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The Human Microbiome: How Our Health is Impacted by Microorganisms
Published in Michael Hehenberger, Zhi Xia, Huanming Yang, Our Animal Connection, 2020
Michael Hehenberger, Zhi Xia, Huanming Yang
An article published in Nature reported that intestinal commensala bacteria can regulate the differentiation of multiple T cells and thus change the immune system of the intestinal mucosa. F. prazilus is located in the mucosal layer of the intestine and produces butyrate by fermentation. This short-chain fatty acid stimulates and modulates T cells to prevent the development of intestinal inflammation. All Clostridium bacteria have similar mechanism. Another article in Science pointed out that under normal circumstances, dendritic cells do not respond to T-cell inflammation in the intestinal mucosa, so they play an important role in maintaining intestinal immune tolerance.80 However, when the environment changes, dendritic cells can activate T cells, and β-chain proteins on T cells play an important role in regulating dendritic cells. When the β-chain protein is cleared, the activity and resistance of T cells are regulated. The effect of inflammatory cytokines was significantly reduced, while pro-inflammatory helper T cells 1 and 17 and their cytokines increased. Mice lacking beta-catenin in dendritic cells exhibit increased sensitivity to enteritis.
The Human Microbiome: How Our Health is Impacted by Microorganisms
Published in Michael Hehenberger, Zhi Xia, Our Animal Connection, 2019
An article published in Nature reported that intestinal commensala bacteria can regulate the differentiation of multiple T cells and thus change the immune system of the intestinal mucosa. F. prazilus is located in the mucosal layer of the intestine and produces butyrate by fermentation. This short-chain fatty acid stimulates and modulates T cells to prevent the development of intestinal inflammation. All Clostridium bacteria have similar mechanism. Another article in Science pointed out that under normal circumstances, dendritic cells do not respond to T-cell inflammation in the intestinal mucosa, so they play an important role in maintaining intestinal immune tolerance.80 However, when the environment changes, dendritic cells can activate T cells, and β-chain proteins on T cells play an important role in regulating dendritic cells. When the β-chain protein is cleared, the activity and resistance of T cells are regulated. The effect of inflammatory cytokines was significantly reduced, while pro-inflammatory helper T cells 1 and 17 and their cytokines increased. Mice lacking betacatenin in dendritic cells exhibit increased sensitivity to enteritis.
Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Dendritic cells are specialized APCs that orchestrate innate and adaptive immune responses. The intestinal mucosa contains numerous DCs, which induce either protective immunity to infectious agents or tolerance to innocuous antigens, including food and commensal bacteria. Several subsets of mucosal DCs have been described that display unique functions dictated in part by the local microenvironment (Figure 2.33).
The modern pharmacological approach to diabetes: innovative methods of monitoring and insulin treatment
Published in Expert Review of Medical Devices, 2022
Iulian Tătaru, Oana M. Dragostin, Iuliu Fulga, Florentina Boros, Adelina Carp, Ariadna Maftei, Carmen L. Zamfir, Aurel Nechita
Encapsulation of insulin in nanoparticles offers new opportunities to control insulin release. Many nanocarrier systems, such as liposomes and polymeric nanoparticles, have been developed to improve their bioavailability and prolong their stability. To achieve an optimal therapeutic effect, these nanoparticles must be stable in the gastrointestinal tract, able to enter the intestinal mucosa, be transported through the intestinal epithelium to reach the systemic circulation and release bioactive insulin. Insulin has represented for many years a correct approach in diabetes treatment and surely will be present in the future. However, the modern pharmacological approach has shifted to newer class drugs with beneficial pleiotropic effect [70].
Overview of methodologies for the culturing, recovery and detection of Campylobacter
Published in International Journal of Environmental Health Research, 2023
Marcela Soto-Beltrán, Bertram G. Lee, Bianca A. Amézquita-López, Beatriz Quiñones
Virulence in Campylobacter consists of multiple pathways, mainly attributed to flagella-mediated motility, bacterial adherence to intestinal mucosa, invasive capability, and the ability to produce toxins, and different sets of determinants are required for the successful colonization by C. jejuni of the host gastrointestinal tract (Table 2). Having arrived at the host’s gastrointestinal epithelial cells, adherence to the cells is required for colonization (Bolton 2015). Important virulence determinants include CadF, a 37-kDa fibronectin-binding outer membrane protein, which is responsible for Campylobacter adhesion to fibronectin (Konkel et al. 1997). FlpA is also a fibronectin binding protein that may work together with CadF (Bolton 2015). Another factor is the CapA autotransporter that is also involved in adhesion. However, some strains use an alternate CapC protein, indicating that adhesion proteins vary between different C. jejuni strains due to diverse mechanisms of interaction and strategies of colonization (Mehat et al. 2020). Moreover, Campylobacter use a Type III protein secretion system (T3SS) for injecting and secreting putative virulence factors into host cells (Table 2), and this flagellar-based T3SS consists of FlhA, FlhB, FliO, FliP, FliQ and FliR (Bolton 2015). Among the various factors secreted from the flagellum are FlaC, CiaC, and CiaI, which are required for colonization, invasion, and intracellular survival (Carrillo et al. 2004; Konkel et al. 2004). Other virulence determinants include IamA and FspA, which are both required for invasion and colonization (Bolton 2015). The most characterized toxin produced by Campylobacter is the cytolethal distending toxin. The toxin consists of three subunits CdtA, CdtB, CdtC; CtdA and CdtC are responsible for the delivery of the active subunit CdtB, which enters the host cell nucleus and acts as a deoxyribonuclease to result in cell cycle arrest and death (Bolton 2015).