Progesterone promotes lung healing after flu

A United States study published in PLOS Pathogens reports that treatment with progesterone protects female mice against the consequences of influenza infection by reducing inflammation and improving pulmonary function, primarily through upregulation of amphiregulin (AREG) in lung cells. In general, progesterone appears to dampen immune responses and reduce inflammation. Although the immunomodulatory effects of progesterone-based contraception have been studied in the context of sexually transmitted diseases such as human immunodeficiency virus and herpes simplex virus, the potential impact of progesterone on viral infections outside of the reproductive tract has not received much attention. In the PLOS Pathogens study, Sabra Klein, from Johns Hopkins University in Baltimore, US, and colleagues examined whether levels of progesterone that mimic physiological concentrations present after ovulation (and equivalent to levels used in contraceptives) influence the host response to influenza infection. The researchers studied female mice whose ovaries had been removed and whose progesterone was supplied by implanted pellets that kept hormone levels constant. When female mice were challenged with influenza virus, the researchers found that the exogenous progesterone was able to protect females from the consequences of influenza infection to some extent. Progesterone did not reduce the level of virus present in the mice, but decreased the amount of inflammation and tissue damage in the lungs and promoted faster recovery from the infection. The researchers found that progesterone treatment was associated with elevated levels of immune cells called T helper 17 cells, which are known to be involved in maintaining mucosal barriers and pathogen clearance at mucosal cell surfaces. Progesterone also increased the levels of the epidermal growth factor, AREG. In mice lacking AREG, progesterone failed to protect against the serious consequences of influenza infection. When the researchers supplied AREG to progesterone-depleted influenza-infected females, their disease and recovery characteristics resembled those of females on progesterone treatment, suggesting that progesterone exerts its effects through boosting of AREG levels in the lungs. The authors suggest that the findings indicate there may be health benefits beyond the reproductive tract for women taking oral contraceptives.

Toxic chemicals found in household dust

Research from the United States has found that household dust exposes people to numerous toxic chemicals that are associated with severe health problems. The researchers said that children are particularly at risk. Published in Environmental Science and Technology, the meta-analysis discovered that the number one chemical identified in household dust was diethylhexyl phthalate, which belongs to a hazardous class of chemicals called phthalates that are used in everything from household cleaners to food packaging to cosmetics, fragrance, and personal hygiene products. Household dust was found to have phthalates in the highest concentration – with a mean of 7682 nanograms per gram of dust – an amount that was several orders of magnitude above the other chemicals. Phenols, chemicals used in cleaning products and other household items, were the second on the list of highest concentrations, followed by flame retardants and highly fluorinated chemicals that are used to make non-stick cookware. Potentially toxic chemicals from consumer products are released into air and amalgamate with dust that settles on household furniture and the floor, the researchers wrote. Families are then exposed to the toxic dust composite through inhaling or ingesting small particles, while some minor amounts can be absorbed through skin. Babies, infants and young children are at a greater risk of chemical exposure because they crawl, play on dusty floors, put their hands in their mouths and also mouth, suck and chew on toys or items that could be lightly covered in dust.

E-cigarette use tied to rise in quit smoking success

Research published in the BMJ concluded that the rise of e-cigarette use in England was linked to higher rates of successful quitting attempts by smokers of regular cigarettes. A linked editorial suggested that the research showed that successful attempts to quit smoking regular cigarettes by switching to e-cigarettes was a likely contributor to the fall in smoking rates in the United Kingdom. In the UK alone there are now over 2 million e-cigarette users. The study analysed two sources of information: the Smoking Toolkit Study, which gave the researchers 10 years of data gathered in a monthly survey of smoking, quitting and e-cigarette use among adults in England; plus quarterly data on numbers of adults using National Health Service stop smoking services in England and their quit rates. The researchers suggested that in 2015, the use of e-cigarettes may have resulted in an extra 18 000 long term smokers joining the ranks of ex-smokers. They remarked that while this was not a big figure, it was “clinically significant because of the huge health gains from stopping smoking”. The researchers found that increased use of e-cigarettes did not appear to be linked with a detectable change in overall attempts to stop smoking (as opposed to successful attempts – where they did find a link). However, they did find that the rise in e-cigarette use was tied to a decline in prescription nicotine replacement treatments. They speculated that this could be because e-cigarette users had already tried these alternatives.

Genetic variant lifts liver damage risk for patients with hepatitis C

A large international team of researchers led by the Westmead Institute for Medical Research in Sydney has found a new genetic variant that puts patients with chronic hepatitis C at risk of developing liver disease. In a study published in Nature Communications, the team led by Professor Jacob George and Dr Mohammed Eslam from the Westmead Institute’s Storr Liver Centre described their analysis of more than 2000 patients, finding that a variant in the MBOAT7 gene was linked to increased liver inflammation and fibrosis. They found that patients with the risk variant had low expression of MBOAT7 – a protective enzyme which reduces inflammation. With low expression, those patients had more severe liver inflammation and inflammatory markers in their blood. The MBOAT7 gene discovery adds another gene to the one identified last year by the same team as a marker for liver fibrosis progression.

 

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