News: Your Lungs Aren't the Same After a Battle with Pneumonia

Once we recover from the respiratory infection pneumonia, our lungs are better equipped to deal with the next infection — thanks to some special cells that take up residence there.

New research led by JP Mizgerd of the Boston University School of Medicine, shows that lung tissue is not the same after pneumonia. Specialized white blood cells infiltrate the lungs and provide immunity to later infections.

The research was published in Nature Immunology.

Pneumonia Isn't an Equal Opportunity Infector

Our lungs have several mechanisms in place to fight pathogens that enter our respiratory tract. We sneeze and cough to blow them out of our system, mucus helps to trap them, tiny hairs in our respiratory tract help to brush them up and out of our body, and immune cells, like macrophages, gobble them up. Yet, some respiratory infections with viruses, bacteria, or fungi end up as pneumonia — where the lung sacs that usually fill with air when we breathe fill with pus and fluid instead.

Three main groups of people are at greater risk for contracting pneumonia: the very young, those over 65, and those with compromised immune systems.

Worldwide, pneumonia is the leading cause of death by infection in children younger than five years old and nearly a million of those children died in 2015. Infection with Streptococcus pneumoniae is the most common cause of bacterial pneumonia in children.

As children grow older, their risk of getting pneumonia decreases and scientists believe this is due to immunity that accumulates with each infection — the immune memory builds. But, until the study by Mizgerd and his team, we didn't know exactly how this specialized immune system response protected patients after pneumonia.

The Benefit of Immune Memory

To investigate which types of cells are involved in generating immune memory after pneumonia, the researchers gave a set of mice one to three mild Streptococcus pneumoniae infections by swabbing the bacteria in their noses — much like the way the infection is usually acquired — to mimic repeated respiratory infections. A control set of mice was not infected.

About four to eight weeks later, when inflammation from the infections resolved, they infected the lungs of the mice with a different, severe, life-threatening strain of pneumonia. Compared to mice that didn't have the prior infections, the mice whose noses the researchers had swabbed with less severe pneumococcal bacteria were much more resistant to the serious infection. Five days after infection with a severe form of Streptococcus pneumoniae, all of the mice that had not previously infected had died, while 90% of the previously infected mice were alive.

Mice the researchers infected twice had a population of white blood cells called CD4 lymphocytes in their lungs. The cells were confined to the previously infected lobe, instead of being dispersed throughout the lower respiratory tract, and are called resident memory T cells. The mice were also only protected against pneumonia in that lobe, a lobe called "immunologically experienced" by the study authors.

To test if the cells were the reason for the protection, the scientists removed the resident memory T cells by binding them to an antibody, then removing the cell-antibody complex. When the researchers exposed these memory cell-less mice the final, severe infection, they no longer had protection against it.

The resident memory T cells even protected the mice against infection with different subtypes — serotypes — of pneumonia than the researchers exposed them to previously.

"The T resident memory cells left behind after prior infections are more broadly effective than vaccine-generated immunity, providing protection against a wider spectrum of microbes that can infect the lungs," said Mizgerd in a press release from Boston University Medical Center.

We propose that this mimics the naturally acquired immune protection that is afforded by most healthy young adult humans but which wanes over time due to aging and comorbidities, such as smoking, alcohol abuse, and chronic disease.

The authors suggested one way to use their findings in the future: Creating vaccines to generate lung resident memory T cells against potential respiratory pathogens, without having had pneumonia first. Activating the lung resident memory T cells using drugs could provide another way to treat infections like pneumonia in people whose defenses to pneumonia are waning due to age and illness.

Instead of finding new antibiotics to treat pneumonia, we may be able to manipulate our immune system to use our natural defenses, including resident T memory cells, to provide protection against or response to respiratory infections.

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