Man flu isn’t a myth after all .

Men get sick because they don’t have the hormones that boost women’s immune system, according to new research

The study by Stanford University School of Medicine, examined the reactions of men and women to vaccination against flu

The study by Stanford University School of Medicine, examined the reactions of men and women to vaccination against flu Photo: Alamy

Scientists from Harvard University have shown that a lack of oestrogen makes men more likely to succumb to pneumonia and other respiratory diseases.

Yet a simple dose of oestrogen was enough to cure both males and females of the serious lung infection.

Professor Lester Kobzik at the Harvard University School of Public Health found females are naturally more resistant to respiratory infections than males.

The study showed that increased resistance to bacterial pneumonia in female mice is linked to the enzyme nitric oxide synthase 3 (NOS3), which is ultimately activated by the release of the female sex hormone estrogen

Female mice and male mice that had been treated with oestrogen were able to clear the bacteria from their lungs more rapidly than normal male mice.

The scientists then took another set of male and female mice and removed the gene responsible for the production of NOS3, an enzyme activated by oestrogen.

They found that deleting this gene meant that the female mice were no longer more resistant to infection.

The team hopes that, in the future, this knowledge could be used to enhance resistance to common and serious lung infections and prevent flu developing into more serious pneumonia.

Professor Kobzik said: “Ultimately, this work could be especially useful in reducing risk of secondary bacterial pneumonias during seasonal or pandemic influenza.

“We were quite pleased that the work led us to NOS3-targeting drugs that are already available and that can indeed improve resistance to pneumonia in our mouse model.”

Would-be drug mimics ‘good’ cholesterol .

A new drug candidate designed to mimic the body’s “good” cholesterol shows a striking ability in mice to lower cholesterol levels in the blood and dissolve artery-clogging plaques. What’s more, the compound works when given orally, rather than as an injection. If the results hold true in humans—a big if, given past failures at transferring promising treatments from mice—it could provide a new way to combat atherosclerosis, the biggest killer in developed countries.

Although doctors already have effective cholesterol-lowering agents, such as statins, at their disposal, there’s room for improvement. Statins have significant side effects in some people and don’t always reduce cholesterol enough in others. “There is still plenty of heart disease out there even among people who take statins,” says Godfrey Getz, an experimental pathologist at the University of Chicago in Illinois.

For that reason, researchers around the globe are searching for novel drugs that affect cholesterol levels in one of two ways. The first has been to reduce levels of low-density lipoprotein (LDL), commonly known as bad cholesterol, which has been associated with higher heart disease risk. This is the goal of statins, which block an enzyme involved in cholesterol production. The second strategy is to increase levels of good cholesterol, or high-density lipoprotein (HDL), which seems to boost heart health in people who have a lot of it. But producing HDL-raising drugs that prevent heart disease has proven difficult. In the body, a large protein called apolipoprotein A-I (apoA-I) wraps around fatty lipid molecules to create HDL particles that sop up LDL and ferry it to the liver where it is eliminated. So for several decades researchers have been designing and testing small protein fragments called peptides to see if they could mimic the behavior of apoA-I. One such peptide, known as 4F, did not reduce serum cholesterol levels, but it did shrink arterial plaques in mice, rabbits, and monkeys. And in an early clinical trial by researchers at Bruin Pharma Inc. in Beverly Hills, California, that was designed only to measure its safety in people, 4F didn’t appear to show any beneficial effect.

Multiple copies of a four-armed peptide wrap around lipids to create particles that mimic the behavior of HDL, the "good" cholesterol.

M. Reza Ghadiri, a chemist at the Scripps Research Institute in San Diego, California, and his colleagues took a slightly different tack, creating a peptide that mimics another part of the apoA-I protein than 4F does. Initial in vitro studies suggested the peptide formed HDL-like particles and sopped up LDL, an encouraging result that prompted them to push it further. Ghadiri and his Scripps colleagues have now tested their compound in mice that develop artery clogging plaques when fed a Western-style high-fat diet. One group of animals received the peptide intravenously. For another group, the researchers simply added the compound to the animals’ water, a strategy they considered unlikely to work, because the gut contains high amounts of proteases designed to chop proteins apart. To their surprise, in both groups, serum cholesterol levels dropped 40% from their previous levels within 2 weeks of starting to take the drug. And by 10 weeks, the number of artery-clogging lesions had been reduced by half, the team reports in the October issue of the Journal of Lipid Research. What remains puzzling, however, is that Ghadiri and his colleagues did not detect their peptides in the blood of their test animal. Ghadiri says this suggests that the new peptide may work by removing cholesterol precursors in the gut before they enter the bloodstream.

“It’s a very interesting result,” Getz says. But he cautions that the work has been tested only in animals, and many therapies—including the closely related 4F peptide—fail to transfer to humans. That said, Getz notes that some of the initial promising results with this peptide and other apoA-I mimics offer hope that researchers may soon come up with novel drugs capable of dissolving artery-clogging plaques before they can wreak their havoc.