Yao-Zhong Liu1, Pooja Maney2, Jyoti Puri3, Yu Zhou4, Melody Baddoo5, Michael Strong5, Yu-Ping Wang6, Erik Flemington5, Hong-Wen Deng4. 1. Center of Genomics and Bioinformatics, Dept. of Biostatistics and Bioinformatics, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, United States. Electronic address: yliu8@tulane.edu. 2. Dept. of Periodontics, School of Dentistry, Louisiana State University Health Sciences Center, New Orleans, LA, United States. Electronic address: pmaney@lsuhsc.edu. 3. Dept. of Periodontics, School of Dentistry, Louisiana State University Health Sciences Center, New Orleans, LA, United States. 4. Center of Genomics and Bioinformatics, Dept. of Biostatistics and Bioinformatics, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, United States. 5. Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA, United States. 6. Dept. of Biomedical Engineering, Tulane University School of Science and Engineering, United States.
Abstract
BACKGROUND: Monocytes are an important cell type in chronic periodontitis (CP) by interacting with oral bacteria and mediating host immune response. The aim of this study was to reveal new functional genes and pathways for CP at monocyte transcriptomic level. METHODS: We performed an RNA-sequencing (RNA-seq) study of peripheral blood monocytes (PBMs) in 5 non-smoking moderate to severe CP (case) individuals vs. 5 controls. We took advantage of a microarray study of periodontitis to support our findings. We also performed pathway-based analysis on the identified differentially expressed (DEx) transcripts/isoforms using DAVID (Database for Annotation, Visualization and Integrated Discovery). RESULTS: Through differential expression analyses at both whole gene (or whole non-coding RNA) and isoform levels, we identified 380 DEx transcripts and 5955 DEx isoforms with a PPEE (posterior probability of equal expression) of <0.05. Pervasive up-regulation of transcripts at isoform level in CP vs. control individuals was observed, suggesting a more functionally active monocyte transcriptome for CP. By comparing with the microarray dataset, we identified several CP-associated novel genes (e.g., FACR and CUX1) that have functions to interact with invading microorganisms or enhance TNF production on lipopolysaccharide stimulation. DAVID analysis of both the RNA-seq and the microarray datasets leads to converging evidence supporting "endocytosis", "cytokine production" and "apoptosis" as significant biological processes in CP. CONCLUSIONS: As the first RNA-seq study of PBMs for CP, this study provided novel findings at both gene (e.g., FCAR and CUX1) and biological process level. The findings will contribute to better understanding of CP disease mechanisms.
BACKGROUND: Monocytes are an important cell type in chronic periodontitis (CP) by interacting with oral bacteria and mediating host immune response. The aim of this study was to reveal new functional genes and pathways for CP at monocyte transcriptomic level. METHODS: We performed an RNA-sequencing (RNA-seq) study of peripheral blood monocytes (PBMs) in 5 non-smoking moderate to severe CP (case) individuals vs. 5 controls. We took advantage of a microarray study of periodontitis to support our findings. We also performed pathway-based analysis on the identified differentially expressed (DEx) transcripts/isoforms using DAVID (Database for Annotation, Visualization and Integrated Discovery). RESULTS: Through differential expression analyses at both whole gene (or whole non-coding RNA) and isoform levels, we identified 380 DEx transcripts and 5955 DEx isoforms with a PPEE (posterior probability of equal expression) of <0.05. Pervasive up-regulation of transcripts at isoform level in CP vs. control individuals was observed, suggesting a more functionally active monocyte transcriptome for CP. By comparing with the microarray dataset, we identified several CP-associated novel genes (e.g., FACR and CUX1) that have functions to interact with invading microorganisms or enhance TNF production on lipopolysaccharide stimulation. DAVID analysis of both the RNA-seq and the microarray datasets leads to converging evidence supporting "endocytosis", "cytokine production" and "apoptosis" as significant biological processes in CP. CONCLUSIONS: As the first RNA-seq study of PBMs for CP, this study provided novel findings at both gene (e.g., FCAR and CUX1) and biological process level. The findings will contribute to better understanding of CP disease mechanisms.
Authors: I Rollinger-Holzinger; B Eibl; M Pauly; U Griesser; F Hentges; B Auer; G Pall; P Schratzberger; D Niederwieser; E H Weiss; H Zwierzina Journal: J Immunol Date: 2000-03-15 Impact factor: 5.422
Authors: Aldo H De-La-Cruz-Montoya; Eric G Ramírez-Salazar; Mayeli M Martínez-Aguilar; Pablo M González-de-la-Rosa; Manuel Quiterio; Cei Abreu-Goodger; Jorge Salmerón; Rafael Velázquez-Cruz Journal: Exp Biol Med (Maywood) Date: 2018-10-15
Authors: Ronaldo Lira-Junior; Sofia Björnfot Holmström; Reuben Clark; Stephanie Zwicker; Mirjam Majster; Gunnar Johannsen; Björn Axtelius; Sigvard Åkerman; Mattias Svensson; Björn Klinge; Elisabeth A Boström Journal: Front Immunol Date: 2020-01-31 Impact factor: 7.561