What happens when someone gets a bacterial infection?  The body responds by making antibodies.  To prevent death, the patient is also often given an antibiotic based on the presumption that the antibiotic will kill the invading microorganisms.  “If you have an infection and an antimicrobial drug is administered, it is supposed to kill the bacteria in your body,” explains Larry Bopp, Associate Professor in the Natural Science and Mathematics Department at SUNY Cobleskill.  “In order to gain FDA approval, it has already been established that the drug is effective and relatively safe.  However, little research is designed to look at more subtle aspects of the interaction between infectious agents, the drugs used to treat the infections they cause, and the responses of the host to the infection and its treatment.”

He goes on to say that if a person gets a bacterial infection, the entire body responds, often with a fever and other inflammatory responses controlled by signaling molecules known as cytokines.  If inflammation is localized, it usually helps the body fight the infection.  Unfortunately, the cytokines produced in response to infection circulate throughout the body, and sometimes the inflammation they cause gets out of control, leading to sepsis, septic shock, and even death.

Over the last 50 years, the survival rate for people suffering from septic shock has not improved. This is partly because we do not fully understand exactly how the cytokine response works, but is mostly because by the time we know that a patient is becoming severely septic or entering septic shock, it is too late to reverse the effects that lead to death.  Bopp and his colleagues are working to determine if there is a pattern of cytokine production early in the development of sepsis that can be detected and would allow doctors to intervene before it is too late.

In the 1970s and 1980s, Dr. Bopp worked for General Electric in Niskayuna, primarily on PCB biodegradation and other areas of environmental microbiology.  After that, he was with the Wadsworth Center of the New York State Health Department as a specialist in infectious diseases, and then became a professor at the University of Southern Mississippi. While at GE, he had collaborated with the infectious disease research staff at the VA Medical Center in Albany, and continued to collaborate with infectious disease researchers at the VA and at the Wadsworth Center while in Mississippi.  In 1996 he returned to the Albany area and became a full-time infectious disease research scientist at the VA.  For the next ten years, he and his colleagues pursued a variety of infectious disease research interests, funded primarily by pharmaceutical companies and the VA.

Bopp’s desire to be back in the classroom, however, brought him to SUNY Cobleskill, where he taught microbiology as an adjunct instructor until a full-time tenure track position opened up in 2006.  He accepted the job with the agreement that he could continue his research, which he often refers to as “drugs and bugs.”

One of the interesting things Bopp and his colleagues have discovered is that the cytokine response of white blood cells to yeast infection is quite different than the response to MRSA infection.  As part of that research, they are investigating whether or not the antibiotics used to treat these infections also influence cytokine reactions in the body.

“What if the antibiotic stimulates cytokine production on its own, even without infection?” Bopp contemplated.    “Or what if the antibiotic represses cytokine production?  And what effect does a drug have on cytokine production in the absence of infection?  That is not normally something that people consider when looking at how antibiotics work in the body.”

To study these complex interactions, Bopp and his colleagues at the VA, as well as Dr. David Lawrence, an immunologist at the Wadsworth Center of the New York State Department of Health, use a model system in which white blood cells from healthy donors are grown in the laboratory and then exposed to antibiotics, infectious agents such as yeast or methicillin-resistant Staphylococcus aureus (MRSA), and combinations of these.  Cytokine levels are then determined to see what effects the treatments have had on cytokine production by the white blood cells.

“You cannot understand the roles microorganisms, antimicrobial drugs, and their combinations play in controlling the inflammatory response to infection unless you study them individually, as well as in combination.  For example, an antibiotic that has no effect on cytokine production when administered alone (without a microorganism present) could have a dramatic effect in the presence of the microorganism.”

These effects have not been widely tested, partly because antimicrobial research has traditionally focused on the microorganisms rather than the hosts (us), but also because measuring cytokine levels is expensive, technically challenging, and requires a larger sample than is generally available.  A game changer for this research, called Luminex microsphere technology, now allows relatively rapid and inexpensive determination of the levels of many cytokines on a very small sample.  Dr. Bopp and his colleagues use this technology to determine the levels of 10 or more cytokines on a sample as small as one drop.

Dr. Bopp has published almost 50 articles in internationally recognized peer-reviewed journals, including 12 articles since joining the faculty at SUNY Cobleskill in 2006.  “We have published a number of papers describing cytokine responses to infection and treatment in a laboratory model system.  Now we are interested in studying these same phenomena in people with varying degrees of sepsis and other inflammatory diseases such as atherosclerosis.”

On February 12, Bopp will give a talk about his work at a Faculty Chat evening at Coby’s restaurant, 549 Main Street in Cobleskill.  To find out more, contact the Office of Community Engagement at x5300 or the Office of Communications at x5631.