Wojciech Dabrowski*, Dorota Siwicka-Gieroba, Katarzyna Kotfis, Sami Zaid, Sylwia Terpilowska, Chiara Robba and Andrzej K. Siwicki Pages 1164 - 1177 ( 14 )
A traumatic brain injury (TBI) initiates an inflammatory response with molecular cascades triggered by the presence of necrotic debris, including damaged myelin, hemorrhages and injured neuronal cells. Molecular cascades prominent in TBI-induced inflammation include the release of an excess of proinflammatory cytokines and angiogenic factors, the degradation of tight junctions (TJs), cytoskeletal rearrangements and leukocyte and protein extravasation promoted by increased expression of adhesion molecules. The brain-gut axis consists of a complex network involving neuroendocrine and immunological signaling pathways and bi-directional neural mechanisms. Importantly, modifying the gut microbiome alters this axis, and in turn may influence brain injury and neuroinflammatory processes. In recent years it has been demonstrated that the activity and composition of the gastrointestinal (GI) microbiome population influences the brain through all of above-mentioned pathways affecting homeostasis of the central nervous system (CNS). The GI microbiome is involved in the modulation of cellular and molecular processes which are fundamental to the progression of TBI-induced pathologies, including neuroinflammation, abnormal blood brain barrier (BBB) permeability, immune system responses, microglial activation, and mitochondrial dysfunction. It has been postulated that interaction between the brain and gut microbiome occurs mainly via the enteric nervous system and the vagus nerve through neuroactive compounds including serotonin or dopamine and activation by bacterial metabolites including endotoxin, neurotransmitters, neurotrophic factors, and cytokines. In recent years the multifactorial impact of selected immunomodulatory drugs on immune processes occurring in the CNS and involving the brain-gut axis has been under intensive investigation.
Traumatic brain injury, secondary brain damage, trauma, cells interactions, microbiome, immunomodulation.
Department of Anesthesiology and Intensive Care, Medical University of Lublin, 20-954 Lublin, Department of Anesthesiology and Intensive Care, Medical University of Lublin, 20-954 Lublin, Department of Anesthesiology, Intensive Therapy and Acute Intoxications, Pomeranian Medical University, 71-204 Szczecin, Department of Anaesthesia, Al-Emadi-Hospital Doha, Laboratory of Environmental Biology, Institute of Environmental Engineering, The John Paul II Catholic University of Lublin, 20-950, Lublin, Department of Anaesthesia and Intensive Care, Policlinico San Martino, Genova, Department of Microbiology and Clinical Immunology, University of Warmia and Mazury in Olsztyn, 10-957 Olsztyn