Monday August 26, 2019

Good Cholesterol may Fail to Protect You against Heart Disease, also increases Inflammatory response of Immune Cells called Macrophages

Lung macrophages ingested disease-causing bacteria upon exposure to high-density lipoprotein (HDL)

0
//
Representational image. Flickr

London, November 18, 2016: Although well associated with lowering cardiovascular disease risk high-density lipoprotein (HDL) — known as good cholesterol — may not always be able to protect against heart disease.

A new study has suggested that it increases the inflammatory response of certain immune cells called macrophages.

NewsGram brings to you current foreign news from all over the world.

This can potentially counteract its well-established anti-inflammatory effect in various other cell types, the study said.

“Good cholesterol’s functions are not as simple as initially thought, and appear to critically depend on the target tissue and cell type,” said Marjo Donners of Maastricht University, the Netherlands.

“In the end, it is the balance between its pro- and anti-inflammatory effects that determines clinical outcome,” Donners added.

NewsGram brings to you top news around the world today.

In the study, the researchers found that HDL treatment enhanced inflammation in macrophages, in contrast to its effects in other cell types. Similarly, macrophages taken from mice with elevated HDL levels showed clear signs of inflammation.

This pro-inflammatory effect induced by HDL showed enhanced pathogen protection, the researchers said.

Lung macrophages ingested disease-causing bacteria upon exposure to HDL. On the other hand, mice with low HDL levels were impaired at clearing these bacteria from the lungs.

The results demonstrate that HDL’s pro-inflammatory activity supports the proper functioning of macrophage immune responses.

Check out NewsGram for latest international news updates.

According to Donners, these findings suggest that patients with persistent infections or specific immune disorders might benefit from HDL-raising therapies.

The research could also lead to the development of cell-specific therapies that exploit the benefits of HDL-targeted therapies while avoiding the side effects, the researchers noted.

The study was published in the journal Cell Metabolism. (IANS)

Next Story

Reduce Heart Disease Risk by Quitting Smoking

The cardiovascular system begins to heal relatively quickly after quitting smoking

0
smoking is injurious
Researchers used data from the Framingham Heart Study, a longitudinal study of men and women from Massachusetts, which began enrolment in 1948. Pixabay

Heavy cigarette smokers can reduce their risk of cardiovascular diseases (CVD) by 39 per cent within five years if they quit, researchers said.

It takes at least five to 10 years and perhaps up to 25 years after quitting, for CVD risk to become as low as that of a person who has never smoked, according to the study published in the Journal of the American Medical Association (JAMA).

“The cardiovascular system begins to heal relatively quickly after quitting smoking, even for people who have smoked heavily over decades,” said Hilary Tindle, Founding Director of the Vanderbilt Center for Tobacco Addiction and Lifestyle (ViTAL).

Researchers used data from the Framingham Heart Study, a longitudinal study of men and women from Massachusetts, which began enrolment in 1948.

smoking is injurious
Heavy cigarette smokers can reduce their risk of cardiovascular diseases (CVD) by 39 per cent within five years if they quit. Pixabay

Also Read: New Study Suggests Living Near Parks and Nature Linked to Greater Happiness

The study used prospective data from 1954 through 2014 from 8,770 participants to determine the effect of lifetime smoking and smoking cessation on the risk of CVD, which includes myocardial infarction, stroke, CVD death and heart failure.

“Our team documented what happens to CVD risk after quitting smoking relative to people who continued to smoke and to those who never smoked,” said study lead author Meredith Duncan from Vanderbilt University. (IANS)