Funded by a grant from the Howard Hughes Medical Institute that supports interdisciplinary undergraduate research, Irwin worked on a pair of related experiments with Paul Chiarot, an assistant professor of mechanical engineering, and Jeffrey Schertzer, an assistant professor of biological sciences. In the first, Schertzer studied how vesicles — small bubbles within a cell, enclosed by lipids — affect communication within a bacterial community; in the second, he examined the ways shear stress affects the growth of biofilms.

“What’s unique about this collaboration is that Rebecca’s device allows Jeff to grow biofilms in situ, to add stress in a controllable way, and to observe the structure of the biofilms, which are actually quite complex,” says Chiarot, who supervised Irwin’s work in designing and building the instruments. “Rebecca took leadership on this project, which requires a lot of initiative and a lot of independence. That would have been challenging for a graduate student, and for an undergraduate, it’s even more impressive.”

With biofilms all around us — between our teeth, in the slime on a rock, inside a medical implant — there’s hope this research will reveal what does and doesn’t make them grow, which would have medical, biological and environmental applications. By learning how to disrupt their growth, scientists can decrease the risk of infection; by learning how to increase their growth, they can create new industrial cleaning agents to reduce pollution.

Both are part of the motivation that drives Irwin, a 2015 graduate who plans to pursue a doctorate in bioengineering, and whose participation on these projects was a life-changing experience. “As an undergraduate, being able to do research at this level is really cool,” she says. “It’s different from being in a lab as part of a class, where there’s a desired outcome that your professor wants you to have.”

If you consistently experience high levels of stress, you may be stimulating bacteria that weaken your blood vessels, Binghamton University researchers have found.

The microbiologists discovered a link between stress hormones and bacteria that may explain how emotional shock or over-exertion can trigger heart attacks or strokes in vulnerable people. Researchers believe that this is how someone could literally be scared to death.

The research, published in mBio, the online open-access journal of the American Society for Microbiology, indicates that hormones released during stress could cause thin sheets of bacteria called biofilms to disperse.

If this happens in your body, biofilms within your arterial walls would be stimulated to release enzymes that might weaken the arterial wall and lead to plaque rupturing into the blood stream. Plaque rupture has long been known to be one of the leading causes of heart attack and stroke.

“Our hypothesis fits the observation that heart attack and stroke often occur following an event where elevated levels of catecholamine hormones are released into the blood and tissues, such as occurs during sudden emotional shock or stress, sudden exertion or over-exertion,” says David Davies, associate professor of biological sciences at Binghamton.

Biofilms, often referred to as slime, form when bacteria undergo a genetic change and then organize within a self-produced matrix of extracellular polymeric substance. Once they are protected within the biofilm, bacteria are harder to detect and to treat with antibiotics.

Davies and his colleagues grew different species of bacteria taken from diseased carotid arteries affected by atherosclerosis, the build-up of thick plaques within the walls of blood vessels. They found multiple bacterial species living as biofilms in the walls of every atherosclerotic carotid artery tested. Certain molecular signals can cause the biofilms to release enzymes that digest the scaffolding anchoring the bacteria in place.

“The release of iron into the blood as a result of increases in stress hormones is what causes the bacteria to release their hold on each other and the plaque,” says study co-author Karin Sauer, professor of biological sciences at Binghamton.

This research suggests that bacteria should be considered to be part of the overall pathology of atherosclerosis. The scientists suggest that management of bacteria within an arterial plaque lesion may be as important as managing cholesterol.

Davies believes this research might someday change the medical community’s view of many conditions. “We’re going one disease at a time and trying to demonstrate whether or not bacteria are involved,” he says. “In most diseases with the letters itis … it means inflammation, it means a biofilm infection.”

Persister cells aren’t naturally resistant to antibiotics, but by entering a dormant state and waiting until the medicine wears off, they’re able to start a new colony and produce a new infection. That’s why some diseases are so hard to shake, biologist Claudia Marques explains.

In her work with Binghamton colleague David Davies, Marques studied the formation of multispecies communities of bacteria called biofilms. The team succeeded in identifying a molecule that signals these colonies to disperse, making the microbes easier to kill with antibiotics. Those findings have been cited more than a hundred times.

“When you take antibiotics, you are only targeting the cells that are creating your symptoms,” says Marques, who came to Binghamton as a post-doctoral researcher in 2004 and is now an assistant professor of biology. “But there are other kinds of cells within the biofilm, and because they live in community, they’re much more protected than the cells that were killed. In theory, if you take an antibiotic in combination with something that will wake these dormant cells, you’ll treat your infection much more efficiently.”

If the Binghamton researchers are right, their discovery could have a significant impact in treating diseases that begin with biofilms, including tuberculosis, sinusitis and urinary tract infections.

“Claudia’s focus on waking the cells is what makes her work so good,” says Thomas K. Wood, endowed biotechnology chair at Pennsylvania State University. “She understands how things happen at the molecular level, and her work is important because it puts the emphasis on the right place, which is in trying to get rid of bacteria that are asleep.”

Marques was born in Angola and grew up in Portugal, where she received her bachelor’s degree before pursuing a master’s in medical microbiology from the University of London and a doctorate from the University of the West of England. Now living on her third continent, she’s starting to feel at home again, and has begun collaborating with researchers in electrical engineering and bioengineering, creating infections to study how different species interact within a single biofilm community.

“The possibility of treating patients better and improving their lives, that’s what excites me about this work,” Marques says. “That’s what got me into this work: to improve the health of the overall population.”

“Bacteria, often viewed as simplistic creatures, are in fact very sociable units of life,” said Alex Rickard, assistant professor of biological sciences. “They can physically and chemically interact with one another and are quite selective about who they hang out with. How bacteria might communicate in chronic wounds, however, was somewhat of a mystery.”

Working with researchers and physicians at the Center for Biofilm Engineering at Montana State University and the Southwest Regional Wound Care Center in Lubbock, Texas, Rickard and a team of undergraduates were able to identify specific types of chronic wound bacteria and to test their ability to produce cell-cell signaling molecules.

Partial gene sequencing allowed the team to identify 46 chronic wound strains belonging to nine genera. Further research found that close to 70 percent of those chronic wound strains produce a specific type of communication molecule – autoinducer-2 (AI-2). A smaller percentage – around 20 percent – produce a different type of communication molecule, called acyl-homoserine-lactones (AHLs). Scientists already know that structurally different bacterial cell-cell signaling molecules are able to mediate cell-cell communication, including A1-2 and AHLs.

“Based on our findings, we think that most resident species – the ‘good’ bacteria that live on us and don’t cause disease – produce AI-2, while the pathogenic species typically produce AHLs,” said Katelynn Manton, who was part of the undergraduate team and is now pursuing her doctorate. “And it didn’t seem to matter what kind of chronic wound we looked at – diabetic ulcers, vascular ulcers or environmentally induced chronic wounds. They all indicated a presence of possible AHLs or AI-2s.”

For Randy Wolcott, director of the Southwest Regional Wound Care Center, a clearer understanding of how these bacteria function is particularly important. “AI-2’s may be the best explanation why our commensal coagulase-negative Staphylococci and other synergistically helpful bacteria are immensely beneficial to us when they reside in a normal skin environment,” he said. “However, when they turn or are coerced to a dark side in a wound or infected medical device, they can cause so much devastation and death.”

According to Rickard and his team, the typically pathogenic bacteria communicate in one language; the “good” bacteria in another. The big question now is whether any of them are bilingual and can listen in on one another’s “conversations.” Being able to interpret – or perhaps even guide – these cell-cell signals could influence wound development.

“Can we steer pathogenic bacteria away from what is, in essence, a ‘mob’ mentality and prevent them from communicating?” asked Rickard. “Or can we tell the mob to do one thing when they should in fact be doing something completely different?”

Manipulation of cell-cell signaling has the potential to be an effective strategy for wound healing, particularly in influencing “bad” bacteria, which are particularly resistant to antimicrobials. Bacteria such as Pseudomonas aeruginosa tend to have a repertoire of aggressive tactics that allow them to maintain a strong presence in chronic wounds. As a result, they are able to multiply rapidly, driving out the resident species and hampering wound healing.

“When bacteria form biofilms, as they do in chronic wounds, they become protected from killing by antimicrobial agents,” said Phil Stewart, director of the Center for Biofilm Engineering at Montana State University. “Topical antiseptics, systemic antibiotics and the body’s own defenses are unable to clear these infections. We need alternative strategies – such as jamming bacterial communication – to help weaken the biofilm defenses. Listening in on the bacterial signals may also provide a way to diagnose the state of a chronic wound.”

With finding from the National Institutes of Health, Rickard hopes to expand the study.

“Our goal is to include a wider range of wound types and compare the types of signals present,” he said. “By doing this, we expect to be able to develop novel methods to monitor wound healing and ultimately prevent the establishment of chronic wounds.”

Biofilms – communities of bacteria in self-produced slime – may be found almost anywhere that solids and liquids meet, whether in nature, in hospitals or in industrial settings. Biofilms are implicated in more than 80 percent of chronic inflammatory and infectious diseases caused by bacteria, including ear infections, gastrointestinal ulcers, urinary tract infections and pulmonary infections in cystic fibrosis patients, according to the Centers for Disease Control.

Biofilms are difficult to eradicate with conventional antimicrobial treatments since they can be nearly 1,500-fold more resistant to antibiotics than planktonic, free-floating cells. Biofilms also pose a persistent problem in many industrial processes, including drinking water distribution networks and manufacturing.

Karin Sauer, associate professor of biology at Binghamton, and graduate student Olga Petrova published their findings of key regulatory events required for the formation and development of Pseudomonas aeruginosa biofilms in PLoS Pathogens, a peer-reviewed open-access journal published online by the Public Library of Science.

“We have found a pathway of how the formation of biofilms is controlled,” Sauer said. “If we can figure out how to make use of this newly discovered genetic program, we can interfere with the formation of biofilms and either prevent or treat biofilm infections more successfully.”

Pseudomonas aeruginosa, an opportunistic pathogenic bacterium, is considered one of the primary causes of death in patients with cystic fibrosis, a common and life-threatening hereditary disease.

Petrova documented a previously unknown genetic program composed of several regulators by looking for changes in phosphorylation patterns in Pseudomonas aeruginosa. These regulators can not only be used to stop the development of biofilms at various stages in their growth but also to revert established biofilms to an earlier developmental stage.

“The problem you have when you have a chronic infection is that your immune system is trying to clear the infection but is unable to,” Sauer said. “And the longer the chronic infection goes on, the more damage there will be to tissue at the site of the infection. That’s because the immune response often involves the release of toxic compounds that have no effect on biofilms but can damage the surrounding tissues.”

Sauer’s research is driven by several key questions, she said: “Can we outsmart the biofilms? Can we interfere with biofilm antibiotic resistance? Can we figure out how to prevent biofilms from forming and becoming resistant to antibiotics?”

Some recent findings seem to offer a resounding yes to these questions.

In addition to regulators required for biofilm formation, Sauer and her team recently identified a regulator that is only expressed in biofilms and which seems to be responsible for regulating antibiotic resistance.

“We can modulate the resistance of biofilms now by over-expressing or inactivating this particular regulator,” she said. “We hope to use these discoveries to treat infections by interfering with the way biofilms are growing and by reverting biofilms back to a state where they’re more easily treatable.”

Sauer’s research is supported by the National Institutes of Health, which has awarded her more than $3 million, and the Army Research Office. Her two major NIH-funded projects, which began this fall, look at different aspects of biofilms. One focuses on antibiotic resistance and the mechanism behind it; the other centers on dispersion, the process by which a biofilm breaks down into individual bacterial cells.

“Dispersed cells — or planktonic cells — are way easier to treat,” Sauer said. “We want to understand how bacteria decide when to leave the biofilm. We can use that as a way to treat chronic infections.”