Statins could boost male resistance to respiratory infection

Drugs that mimic part of the role of oestrogen - including statins - could increase resistance to respiratory infection in men at high risk, research suggests.

Sneeze: statins could boost resistance to respiratory infection (Photo: iStock)

An international study, headed by researchers at Harvard University, found that the nitric oxide synthase-3 (NOS3) enzyme improved bacterial clearance in the lungs and played a crucial role in preventing associated respiratory diseases such as pneumonia.

Activation of the NOS3 enzyme is dependent on the female sex hormone oestrogen, which may help explain why women tend to be naturally more resistant to respiratory infections than men.

Drugs that mimic oestrogen’s role in targeting NOS3 activation – such as statins – could be used as a preventative measure to help raise resistance in men at high risk of respiratory infection, the findings suggest.

In a series of experiments, published in the eLife journal, the researchers introduced Streptococcus pneumoniae into the lungs of mice.

To observe the effects of NOS3 on the bacteria, they treated some of the male mice with oestrogen. They found that female mice and these treated male mice were better at clearing out bacteria responsible for pneumonia and other infections than the ordinary males. They also had less acute inflammation after 24 hours.

Drugs that target NOS3 activation

In mice with the gene responsible for producing NOS3 removed, female bacterial resistance fell to be more in line with their male counterparts, further suggesting activation of this enzyme was driving the heightened resistance normally observed in females.

‘Ultimately, this work could be especially useful in reducing risk of secondary bacterial pneumonias during seasonal or pandemic influenza,’ said Professor Lester Kobzik, the senior author.

‘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.’

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