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      Importance of cortactin for efficient epithelial NF-κB activation by Helicobacter pylori, Salmonella enterica and Pseudomonas aeruginosa, but not Campylobacter spp.

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          Abstract

          Transcription factors of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) family control important signaling pathways in the regulation of the host innate immune system. Various bacterial pathogens in the human gastrointestinal tract induce NF-κB activity and provoke proinflammatory signaling events in infected epithelial cells. NF-κB activation requires the phosphorylation-dependent proteolysis of inhibitor of κB (IκB) molecules including the NF-κB precursors through ubiquitin-mediated proteolysis. The canonical NF-κB pathway merges on IκB kinases (IKKs), which are required for signal transduction. Using CRISPR-Cas9 technology, secreted embryonic alkaline phosphatase (SEAP) reporter assays and cytokine enzyme-linked immunosorbent assay (ELISA), we demonstrate that the actin-binding protein cortactin is involved in NF-κB activation and subsequent interleukin-8 (IL-8) production upon infection by Helicobacter pylori, Salmonella enterica and Pseudomonas aeruginosa. Our data indicate that cortactin is needed to efficiently activate the c-Sarcoma (Src) kinase, which can positively stimulate NF-κB during infection. In contrast, cortactin is not involved in activation of NF-κB and IL-8 expression upon infection with Campylobacter species C. jejuni, C. coli or C. consisus, suggesting that Campylobacter species pluralis (spp.) induce a different signaling pathway upstream of cortactin to trigger the innate immune response.

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          Most cited references55

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          The nuclear factor NF-kappaB pathway in inflammation.

          The nuclear factor NF-kappaB pathway has long been considered a prototypical proinflammatory signaling pathway, largely based on the role of NF-kappaB in the expression of proinflammatory genes including cytokines, chemokines, and adhesion molecules. In this article, we describe how genetic evidence in mice has revealed complex roles for the NF-kappaB in inflammation that suggest both pro- and anti-inflammatory roles for this pathway. NF-kappaB has long been considered the "holy grail" as a target for new anti-inflammatory drugs; however, these recent studies suggest this pathway may prove a difficult target in the treatment of chronic disease. In this article, we discuss the role of NF-kappaB in inflammation in light of these recent studies.
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            The non-canonical NF-κB pathway in immunity and inflammation

            Defects in the non-canonical pathway of NF-κB activation are associated with severe immune deficiencies, and aberrant activation of this pathway can cause autoimmune and inflammatory diseases. Here, the author investigates the activation, signalling mechanisms and the biological function of the non-canonical NF-κB pathway.
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              Salmonella enterica serovar Typhimurium skills to succeed in the host: virulence and regulation.

              Salmonella enterica serovar Typhimurium is a primary enteric pathogen infecting both humans and animals. Infection begins with the ingestion of contaminated food or water so that salmonellae reach the intestinal epithelium and trigger gastrointestinal disease. In some patients the infection spreads upon invasion of the intestinal epithelium, internalization within phagocytes, and subsequent dissemination. In that case, antimicrobial therapy, based on fluoroquinolones and expanded-spectrum cephalosporins as the current drugs of choice, is indicated. To accomplish the pathogenic process, the Salmonella chromosome comprises several virulence mechanisms. The most important virulence genes are those located within the so-called Salmonella pathogenicity islands (SPIs). Thus far, five SPIs have been reported to have a major contribution to pathogenesis. Nonetheless, further virulence traits, such as the pSLT virulence plasmid, adhesins, flagella, and biofilm-related proteins, also contribute to success within the host. Several regulatory mechanisms which synchronize all these elements in order to guarantee bacterial survival have been described. These mechanisms govern the transitions from the different pathogenic stages and drive the pathogen to achieve maximal efficiency inside the host. This review focuses primarily on the virulence armamentarium of this pathogen and the extremely complicated regulatory network controlling its success.
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                Author and article information

                Journal
                Eur J Microbiol Immunol (Bp)
                Eur J Microbiol Immunol (Bp)
                EUJMI
                European Journal of Microbiology & Immunology
                Akadémiai Kiadó (Budapest )
                2062-509X
                2062-8633
                03 February 2022
                February 2022
                : 11
                : 4
                : 95-103
                Affiliations
                [1 ] Department of Biology, Division of Microbiology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) , Germany
                [2 ] Institute of Experimental Internal Medicine, Medical Faculty, Otto von Guericke University Magdeburg , Germany
                [3 ] Institute of Food Safety and Food Hygiene, Centre for Veterinary Public Health, Freie Universität Berlin , Germany
                Author notes
                *Corresponding author. Tel.: +49 9131 85 20314 E-mail: Nicole.Tegtmeyer@ 123456fau.de
                Article
                10.1556/1886.2021.00023
                8830411
                35060920
                9fca1ff6-7442-4226-9880-f5f0f664a344
                © 2021, The Author(s)

                Open Access. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License ( https://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted use, distribution, and reproduction in any medium for non-commercial purposes, provided the original author and source are credited, a link to the CC License is provided, and changes - if any – are indicated.

                Page count
                Figures: 4, Tables: 1, Equations: 0, References: 55, Pages: 9
                Categories
                Original Research Paper

                adp-heptose,nf-κb,helicobacter pylori,t4ss,cortactin,src,interleukin-8,inflammation

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