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Immunology, Inflammation, and an Oddly Intrigued Conservation Biologist

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Immunology, Inflammation, and an Oddly Intrigued Conservation Biologist Immunology, Inflammation, and an Oddly Intrigued Conservation Biologist Author: Melanie Quain Edited by: Jessica Packard Speaker: Ruslan Medzhitov, Professor of Immunobiology at Yale University School of Medicine “Host Defense Strategies” Pitt Science 2019 Thursday, October 17th 2019 Every year, the University of Pittsburgh holds Pitt Science, a conference open to anyone who is interested in learning about some ground-breaking research happening around the country. At each conference, the most prestigious annual award is given out to that years’ worthy scientist; the Dickson Prize in Medicine is annually awarded to one of the country’s leading researchers who engages themselves in innovative biomedical research. Who will win? Who has what it takes? Why am I asking so many questions when I already know the answer?? This year, the recipient of the 2019 Dickson Prize in Medicine is Ruslan Medzhitov, PhD, one of the world’s leading immunology researchers. Born in Uzbekistan, it was mandatory for Medzhitov to enroll in the Russian army at the age of 18 for two years. Following his service in the army, he dedicated his life to his education and eventually earned his B.S. and followed that degree to pursue his PhD at Moscow State University. He ran into funding issues due to the economic crisis in the Soviet Union in 1990 and later finished his PhD at the University of California, San Diego with Dr. Russell Doolittle and later worked with Dr. Charlie Janeway during his postdoc through researching immunity and inflammation[3]. From not backing down in the world of academics, Medzhitov has been able to achieve a number of accomplishments including being credited with many fundamental discoveries around the importance of Toll-like receptors in controlling adaptive immunity, infections, chronic inflammation, and tumor growth. The list of Dr. Medzhitov’s additional accomplishments and awards could go on and on, and with such a stacked resume, I was ready to see how he was going to draw me in with his immunology presentation! After receiving the Dickson Award, Medzhitov appeared very humbled after receiving this award along with the kind words said by the Pitt scientists. He thanked the community for recognizing him and gave a brief speech on how grateful he was to be able to work on ground- breaking research in the field of immunobiology. From there, he opened up his presentation giving a background on immunology and inflammation. Medzhitov began with the relation of homeostasis and inflammation, showing that homeostasis maintains stability of biological systems in the face of perturbance, while inflammation is induced by perturbations that cannot be handled by homeostatic mechanisms. This segwayed into the 4 causes of inflammation (infections; tissue damage; modern lifestyle; and noxious substances) and the inflammatory Pathway that are both demonstrated in the illustrations below! To break it down, once outside damage occurs the inflammatory pathway kicks into gear in order to fight off invading pathogens. The initial infection or tissue damage is classified in the inducer phase of the pathway and the tissue damaged is classified as the effector, mast cells and macrophages patrol for potential invading pathogens during the sensory phase, cytokines act during the mediator phase by helping fight off the invasive infection. Though it reaps good benefits, inflammatory response can be costly in terms of lost energy and can lead to the loss of fitness when responding to a variety of factors. Inflammatory response can be divided into two categories: intentional suppression of incompatible lower priority functions and unintentional suppression, or loss of function, both of which contribute to inflammatory disease[3]. To sum it all up, the higher the benefit, the higher the cost! Need a visual? Check out the graph below! You can see in Dr. Medzhitov’s graph that the further you move to the right, into the red zone, the cost is higher, but the benefit is high. As your body is fighting off this infection, you can fall ill to side effects from driving out the infection[2,3]. These side effects are what drive his research … what diseases are caused by this process of B=C?[3] The presentation then continued into their laboratory’s particular interest in disease induced anorexia. Basically, in most cases, when you have an acute infection such as a flu, your appetite decreases and you just want to cozy up in bed and binge SpongeBob SquarePants for the rest of your life. Oh, is that just me? Alright, let’s just move on… In order to study this phenomenon, the laboratory studied a pathogen known as Listeria, a common bacterium that causes food poisoning. Mice were infected with a sub-lethal dose of Listeria and their food consumption was monitored, and surprise, surprise there was a decrease in their food consumption until the infection left their bodies[3]. Next, they force fed the mice even when they were experiencing disease induced anorexia… guess what happened … the little guys didn’t make it, which indicated that eating during infection is lethal. So, what causes this affect? Glucose … so what would happen if you prevent glucose utilization? Instead of glucose, they used 2DG a glucose variant that can be taken into the cells by not metabolize. From this, they found that 2DG was able to allow 100% of the mice in the study to survive the infection[3]. Now… is this only exclusive in the Listeria infection? Or can this work in others? For this, they used a model of bacterial sepsis, Lipopolysaccharide (LPS) that is known to induce a dramatic inflammatory response. From this it was found that most mice would die when given food. Was this caused by glucose again? When they looked further and gave some mice glucose and others 2DG, all mice given glucose had deceased while all mice given 2DG had a 100% survival rate[3]. Dr. Medzhitov expressed that they were excited about this because they were able to produce these results under a pretty simple simulation and still be able to show profound results. It turns out that LPS produces a very high mortality rate! So… how is this all happening? When mice don’t eat, they undergo a fasting metabolic state. So, does this fasting metabolism have a more important factor than once thought, in terms of inflammation? Dr. Medzhitov breaks down fasting metabolism in this flow chart to your left. During fasting, glucose levels go down and therefore insulin levels go down. The organism then switches from using glucose to using fatty acids for energy; only the brain continues to use glucose in this fasting state[3]. Medzhitov and his team hypothesized that the regulated process of fasting may be involved in controlling the survival of the individual, because when we eat (consume food or glucose) insulin production is induced which suppresses the fasting process[3]. Maybe this could be why glucose killed the mice! The presentation then continued into their laboratory’s discovery of the function of the hormone, GDF15. This hormone is present whenever something in the body “goes wrong,” i.e. morning sickness, infection, anorexia, nausea, cell stress, toxins, chemotherapy, etc. GD15 has recently been identified as an emergency appetite suppressor that is exclusively expressed in the Postrema of the brain[1]. Is this hormone responsible for anorexia? … no HOWEVER, it is necessary for the survival of bacterial and viral inflammation, this was discovered through mouse models; most mice would survive with normal to high levels of GDF15 but would die when these levels of GDF15 decreased[1]. Dr. Medzhitov then posed the question… “How does GDF15 promote survival of the organism during infections?” As it turns out, the area of postrema activation by inflammation is dependent on GDF15. Further, the GDF15 blockade does not affect blood glucose, fatty acids, or ketone bodies in LPS sepsis. To answer another question on how GDF15 interacts with the heart, it has been shown that GDF15 helps sustain blood pressure within an individual, and without it (or decreased levels) the individual runs a risk of heart failure. GDF15 controls the hepatic sympathetic output in the heart, which works with triglycerides (or liver, if the individual is in a fasted state)[1]. So... what does this all mean? To wrap things up, Dr. Medzhitov’s research showed that GDF15 coordinates tolerance to inflammatory damage through regulation of triglyceride metabolism. In addition, the laboratory’s study provides additional evidence to support the emerging concept that metabolic reprogramming is essential to disease tolerance[1]. With further investigation of disease tolerance mechanisms, it’s highly possible to provide a new class of therapies for acute inflammatory diseases! If I’m going to be honest, I was not expecting to enjoy the presentation as much as I did. Dr. Medzhitov kept my attention the entire presentation through his ability to break down his research so that scientists of all backgrounds would be able to follow him on his journey of making this discovery through novel research methods. Never did I think I would be sitting in a lecture hall entranced by a lecture on inflammatory response, but here I am to say that I have! Kudos to you, Dr. Medzhitov and congratulations on receiving the Dickson Prize! Also… can we take the time to appreciate that Dr. Medzhitov created his own YouTube videos to get his research to a larger audience? We love a good SciComm moment! References: 1. Luan, H.H., Wang, A., Hilliard, B.K., Carvalho, F., Rosen, C.E., Ahasic, A.M., Herzog, E.L., Kang, I., Pisani, M.A., Yu, S., Zhang, C., Ring, A.M., Young, L.H., Medzhitov, R (2019). GDF15 is an Inflammation-Induced Central Mediator of Tissue Tolerance.
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