Biofilm‐induced profiles of immune response gene expression by oral epithelial cells

Abstract

This study examined the oral epithelial immunotranscriptome response patterns modulated by oral bacterial planktonic or biofilm challenge. We assessed gene expression patterns when epithelial cells were challenged with a multispecies biofilm composed of Streptococcus gordonii, Fusobacterium nucleatum, and Porphyromonas gingivalis representing a type of periodontopathic biofilm compared to challenge with the same species of planktonic bacteria. Of the 579 human immunology genes, a substantial signal of the epithelial cells was observed to 181 genes. Biofilm challenged stimulated significant elevations compared to planktonic bacteria for IL32, IL8, CD44, B2M, TGFBI, NFKBIA, IL1B, CD59, IL1A, CCL20 representing the top 10 signals comprising 55% of the overall signal for the epithelial cell responses. Levels of PLAU, CD9, IFITM1, PLAUR, CD24, TNFSF10, and IL1RN were all elevated by each of the planktonic bacterial challenge vs the biofilm responses. While the biofilms up‐regulated 123/579 genes (>2‐fold), fewer genes were increased by the planktonic species (36 [S gordonii], 30 [F nucleatum], 44 [P gingivalis]). A wide array of immune genes were regulated by oral bacterial challenge of epithelial cells that would be linked to the local activity of innate and adaptive immune response components in the gingival tissues. Incorporating bacterial species into a structured biofilm dramatically altered the number and level of genes expressed. Additionally, a specific set of genes were significantly decreased with the multispecies biofilms suggesting that some epithelial cell biologic pathways are down‐regulated when in contact with this type of pathogenic biofilm.

Long Term Delta-9-tetrahydrocannabinol Administration Inhibits Proinflammatory Responses in Minor Salivary Glands of Chronically Simian Immunodeficieny Virus Infected Rhesus Macaques

“…Table S1 lists the Top 50 differentially upregulated genes in OPM of VEH-untreated SIV rhesus macaques. Notable genes that were significantly upregulated exclusively in OPM of VEH-untreated/SIV rhesus macaques ( Figure 1 A) included IL1RN (inhibits activity of interleukin-1) [ 40 ], PELI3 (interacts with complex containing IRAK kinases and TRAF6 of IL1 and TLR signaling pathways) [ 41 ], BST2 (Interferon induced anti-viral protein) [ 42 ], alarmins ( IL1A , IL36A and S100A9 ) [ 43 , 44 ], IRF1 (innate and adaptive immune response) [ 45 ], DEFB103A (antimicrobial peptide), CD207 (major receptor on langerhans cells for Candida species) [ 46 ], STAT2 (type 1 interferon signaling) [ 45 ] and MYD88 (adapter protein in Toll-like receptor signaling) [ 47 ].…”

Clinical and molecular characterization of COVID-19 hospitalized patients

“…We explored the hypothesis that each patient could have one unique combination of rare pathogenic/highly relevant variants related for different reasons to infection susceptibility [9] (Fig 1): G6PD-deficient cells are more susceptible to several viruses including coronavirus and have down-regulated innate immunity (in line with the observed very low levels of IL-6) ( Fig 1) [25]; ZEB1-linked corneal dystrophy, known to function in immune cells, and playing an important role in establishing both the effector response and future immunity in response to pathogens [26]; TGFBI mutations (associated with corneal dystrophy); ABCC6 gene mutations (associated with pseudoxanthoma elasticum); likely hypomorphic mutations in CHD7 or COL5A1/2 variants, playing a role as modulators of immune cells activity and/or response to infections [27][28][29][30][31][32][33][34]; ADAR, involved in viral RNA editing; CLEC4M, an alternative receptor for SARS-CoV [35] HCRTR1/2, receptors of Hypocretin, important in the regulation of fatigue during infections [36]; FURIN, a serine protease that cleaves the SARS-Cov-2 minor capsid protein important for ACE2 contact and viral entry into the host cells [37,38].…”

Biliary Tract Carcinogenesis Model Based on Bile Metaproteomics

“…Biofilm formation by bacteria such as F. nucleatum and A. naeslundii, and not the planktonic form, stimulates the synthesis of IL-8 by human squamous epithelial cells (51). Supporting the latter concept, several surveys have proved that bacteria biofilm not only stimulates IL-8 synthesis by human squamous epithelial cells, but that stimulation is stronger when the biofilm is formed by multiple bacterial species (52,53). Furthermore, the similarity of some amino acids in the carboxyterminal region of IL-8 with cecropins, proteins with antibiotic properties, elicit the analysis of the antibiotic properties of IL-8 through the synthesis of synthetic peptides.…”