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Archive - Sep 29, 2017

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Confronted with Bacteria, Infected Cells Die Allowing Others to Live, Penn Study Finds

The immune system is constantly performing surveillance to detect foreign organisms that might do harm. But pathogens, for their part, have evolved a number of strategies to evade this detection, such as secreting proteins that hinder a host's ability to mount an immune response. In a new study, a team of researchers led by Dr. Igor E. Brodsky of the University of Pennsylvania, identified a "back-up alarm" system in host cells that responds to a pathogen's attempt to subvert the immune system. "In the context of an infection, the cells that are dying are talking to the other cells that aren't infected," said Dr. Brodsky, an Assistant Professor in the Department of Pathobiology in Penn's School of Veterinary Medicine and senior author on the study. "I don't think of it as altruistic, exactly, but it's a way for the cells that can't respond any longer to still alert their neighbors that a pathogen is present." The findings address the long-standing question of how a host can generate an immune response to something that is designed to shut off that very response. A potential future application of this new understanding may enable the cell-death pathway triggered by bacteria to be harnessed in order to target tumor cells and encourage their demise. The work was published online on August 30, 2017 in the Journal of Experimental Medicine. The article is titled “RIPK1-Dependent Apoptosis Bypasses Pathogen Blockade of Innate Signaling to Promote Immune Defense.” A major way that the immune system recognizes pathogens is by detecting patterns that are shared among microbes but are distinct from a host's own cells. Pathogens, however, don't make it easy for immune cells to destroy them. Some can inject proteins into host cells that interfere with this detection, allowing an infection to become established.

Novel Class of Lipid Mediators (Elovanoids) May Protect Brain from Stroke, Neurodegenerative Diseases

Research led by Nicolas Bazan (photo), MD, PhD, Boyd Professor and Director of the Neuroscience Center of Excellence at LSU Health New Orleans, has discovered a new class of molecules in the brain that synchronize cell-to-cell communication and neuroinflammation/immune activity in response to injury or diseases. Elovanoids (ELVs) are bioactive chemical messengers made from omega-3 very-long-chain polyunsaturated fatty acids (VLC-PUFAs, n-3). They are released on demand when cells are damaged or stressed. "Although we knew about messengers from omega-3 fatty acids such as neuroprotectin D1 (22 carbons) before, the novelty of the present discovery is that elovanoids are made of 32 to 34 carbon atoms in length," notes Dr. Bazan. "We expect that these structures will profoundly increase our understanding of cellular cross talk to sustain neuronal circuitry and particularly to restore cell equilibrium after pathological insults." Working in neuronal cell cultures from the cerebral cortex and from the hippocampus and a model of ischemic stroke, the researchers found that elovanoids not only protected neuronal cells and promoted their survival, but helped maintain their integrity and stability. The work was published online on September 27, 2017 in Science Advances. The open-access article is titled “Elovanoids Are a Novel Class of Homeostatic Lipid Mediators That Protect Neural Cell Integrity Upon Injury.” "Our findings represent a breakthrough in the understanding of how the complexity and resiliency of the brain are sustained when confronted with adversities such as stroke, Parkinson's, or Alzheimer's and neuroprotection signaling needs to be activated," says Dr. Bazan. "A key factor is how neurons communicate among themselves.