Healthy Immune Response to COVID-19 Vaccines Seen in Patients
Immune responses to COVID-19 vaccination were similar in people with chronic obstructive pulmonary disease (COPD) to those of healthy adults, a U.K. study found.
“The results of this study will be a great relief for patients with COPD who can rest assured they can derive protection from COVID-19 vaccination, despite an impaired immune system,” Thomas Southworth, PhD, an honorary research associate at the University of Manchester and senior scientist at the Medicines Evaluation Unit, said in a university press release.
“Airway immune responses to COVID-19 vaccination in COPD patients and healthy subjects,” was published as a research letter in the European Respiratory Journal.
Evidence suggests COPD patients may be at a higher risk of severe illness upon infection with SARS-COV-2, the virus that causes COVID-19, relative to that risk in those who are healthy.
COVID-19 vaccines broadly act to stimulate the immune system to produce antibodies against the virus, helping to protect against infection and severe disease. But data generally show an altered immune system and lower antibody responses in COPD patients, raising the possibility that COVID-19 vaccines could be less effective for these people.
Researchers at the University of Manchester evaluated immune responses to COVID-19 vaccination among COPD patients and healthy adults older than 40, comparing them to unvaccinated people with or without COPD.
Included in the study were 11 vaccinated COPD patients, 16 vaccinated healthy adults as controls, and 43 people yet to be vaccinated (24 with COPD and 19 without it), all without a prior COVID-19 infection.
Patients’ mean age was 66.1, and that of healthy adults was 58.8. COPD was moderate or severe in all patients, and 10 were former smokers.
Vaccinated participants had been given two doses of the Pfizer/BioNTech or AstraZeneca vaccine, and provided blood and nasal samples at least two weeks later. Some also provided samples of sputum, a mixture of saliva and mucus from the lungs.
COPD patients and healthy people who received the vaccine mounted similar immune responses, marked by elevations in antibodies, called immunoglobulins, against the virus, results showed.
Antibody levels were significantly higher in vaccinated than in unvaccinated people, regardless of whether they had COPD, “providing reassurance that current vaccines cause the desired immune responses in COPD, despite the presence of immune dysregulation,” the researchers wrote.
More specifically, vaccinated people had higher levels of IgG antibodies, a type of antibody that protects against viral infections, in blood and sputum samples. Levels of another anti-viral antibody called IgA also rose after vaccination in the blood, but not in sputum.
An analysis of nasal swabs found higher IgG, but not IgA, levels in vaccinated people compared with unvaccinated individuals.
“Vaccination did not induce a sustained IgA antibody response in the airways of either COPD patients or healthy subjects. IgA antibodies act to block viral infections as they initially enter our nose and airways,” Southworth said.
“Future vaccines, which do induce sustained anti-SARS-COV-2 IgA antibody responses in the upper airways, may offer additional protection for both COPD patients and healthy individuals equally,” Southworth added.
Those vaccinated also showed increases in interferon-gamma, a molecule released by T-cells during an immune response, compared with the unvaccinated group.
Nine healthy people with a history of COVID-19 who were given one vaccine dose also saw an increased immune response similar to fully vaccinated individuals.
Blood and nasal IgG levels were higher among those given the Pfizer/BioNTech vaccine than the AstraZeneca vaccine, with nonsignificant trends observed for sputum IgG and blood IgA levels, similar to previous observations, the researchers noted.
“Our results demonstrate that COPD patients develop immune responses to COVID-19 vaccines that are similar to [healthy controls],” the researchers concluded.