Nuclear factor-kappa B activation and innate immune response in microbial pathogen infection.
Human pathogenic microorganisms have developed a variety of strategies to infect the host organism successfully, whereas the host has evolved a series of defense mechanisms. In most cases, the epithelial cell layer represents the first barrier for the bacterial pathogen and triggers the innate and inflammatory responses in the host. Epithelial cells release proinflammatory mediators including cytokines and chemokines, leading to the subsequent attraction of monocytes/macrophages. Therefore, epithelial cells represent an immediate-early warning system in the host organism. Subsequent to the colonization of the epithelial layer, invasive microbial pathogens often induce an acute inflammatory response, which functions to activate residential macrophages and recruits blood leukocytes to the site of infection. Distinct receptors of the Toll family on the cell surface of immune cells mediate antibacterial responses in mammals as well as in Drosophila. One of the most important cellular factors involved in the regulation of the host innate antimicrobial response is the immediate-early response transcription factor nuclear factor (NF)-kappa B. Microbial pathogens activate cellular signal transduction pathways that induce NF-kappa B activation, but pathogens also find ways to overcome the innate immune response through active manipulation of the NF-kappa B signal transduction pathways. Exploration of the mechanisms that influence NF-kappa B activity could contribute to a better understanding of the molecular pathogenesis of microbial infections and could be important for potential therapeutic intervention that may be relevant in a wide variety of inflammatory diseases.
Naumann
M
M
Department of Molecular Biology, Max-Planck-Institute for Infection Biology, 10117 Berlin, Germany. naumann@mpiib-berlin.mpg.de
D000818:Animals; D000917:Antibody Formation; D029721:Drosophila Proteins; D004847:Epithelial Cells / Q000276:immunology / Q000382:microbiology; D016481:Helicobacter Infections / Q000276:immunology*; D016480:Helicobacter pylori / Q000276:immunology; D006801:Humans; D008562:Membrane Glycoproteins / Q000276:immunology / Q000378:metabolism; D016328:NF-kappa B / Q000276:immunology / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000276:immunology / Q000378:metabolism; D051193:Toll-Like Receptors
D029721:Drosophila Proteins; D008562:Membrane Glycoproteins; D016328:NF-kappa B; D011956:Receptors, Cell Surface; D051193:Toll-Like Receptors