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Dental Disease, Inflammation, Cardiovascular Disease, Nutrition and Nutritional Supplements
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Douglas G. Thompson, Gregori M. Kurtzman, Chelsea Q. Watkins
Utilizing modern salivary diagnostic tests or a combination of them can significantly enhance the practitioner’s knowledge about the initiators of the periodontal disease process. Just like the tests for oral pathogens, tests also exist for genetic mutations that may affect the disease process. These tests identify potential genetic mutations that may increase the risk of acquiring periodontal disease or reacting more severely to the disease if the patient already has it. Examples of some of the genes significant to this and other inflammatory disease processes are beta-defensin 1, CD14, toll-like receptor 4, tumor necrosis factor-alpha, interleukin-1, interleukin-6, interleukin-17A and matrix metallopeptidase 3. The Celsus OneTM (OralDNA® Labs, Eden Prairie, MN) test evaluates for mutations in eight gene markers related to a potential exaggerated inflammatory response: IL-1 composite genotype, IL-6, IL-17 A, beta-defensin 1, CD14, tumor necrosis factor-alpha, toll-like receptor 4 composite genotype and matrix metalloproteinase 3. These gene mutations are associated with an increased risk for more severe periodontal infections, as well as increased risk for periimplantitis (periodontal disease associated with dental implants), diabetes and cardiovascular disease (Figure 14.2).95,96
Understanding the genetic basis of immune responses to fungal infection
Published in Expert Review of Anti-infective Therapy, 2022
Samuel M. Gonçalves, Cristina Cunha, Agostinho Carvalho
Genetic variation in IL-1β and beta-defensin 1 (DEFB1) was also associated with susceptibility to mold infection after solid-organ transplantation through altered production of monocyte-derived proinflammatory cytokines [69]. In addition, the promoter rs2069705 SNP in IFN-γ was found to confer resistance to IPA through a mechanism that involved the enhanced fungicidal activity of macrophages [70]. Recent work based on homozygosity mapping of blastomycosis patients from endemic areas in the US implicated a block of variants near IL-6 [71]. Endemic carriers were found to display impaired IL-6 and Th17 responses compared to European donors, a finding consistent with population differences in IL-6-mediated responses and T cell development. Cellular immunity to fungal infection, particularly in the context of recurrent vulvovaginal candidiasis (RVVC), was also shown to be affected by genetic variation in IL-22 [28]. In this case, the risk variant was associated with decreased production of IL-22 and downstream defects in calprotectin levels in patients.
Characterization of host defense molecules in the human pancreas
Published in Islets, 2019
Anton Stenwall, Sofie Ingvast, Oskar Skog, Olle Korsgren
The alpha- and beta defensins are hitherto known to be expressed both constitutively and inductively in various types of tissue, as reviewed by Ramasundara et al. The alpha defensins 1–4 are expressed in neutrophils in the lamina propria of the GI tract, and their expression is induced in intestinal epithelial cells in an inflammatory setting. Beta defensin 1 is constitutively expressed in colonic epithelial while the expression of beta defensins 2–4 is induced by bacteria and IL-1α.22,23 The expression of REG3A is induced by injury and inflammation in the colon.24 When considering inter-individual differences in the expression of defensins in the light of constitutive and induced expression, we hypothesized that the inter-individual differences in our material could be due to varying exposure to inflammatory and infectious stimuli as well as varying sensitivity and capacity to respond to these. The presence of bacteria in pancreases retrieved for organ donation is high and varies between donors.25-32 This is indeed expected due to the direct communication between the duodenum and the pancreas. However, we find no correlation to host defense expression levels and the levels of CD3 or CD45 positive cell infiltrates in the tissue. An observation tentatively explained by the fact that the pancreases were obtained from organ donors. However, since autolysis of the pancreas occurs rapidly after death, biopsies without severe artifacts cannot be obtained from autopsies.
Human platelets and megakaryocytes express defensin alpha 1
Published in Platelets, 2020
Xareni Valle-Jiménez, Adriana Ramírez-Cosmes, Alba Soledad Aquino-Domínguez, Francisco Sánchez-Peña, José Bustos-Arriaga, María De Los Ángeles Romero-Tlalolini, Honorio Torres-Aguilar, Jeanet Serafín-López, Sergio Roberto Aguilar Ruíz
Recent findings indicate that PMPs are not the only proteins with antimicrobial activity in platelets. Another important group of active proteins is antimicrobial peptides (AMPs); peptides from 10 to 150 amino acids of which approximately 60% are positively charged. AMPs are stored in cells as propeptides or mature peptides, and when secreted not only lyse bacteria, but also induce apoptosis in target cells, regenerate tissues, and modulate the immune response [13]. In humans, three groups of AMPs have been described: α and β-defensins, cathelicidins, and granulysins [13]. In platelets, the defensins expression has not been fully described. Platelets contain mRNA and the peptide of beta-defensin 1 (hBD-1), which is expressed primarily in epithelial cells. This peptide is found extra-granularly in the cytoplasm and is secreted after platelet activation, and can induce the formation of extracellular traps in polymorphonuclear cells [14]. Only the defensin alpha 1 has been found in a proteomic study of platelets [15]; however, the authors did not confirm the presence of mRNA or peptide. Whether platelets contain other AMPs and whether these peptides are derived from the megakaryocytic cell line and can be secreted is also unknown. The goal of this work was to evaluate the expression and transference of the mRNA and peptide of DEFA1 in the megakaryocytic lineage (megakaryoblast-platelets) and their potential capability to secrete it. Therefore, a gene expression microarray was performed to identify the expression of genes with reported antimicrobial activity in platelets, and in accordance with the previous proteomics evidence, mRNA of DEFA1 was detected. Our work confirmed the presence and secretion of DEFA1 in peripheral blood platelets, the megakaryoblast cell line (MEG-01), and platelet-like particles (PLPs) derived from MEG-01 cells, additionally, this secreted DEFA1 can rebind to platelet’s surface and have antibacterial activity against Escherichia coli, demonstrating that this AMP can be secreted after activation of the megakaryocytic lineage with different agonists.