Prostate Restored
Prostate Restored
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Moreover, zinc acts as a direct or indirect regulator to affect the communication between nociceptor neurons and immune systems in the host, modulating the inflammatory response and host defence against bacterial infection [10,11,12].
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Read More »In a recent study, zinc was found to affect the biological activity of host receptors and influence the interaction between pathogenic microbes and the host. For example, porcine aminopeptidase N (APN) is a Zn2+-dependent membrane-bound exopeptidase that is widely expressed in various tissues and cells, especially in the small intestine mucosa [90]. It has been proven to be a fimbrial receptor protein for ETEC F4 and mediates the endocytosis of F4 bacteria in the host [91]. In our previous study, we observed that APN directly interacted with the major FaeG subunit of F4 fimbriae and affected F4 bacterial adherence to host cells [92]. The binding determinants of the APN-FaeG interaction contain residues important for zinc binding, and in a certain concentration range, the change in Zn2+ concentrations affects the biological activity of the APN protein as well as the adherence between E. coli F4 and host intestinal epithelial cells [90, 93]. In addition to cleaving N-terminal amino acids from small oligopeptides on the apical surface of intestinal epithelial cells, APN participates in regulating the MAPK/ERK1/2 signalling pathway in monocytes, while its zinc-binding site is blocked by inhibitory antibodies [91, 94]. APN has also been described as a cancer-specific biomarker and reported to be involved in the progression of tumour metastasis, angiogenesis and prognosis, as well as protein overexpression in cancer cells, while tissue invasion and metastasis in human prostate cancer could be attenuated by using Zn2+ to inhibit APN biological activity in a dose-dependent manner [95,96,97]. Zinc is also closely related to some transmembrane receptor proteins, including B cell receptors (BCRs), TLRs and nucleotide-binding oligomerization domain (NOD)-like receptors, which are responsible for the recognition of microbes or antigen molecules and involved in the development and modulation of intestinal homeostasis [72, 98, 99]. ZIP9 increased the intracellular zinc level and enhanced Akt and Erk phosphorylation in response to BCR activation [100]. ZIP7 plays an important role in B cell development and positively regulates pre-BCR and/or BCR signalling, while ZIP10 deficiency leads to impairment of BCR signalling in immune responses [99, 101, 102]. In addition, zinc induces inflammatory responses via the TLR/nuclear factor kappa-B (NF-κB) pathway and indirectly regulates TLR signalling via zinc transporters [103, 104]. Interestingly, the antimicrobial roles of macrophages vary in defending against different pathogens. Macrophages deploy both zinc starvation and/or zinc toxicity as an antimicrobial strategy [72, 98, 105]. The clearance of Streptococcus in macrophages is promoted by both calprotectin-mediated zinc starvation and intracellular zinc toxicity [106], whereas zinc starvation is utilized as a strategy against Histoplasma capsulatum infection, and excessive zinc poisoning within the macrophage phagolysosome exerts direct bactericidal effects on M. tuberculosis and UPEC [98, 107, 108]. In addition, continuous stimulation of TLRs and NOD2 alters the expression of MT and increases the level of intracellular zinc, leading to increased autophagy and enhanced bacterial clearance of S. typhimurium, S. aureus, and adherent invasive E. coli in intestinal macrophages [98, 109,110,111]. Zinc also causes macrophage malfunction, further triggering an abnormal inflammatory response, and impairs the innate immune system [111, 112]. For example, IRF/IL-23-mediated M1 macrophage activation and GATA3/IL-4-mediated M2 macrophage inhibition are both aggravated by zinc deficiency, resulting in severe intestinal inflammation and nitrogen metabolism disorder in patients with liver cirrhosis, whereas zinc supplementation can improve ammonia and protein metabolism and regulate the activation of M1/M2 macrophages [113]. Alternative activation of macrophages does not contribute to defending against intracellular pathogens in some cases. IL-4 induces macrophage polarization to the M2 phenotype and increases the expression of MT3 and ZnT4 but not MT1 and MT2. In addition to promoting zinc uptake by intracellular pathogens, MT3 and ZnT4 augments intracellular labile Zn2+ and contributes to pathogen persistence in M2 macrophages [114].
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Read More »Moreover, zinc itself has a regulatory role in intestinal immune responses and the healthy balance of the intestinal flora [3, 108]. After antigen stimulation, zinc attenuates the intestinal stress response and promotes the secretion of proteins and pro-inflammatory cytokines, such as sIgA, antimicrobial peptides, IL-1β, and IL-6 [54]. By regulating the MAPK and Akt signalling pathways, zinc can enhance intestinal mucosal barrier integrity and reduce inflammation and diarrhoea caused by bacterial infections [115]. Zinc also increases the expression of zinc finger protein A20 (also known as tumour necrosis factor alpha-induced protein 3) in intestinal epithelial cells to inhibit the inflammatory response and apoptosis mediated by some signal transduction pathways, such as NF-κB, and subsequent TNF-α production [116, 117]. However, A20 is a potent inhibitor of NF-κB-, TLR3-, and retinoic acid-inducible gene I-mediated IFN induction; thus, along with increased activation of NF-κB, interferon regulatory factor (IRF)-3, and IRF7, viral clearance was improved in A20-deficient cells, and this deficiency may protect the host against viral infection [118, 119]. As reported, zinc could optimize anti-tumour effects by inhibiting LPS-, ROS- or other immune factor-induced oncogenic signalling pathways, such as NF-κB, activator protein-1, Janus tyrosine kinase/signal transducer and activator of transcription (JAK/STAT), and PI3K/Akt; decrease oxidative stress and inflammatory responses induced by chemo- and radiotherapy; promote the development and differentiation of T and B lymphocytes; and improve the tumour microenvironment to reduce the risk of prostate, oesophageal, lung, and oral cancers [120,121,122]. High dietary zinc treatment has a beneficial effect on the modulation of mucosal structure and immune responses in the gut. It blocked TNF-α-mediated degradation of IκBα, decreased the mRNA expression of IFN-γ and IL-8, and upregulated the mRNA expression of ZO-1, occludin and transforming growth factor-β, resulting in an improvement in the antioxidant capacity and prevention of postweaning diarrhoea in piglets [63, 123]. Additionally, zinc is also reported to influence the modulation of biological rhythm and activity. By effectively stabilizing the binding of period proteins and cryptochrome proteins, zinc ions help to sustain the rhythmicity of the mammalian circadian clock in resisting the interference of negative factors, such as improper diet and drug abuse [124]. Previous studies have shown that zinc can regulate the absorption of water and electrolytes in the intestine and has a general inhibitory effect on voltage-gated ion channels, i.e., those for K+, Na+, Ca2+, and Cl− [125]. A new type of selective chloride channel regulated by Zn2+ in enteroendocrine cells of Drosophila larvae’s digestive tract, called Hodor, was found to act as a zinc ion sensor in the intestine and regulate individual feeding behaviour [126, 127]. Zn2+ is also used to promote the efficiency of antibiotics, such as vancomycin, quinolones, aminoglycosides, tetracycline, and macrolides [128]. For example, in gram-negative bacteria, the presence of zinc ions leads to an increase in the absorption of quinolones by changing the permeability of the bacterial outer membrane porin OmpF protein, while Zn2+ can effectively inhibit the acetylation of aminoglycosides catalysed by aminoglycoside 6′-N-acetyltransferase type Ib [AAC(6′)-Ib] and enhance the sensitivity of bacteria, especially for some aminoglycoside-resistant bacteria [128, 129].
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Read More »When zinc deficiency occurs, the cytotoxicity of natural killer cells, the phagocytic activity of neutrophils and the chemotaxis of monocytes are significantly decreased, but the phagocytosis and oxidative burst of monocytes are not affected. Zinc shortage has an influence on only IL-6 and TNF-α production in monocytes [54, 112]. In addition, the loss of copper-zinc superoxide dismutase activities results in damage to the stability of the cell membrane structure and dysfunction in host defensive systems, such as the regulation of neutrophil apoptosis and neutrophil-mediated tissue injury [117]. Because of this dysfunction, zinc deficiency enhances the severity of infectious diseases and illness in animals, whereas probiotics were reported to overcome the host defence defect in zinc-deficient cells by abolishing the activation of pro-inflammatory signalling via the ERK and p38 pathways [130].
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