How stress can make you sick explained

January 11, 2018

Washington, Jan 11: Stress can interact with immune cells and regulate how they respond to allergens, causing physical symptoms and disease, a study has found.

Published in the Journal of Leukocyte Biology, the study showed how a stress receptor, known as corticotropin-releasing factor (CRF1) can send signals to certain immune cells, called mast cells, and control how they defend the body.

For the study, researchers from the Michigan State University (MSU) in the US compared the histamine responses of mice to two types of stress conditions - psychological and allergic - where the immune system becomes overworked.

One group of mice was considered "normal" with CRF1 receptors on their mast cells and the other group had cells that lacked CRF1.

"While the 'normal' mice exposed to stress exhibited high histamine levels and disease, the mice without CRF1 had low histamine levels, less disease and were protected against both types of stress," said Adam Moeser, from MSU.

"This tells us that CRF1 is critically involved in some diseases initiated by these stressors," Moeser said.

The CRF1-deficient mice exposed to allergic stress had a 54 per cent reduction in disease, while those mice who experienced psychological stress had a 63 per cent decrease.

The results could change the way everyday disorders such as asthma and the debilitating gastrointestinal symptoms of irritable bowel syndrome are treated.

"This work is a critical step forward in decoding how stress makes us sick and provides a new target pathway in the mast cell for therapies to improve the quality of life of people suffering from common stress-related diseases," said Moeser.

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Agencies
May 19,2020

New York, May 19: Cigarette smoke spurs the lungs to make more of the receptor protein which the novel coronavirus uses to enter human cells, according to a study which suggests that quitting smoking might reduce the risk of a severe coronavirus infection.

The findings, published in the journal Developmental Cell, may explain why smokers appear to be particularly vulnerable to severe COVID-19 disease.

"Our results provide a clue as to why smokers who develop COVID-19 tend to have poor clinical outcomes," said study senior author Jason Sheltzer, a cancer geneticist at Cold Spring Harbor Laboratory in the US.

"We found that smoking caused a significant increase in the expression of ACE2, the protein that SARS-CoV-2 uses to enter human cells," Sheltzer said.

According to the scientists, quitting smoking might reduce the risk of a severe coronavirus infection.

They said most individuals infected with the virus suffer only mild illness, if they experience any at all.

However, some require intensive care when the sometimes-fatal virus attacks, the researchers said.

In particular, they said three groups have been significantly more likely than others to develop severe illness -- men, the elderly, and smokers.

Turning to previously published data for possible explanations for these disparities, the scientists assessed if vulnerable groups share some key features related to the human proteins that the coronavirus relies on for infection.

First, they said, they focused on comparing gene activity in the lungs across different ages, between the sexes, and between smokers and nonsmokers.

The scientists said both mice that had been exposed to smoke in a laboratory, and humans who were current smokers had significant upregulation of ACE2.

According to Sheltzer, smokers produced 30-55 per cent more ACE2 than their non-smoking counterparts.

While the researchers found no evidence that age or sex impacts ACE2 levels in the lungs, they said the influence of smoke exposure was surprisingly strong.

However, they said, the change seemed to be temporary.

According to the data, the level of the receptors ACE2 in the lungs of people who had quit smoking was similar to that of non-smokers.

The study noted that the most prolific producers of ACE2 in the airways are mucus-producing cells called goblet cells.

Smoking is known to increase the prevalence of such cells, the scientists said.

"Goblet cells produce mucous to protect the respiratory tract from inhaled irritants. Thus, the increased expression of ACE2 in smokers' lungs could be a byproduct of smoking-induced secretory cell hyperplasia," Sheltzer explained.

However, Sheltzer said other studies on the effects of cigarette smoke have shown mixed results.

"Cigarette smoke contains hundreds of different chemicals. It's possible that certain ingredients like nicotine have a different effect than whole smoke does," he said.

The researchers cautioned that the actual ACE2 protein may be regulated in ways not addressed in the current study.

"One could imagine that having more cells that express ACE2 could make it easier for SARS-CoV-2 to spread in someone's lungs, but there is still a lot more we need to explore," Sheltzer said.

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Agencies
June 23,2020

The record levels of new daily COVID-19 cases are due to the fact that the pandemic is peaking in a number of big countries at the same time and reflect a change in the virus' global activity, the World Health Organisation said.

At a media briefing on Monday, WHO's emergencies chief Dr Michael Ryan said that the numbers are increasing because the epidemic is developing in a number of populous countries at the same time.

Some countries have attributed their increased caseload to more testing, including India and the US But Ryan dismissed that explanation.

We do not believe this is a testing phenomenon, he said, noting that numerous countries have also noted marked increases in hospital admissions and deaths neither of which cannot be explained by increased testing.

There definitely is a shift in that the virus is now very well established, Ryan said. The epidemic is now peaking or moving towards a peak in a number of large countries.

He added the situation was definitely accelerating in a number of countries, including the US and others in South Asia, the Middle East and Africa.

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Agencies
June 21,2020

Lower neighbourhood socioeconomic status and greater household crowding increase the risk of becoming infected with SARS-CoV-2, the virus that causes COVID-19, warn researchers.

"Our study shows that neighbourhood socioeconomic status and household crowding are strongly associated with risk of infection," said study lead author Alexander Melamed from Columbia University in the US.

"This may explain why Black and Hispanic people living in these neighbourhoods are disproportionately at risk for contracting the virus," Melamed added.

For the findings, published in the journal JAMA, the researchers examined the relationships between COVID-19 infection and neighbourhood characteristics in 396 women who gave birth during the peak of the Covid-19 outbreak in New York City. Since March 22, all women admitted to the hospitals for delivery have been tested for the virus, which gave the researchers the opportunity to detect all infections -- including infections with no symptoms -- in a defined population

The strongest predictor of COVID-19 infection among these women was residence in a neighbourhood where households with many people are common.The findings showed that women who lived in a neighbourhood with high household membership were three times more likely to be infected with the virus. Neighbourhood poverty also appeared to be a factor, the researchers said.Women were twice as likely to get COVID-19 if they lived in neighbourhoods with a high poverty rate, although that relationship was not statistically significant due to the small sample size.

The study revealed that there was no association between infection and population density.

"New York City has the highest population density of any city in the US, but our study found that the risks are related more to density in people's domestic environments rather than density in the city or within neighbourhoods," says co-author Cynthia Gyamfi-Bannerman."

The knowledge that SARS-CoV-2 infection rates are higher in disadvantaged neighbourhoods and among people who live in crowded households could help public health officials target preventive measures," the authors wrote.

Recently, another study published in the Journal of the American Planning Association, showed that dense areas were associated with lower COVID-19 death rates.

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