A new study published in Science Translational Medicine found that medicines used to treat high blood pressure and heart failure can reduce the immune system’s ability to fight dangerous bacterial infections.
They believe that these common medicines may make patients more prone to bacterial infections like methicillin-resistant Staphylococcus aureus (MRSA), which are common in hospitals.
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Angiotensin receptor blockers, a different class of medicine commonly used to treat similar conditions, were also evaluated by the researchers. These medications didn’t have the same immune-suppressing effects on white blood cells as Angiotensin-converting enzyme – ACE inhibitors, but the researchers stress that more research in humans is needed to confirm this.
“These findings have potential clinical implications as physicians decide whether to put patients on an ACE inhibitor or angiotensin receptor blocker to treat high blood pressure, especially immunocompromised patients who are more vulnerable to infections,” said Zakir Khan, assistant professor at Cedars-Sinai Medical Center in Los Angeles and senior author of the new study.
Patients, on the other hand, typically take ACE inhibitors for a long time to control their blood pressure. As the researchers only looked at the effects of ACE inhibitors on human cells after a week of treatment, it’s still unknown whether the drug’s effects will vary over time.
Benazepril (Lotensin) and lisinopril (Qbrelis, Prinivil) are ACE inhibitors that reduce blood pressure by relaxing blood arteries. They function by inhibiting an enzyme called ACE, which is found in a variety of tissues and regulates blood pressure.
Because of these characteristics, ACE inhibitors are one of the most commonly prescribed treatments for high blood pressure, either alone or in combination with other medications such as statins. According to a report published in the Journal of Managed Care and Specialty Pharmacy, 162.8 million were prescribed for ACE inhibitors in the United States in 2009.
According to the new study, ACE inhibitors are also used to treat heart failure and diabetic renal disease, as well as to manage patients undergoing invasive cardiac surgery.
However, some research suggests that the ACE enzyme may also help immune cells like neutrophils defend the body against bacteria and other microbes. Scientists are still debating whether ACE inhibitors may have unforeseen immune system consequences.
“While these drugs have been largely thought to be safe, published studies have noted an association between the use of ACE inhibitors and some forms of infection,” said Khan. “We wanted to further explore this association.”
Khan, study lead author Duo-Yao Cao, and colleagues treated mice with the approved ACE inhibitors ramipril (Altace) and lisinopril. They then tested whether neutrophils in the animals’ blood could kill MRSA, Klebsiella pneumoniae, and Pseudomonas aeruginosa, bacteria that frequently cause pneumonia and other infections in hospital patients.
Cao, a researcher at Cedars-Sinai Medical Center, and his team found that the neutrophils killed fewer bacteria compared to neutrophils from untreated mice. Treating mice with ramipril also left them more susceptible to severe MRSA infections.
ACE inhibitors are also used in patients who might be vulnerable to heart infections, so the research team tested the effects of ACE inhibitors in mice with damaged heart valves. Like the first experiments, the scientists observed that the animals were more vulnerable to MRSA infections in the heart after they received ramipril.
The team repeated the experiments with the angiotensin receptor blocker losartan (Cozaar), one of the most common blood pressure medications. Unlike the ACE inhibitor ramipril, losartan didn’t weaken neutrophil’s bacteria-fighting capabilities or leave mice more susceptible to MRSA infections.
In a small pilot clinical study, Cao’s team gave ramipril to seven human volunteers every day for one week. The study subjects provided blood samples before, during, and after treatment, which the researchers analyzed to assess the antibacterial functions of the neutrophils in the people.
The team found that neutrophils isolated from the volunteers couldn’t properly produce superoxides and reactive oxygen species, which are molecules involved in antibacterial immune responses. The neutrophils’ ability to kill MRSA, K. pneumoniae, and P. aeruginosa bacteria also declined as the patients began taking ramipril.
Khan made sure to note that his team’s study has several limitations. For example, the researchers didn’t treat the volunteers with angiotensin receptor blockers, so they can’t yet conclude whether these drugs might have similar suppressing effects on neutrophils in humans.
For future work, Khan stressed the importance of understanding the exact mechanism by which the ACE enzyme supports antibacterial immunity from neutrophils. He added that his team is planning to compare in more detail the effects of ACE inhibitors and angiotensin receptor blockers on neutrophils in a large group of patients who received treatment at their hospital.
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