Research News

New model sheds light on secondary bacterial pneumonia

By UB REPORTER STAFF

Published August 12, 2016 This content is archived.

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“We don’t know why the viral infection induces the bacteria to disseminate to the lung, but now we can evaluate potential mechanisms more closely because of this model. ”
Anthony Campagnari, professor
Jacobs School of Medicine and Biomedical Sciences

For years, researchers have known that the bacteria Staphylococcus aureus (S. aureus) can trigger severe, sometimes deadly secondary bacterial pneumonia in some people who are subsequently infected with influenza A virus, but scientists have not known exactly how this happens.

Now, UB scientists have developed a new model for studying this phenomenon, which could lead to new ways to prevent secondary bacterial infections. The findings were published this week in mBio, an online open-access journal of the American Society for Microbiology.

“This study has established a physiologically relevant model so we can now more carefully evaluate the actual events involved after colonization with S. aureus and identify the primary factors that can lead to secondary bacterial pneumonia,” says Anthony Campagnari, senior author and professor in the Department of Microbiology and Immunology, and the Department of Medicine in the Jacobs School of Medicine and Biomedical Sciences at UB.

S. aureus is one of the most common causes of secondary bacterial pneumonia in cases of seasonal influenza. Scientists have been studying this phenomenon by introducing S. aureus directly into the lungs of mice. However, this does not mimic the natural pathogenesis of infection.

In the new model, Ryan Reddinger, a doctoral candidate in the Department of Microbiology and Immunology who is working in Campagnari’s lab, developed a technique where S. aureus stably colonizes the nares (nostrils) of mice and these animals are subsequently infected with influenza A virus to see what would happen.

“Ryan’s work demonstrated that influenza A virus infection leads to the dissemination of S. aureus from the nasal cavity into the lungs, resulting in the development of secondary bacterial pneumonia in these mice,” Campagnari says. “The model is very relevant to the current physiologic state in humans where individuals are colonized by S. aureus in the nares and subsequently acquire a viral infection.

“The fascinating thing about this model is when we colonize mice with S. aureus, it remains in the nares for up to seven days, without obvious signs of disease, and does not appear to move to the lungs on its own,” he notes. “The bacteria only disseminates to the lungs in response to the subsequent viral infection.”

When someone has a viral infection, certain physiologic changes occur in the nasopharynx that are related to damage of host cells and host responses, including increased body temperature and release of glucose, norepinephrine and the cellular energy carrier adenosine triphosphate, or ATP. With their model, the UB researchers discovered that a combination of these factors, in the absence of influenza A virus, will cause S. aureus to leave the nasopharynx and travel to the lungs.

“We don’t know why the viral infection induces the bacteria to disseminate to the lung, but now we can evaluate potential mechanisms more closely because of this model,” Campagnari says. “In addition, this model could be adapted to study other virus-bacterial interactions.”