Update on the role of Toll-like receptors during bacterial infections and sepsis.
Toll-like receptors (TLRs) are recognition molecules that importantly contribute to the innate immune response to bacterial and viral infections. Once TLRs sense the presence of invading pathogens a signal transduction cascade is initiated that eventually leads to the production of pro-inflammatory mediators and attraction of neutrophils to the site of infection. While the ultimate goal of this defense pathway is the successful elimination of invading microbes, prolonged or exaggerated stimulation of TLR-associated events can lead to systemic inflammation and clinical symptoms of sepsis. This brief review summarizes the impact of selected TLRs in the host response to clinically important bacteria and provides insights into TLR-associated therapeutic approaches during sepsis and inflammation.
Knapp
Sylvia
S
Center for Molecular Medicine of the Austrian Academy of Sciences (CeMM) and Division of Infectious Diseases and Tropical Medicine, Department of Medicine 1, Medical University of Vienna, Vienna, Austria. sylvia.knapp@meduniwien.ac.at
D000818:Animals; D000942:Antigens, Bacterial / Q000276:immunology; D001424:Bacterial Infections / Q000188:drug therapy / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology; D018836:Inflammation Mediators / Q000097:blood; D008070:Lipopolysaccharides / Q000276:immunology; D051379:Mice; D009504:Neutrophils / Q000276:immunology; D018805:Sepsis / Q000188:drug therapy / Q000276:immunology*; D015398:Signal Transduction / Q000502:physiology; D051193:Toll-Like Receptors / Q000037:antagonists & inhibitors / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
D000942:Antigens, Bacterial; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D051193:Toll-Like Receptors; D014409:Tumor Necrosis Factor-alpha