Steven R Blanke
University of Illinois, USA
Title: Extending the Gut-Brain Axis: The Curious Case of Helicobacter pylori
Biography
Biography: Steven R Blanke
Abstract
There is increasing recognition that localized microbe-host interactions inrnhumans can influence the physiology and function of distal tissue and organrnsystems in a manner that can have profound impact on human health andrndisease. For example, human gut microbiota communicate with the centralrnnervous system (CNS) via the neural, endocrine and/or immune systems,rnthereby influencing brain function. Cytokines from the peripheral immune systemrninteract with the central nervous system (CNS) via active transport across thernblood brain barrier as well as direct entry via the circumventricular organs. Here,rnwe evaluated the hypothesis that chronic gastric infection with the humanrnpathogenic bacterium Helicobacter pylori (Hp) is causal for elevated systemicrninflammation and neuro-inflammation. Chronic Hp infection is characterized byrnsustained inflammation of the gastric mucosa, which is highly associated withrnprogression to gastric ulcer disease or gastric cancer in approximately 10% andrn2% of infected individuals, respectively. Our studies employing a Sprague-rnDawley rat model for chronic Hp infection revealed sustained gastricrninflammation and tissue damage. What is more, Hp-infected rats demonstratedrnelevated inflammation with the bloodstream and CNS, with activated microgliarnand elevated TNF-α detected in the brain of the infected animals. The causalrnrelationship between gastric Hp infection and brain sequelae was supported byrnthe loss of elevated systemic and CNS inflammation upon clearance of Hprn infections following antibiotic administration. Because approximately half thernworld’s population is infected with Hp, these results have implications for thernimpact of microbes on cognition and behavior during human brain development.
