are known to release acetylcholine. Instead, B cells, which are themselves a type of white blood cell (most known for making antibodies), supplied the acetylcholine in the bone marrow. “Thus, B cells counter inflammation—even in the heart and the arteries—via dampening white blood cell production in the bone marrow. Surprisingly, they use a neurotransmitter to do so,” says Nahrendorf.


Tapping into this process may help investigators develop strategies to block inflammation in cardiovascular conditions such as atherosclerosis. “Ultimately this may lead to new therapeutics that combat myocardial infarction, stroke, and heart failure,” says Nahrendorf. 


Reference: Schloss MJ, Hulsmans M, Rohde D, et al. B lymphocyte-derived acetylcholine limits steady-state and emergency hematopoiesis. Nat Immunol. Published online March 28, 2022:1-14. doi:10.1038/s41590-022-01165-7


This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.


Advertisement