How COVID-19 triggers massive inflammation

SARS-CoV-2 (shown here in the electron microscope). Credit: National Allergy and Disease Control Center, NIH

A study led by researchers at Boston Children’s Hospital has revealed for the first time why COVID-19 causes severe inflammation in some people, leading to severe respiratory distress and multiple organ damage. Surprisingly, the study also found that the antibodies that people develop when they contract COVID-19 can cause further inflammation in some cases, while the viruses that cause mRNA COVID-19 resistance do not seem to not.

The researchers, led by Judy Lieberman, MD, Ph.D. and Caroline Junqueira, Ph.D. in the Boston Children’s Program in Medicine and Molecular Biology, with Michael Filbin, MD, at Massachusetts General Hospital, published their study April 6 in Nature.

“We want to understand what differentiates soft tissue patients from COVID-19 severity,” Lieberman said. “We know a lot alamomin kumburi are among the people who severe diseaseand inflammation is the root cause of the disease, but we do not know what causes it.

The researchers examined new blood samples from patients with COVID-19 heading to the emergency department at Massachusetts General Hospital. They compared these with samples from healthy and sick people with other respiratory conditions. They also looked at pneumonia tests from people who had died from COVID-19.

Fire death by antibiotics

They found that SARS-CoV-2 can infect monocytes – antibodies in the blood that act as “sentinels” or progenitors – and macrophages, the same bacteria in the lungs. Once infected, two cell types die violently (called pyroptosis) which releases a powerful alarm signal.

“In patients with the disease, about 6 percent of blood monocytes die from inflammation,” Lieberman said. “This is a huge number to identify, because dead cells are quickly eliminated from the body.”

Study the huhu nama from people who died from COVID-19, they found that nearly a quarter of macrophages in tissue are dying.

When researchers examined cells for symptoms of SARS-CoV-2, they found that about 10 percent of monocytes and 8 percent of lung macrophages were infected.

The fact that monocyte and macrophages are susceptible to SARS-CoV-2 infection is surprising, since monocytes do not carry ACE2 receptors, a major signaling pathway. virus, and macrophages have low ACE2 levels. Lieberman thinks the SARS-CoV-2 infection of monocytes may have previously been missed in part because researchers are usually studying frozen blood samples, in which dead cells do not emerge.

The study also showed that while SARS-CoV-2 was able to infect monocytes and macrophages, it was unable to produce new viruses. Researchers believe that cells die faster from pyroptosis before new viruses can become fully formed.

“In some ways, transmission of these sentinel cells is protective: it destroys the virus and takes on more activity. antibiotics, says Lieberman. “But the bad news is that all of these viruses are coming out. In people who are more prone to inflammation, such as the elderly, this may go out of control.”

Antibodies facilitate infection?

It is possible to infect certain groups of monocytes in particular: those containing the CD16 receptor. These “abnormal” monocytes make up about 10 percent of all monocytes, but their number increased in patients with COVID-19, the researchers found. They are also more susceptible to infection: almost half are infected, compared to none of the normal blood monocytes.

The CD16 receptor appears to recognize it vaccine and SARS-CoV-2 increased protein. Researchers believe that these antibiotics may ease the risk of infection monocytes carrying the receiver. “Antibiotics cover the virus, and cells with the CD16 receptor then carry the virus,” Lieberman said.

However, when the team examined healthy patients who received mRNA vaccine on COVID-19, the enhanced antibodies did not appear to facilitate infection. The reason for this is still unknown; the researchers believe that the produced viruses have different properties than the viruses that develop during infection and do not bind to the CD16 receptor. As a result, the Cells do not transmit the virus.

Lieberman and her colleagues believe these findings may be effective for the use of monoclonal antibodies to control COVID-19, helping to explain why treatment only works when given early. “Maybe later, antibiotics can help increase inflammation,” she said. “We may need to look at the properties of antibiotics.”

New research may shed light on the potential for viral infections on the lungs

Learn more:
Judy Lieberman, FcγR-moderate SARS-CoV-2 infection of monocytes activated inflammation, Nature (2022). DOI: 10.1038 / s41586-022-04702-4.

hintHow COVID-19 Causes Inflammation (2022, April 6) Retrieved 6 April 2022 from

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