A new study has uncovered a mechanism that appears to explain why obesity predisposes to developing acute respiratory distress syndrome (ARDS), discovering a novel strategy for preventing ARDS in obese individuals.
Thomas Jefferson University's Ross Summer said that although their work needs to be confirmed in humans, the studies in animals suggest that obese patients with ARDS may have a biologically different disease than their non-obese counterparts and the research could point to a new therapeutic avenue for these patients.
Summer added that while immune activation is usually protective and beneficial in the body, in the case of ARDS, the immune system acts like a runaway train, gaining speed and momentum as it goes, without the breaks that would normally slow it down and keep it from causing too much damage in the body, noting that inflammation together with fluid build-up cause the lungs lose their ability to exchange oxygen and carbon dioxide, and can lead to death.
Researchers used gene therapy techniques to restore the decreased adiponectin levels in obese mice and found that by replacing this hormone obese mouse were less vulnerable to developing ARDS.
Summer noted that it's unclear whether adiponectin acts directly on the blood vessels of the lung, adding that it is possible that this hormone initiates other protective and anti-inflammatory signals that prevent the loss of junction proteins and the increase of the immune adhesion proteins.
Although drugs which can increase adiponectin levels already exist, the first step, says Summer is to confirm that low adiponectin levels are linked to higher rates of ARDS in humans. However, if this association proves to be true, Summer believes adiponectin replacement therapy may be an easy way to prevent ARDS in at-risk individuals.
The study appears online in the journal Scientific Reports, a Nature publication.