Dataset Information

Gene expression data of inflammatory mediators in apical periodontitis in 129 (wild type) and 5-lipoxygenase knockout mice.

ABSTRACT: Apical periodontitis is an immune inflammatory response around periapical tissues as a result of pathogens invasion into the root canal. The host immunoinflammatory response could determine the progression of this disease, which involves the recruitment of immune cells, and the release of several cytokines in the lesion site. The 5-lipoxygenase pathway has been activated in some osteolytic diseases due to its capacity to interfere in the proliferation and differentiation of bone cells, including the osteoclasts. As mean to understand the inflammatory genes regulation in the apical periodontitis progression, we evaluated the network of 66 genes related to cytokines, chemokines and other inflammatory mediators and receptors in the wild-type (WT) and 5-lipoxygenase enzyme genetically deficient mice (KO). This article presents data not published but related to the research article "Effects of 5-lipoxygenase gene disruption on inflammation, osteoclastogenesis and bone resorption in polymicrobial apical periodontitis" .

SUBMITTER: Taira TM

PROVIDER: S-EPMC8762048 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature

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Gene expression data of inflammatory mediators in apical periodontitis in 129 (wild type) and 5-lipoxygenase knockout mice.

Taira Thaise Mayumi TM Ribeiro Vítor Luís VL Ribeiro Yuri Jivago Silva YJS da Silva Raquel Assed Bezerra RAB da Silva Léa Assed Bezerra LAB Politi Marília Pacífico Lucisano MPL Faccioli Lúcia Helena LH Paula-Silva Francisco Wanderley Garcia FWG

Data in brief 20220110

Apical periodontitis is an immune inflammatory response around periapical tissues as a result of pathogens invasion into the root canal. The host immunoinflammatory response could determine the progression of this disease, which involves the recruitment of immune cells, and the release of several cytokines in the lesion site. The 5-lipoxygenase pathway has been activated in some osteolytic diseases due to its capacity to interfere in the proliferation and differentiation of bone cells, including ...[more]

PMID: 35071699

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Project description:AimsApical Periodontitis (AP) involves complex interactions between the root canal microbiome and the host immune response, with potential risk of local and systemic inflammatory burden, however there is no evidence available regarding correlation between microbiome and inflammatory marker levels. This study aims to identify the microbiome of saliva, intracanal and blood samples in AP subjects and investigate the correlation between intracanal and blood microbiomes with serum inflammatory biomarker levels, and salivary microbiomes with salivary inflammatory biomarker levels.MethodologySaliva, Intracanal and blood samples were collected from AP patients undergoing root canal retreatment. Following DNA extraction, 16SrRNA gene-sequence analysis (V1-V2) was performed using Illumina MiSeq 300 platform. Serum and salivary inflammatory marker levels were measured using the magnetic multiplex-microbead assay. The alpha and beta diversities were tested using the phyloseq package in R (version 4.1). The abundance of the identified phyla and genera were analysed using non-parametric tests. Spearman´s correlation coefficient was used for correlation between microbial abundance and biomarker levels.ResultsStreptococcus and Prevotella were prevalent in saliva; Enterococcus, Streptococcus and Bacteroidaceae_(G-1) in intracanal; and Cutibacterium and Staphylococcus in blood samples. Streptococcus, Prevotella, Actinomyces and Rothia were the most abundant common genera among all three sample sources. In saliva, Haemophilus, Gemella, Prevotella, and Alloprevotella were positively correlated with salivary levels of IL-8, MMP-2, TNF-α, and IL-6, respectively. Intracanal genera, Enterobacter, and Parvinomonas, were positively correlated serum FGF-23. Finally, the abundance of Novosphingobium, Streptococcus, Bosea, and Corynebacterium genus in blood were positively correlated with FGF-23, MMP-9, CRP, IL-8, and ICAM-1.ConclusionMicrobiome in saliva, blood and intracanal samples were correlated with some of the inflammatory biomarker levels of saliva and serum, suggesting that the effect of AP goes beyond a periapical infection and may pose a potential systemic inflammatory burden risk if left untreated.

Project description:Periodontitis is a microbial-induced chronic inflammatory disease, which may not only result in tooth loss, but can also contribute to the development of various systemic diseases. The transition from healthy to diseased periodontium depends on microbial dysbiosis and impaired host immune response. Although periodontitis is a common disease as well as associated with various systemic inflammatory conditions, the taxonomic profiling of the salivary microbiota in periodontitis and its association with host immune and inflammatory mediators has not been reported. Therefore, the aim of this study was to identify key pathogens and their potential interaction with the host's inflammatory mediators in saliva samples for periodontitis risk assessment. The microbial 16S rRNA gene sequencing and the levels of inflammatory mediators were performed in saliva samples from patients with chronic periodontitis and periodontally healthy control subjects. The salivary microbial community composition differed significantly between patients with chronic periodontitis and healthy controls. Our analyses identified a number of microbes, including bacteria assigned to Eubacterium saphenum, Tannerella forsythia, Filifactor alocis, Streptococcus mitis/parasanguinis, Parvimonas micra, Prevotella sp., Phocaeicola sp., and Fretibacterium sp. as more abundant in periodontitis, compared to healthy controls. In samples from healthy individuals, we identified Campylobacter concisus, and Veillonella sp. as more abundant. Integrative analysis of the microbiota and inflammatory mediators/cytokines revealed associations that included positive correlations between the pathogens Treponema sp. and Selenomas sp. and the cytokines chitinase 3-like 1, sIL-6Rα, sTNF-R1, and gp130/sIL-6Rβ. In addition, a negative correlation was identified between IL-10 and Filifactor alocis. Our results reveal distinct and disease-specific patterns of salivary microbial composition between patients with periodontitis and healthy controls, as well as significant correlations between microbiota and host-mediated inflammatory cytokines. The positive correlations between the pathogens Treponema sp. and Selenomas sp. and the cytokines chitinase 3-like 1, sIL-6Rα, sTNF-R1, and gp130/sIL-6Rβ might have the future potential to serve as a combined bacteria-host salivary biomarker panel for diagnosis of the chronic infectious disease periodontitis. However, further studies are required to determine the capacity of these microbes and inflammatory mediators as a salivary biomarker panel for periodontitis.

Dataset Information

Gene expression data of inflammatory mediators in apical periodontitis in 129 (wild type) and 5-lipoxygenase knockout mice.

Publications

Gene expression data of inflammatory mediators in apical periodontitis in 129 (wild type) and 5-lipoxygenase knockout mice.

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