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H₂S mediates increased interleukin (IL)-1? and IL-18 production in leukocytes from patients with periodontitis.

ABSTRACT: Background: The mechanisms involved in the interplay between the bacteria and the host cells in periodontitis are not fully understood. Aim: To investigate the effect of the bacterial metabolite H₂S on the pro-inflammatory cytokines interleukin (IL)-1? and IL-18 from periodontitis patients and healthy controls, and to evaluate the composition of the subgingival microbiota with its capacity to produce H₂S. Methods: Subgingival bacterial samples from patients with periodontitis (N=32) and healthy controls (N=32) were investigated for H₂S production and bacterial composition. Peripheral blood mononuclear cells (PBMCs) were cultured in the presence/absence of 1mM H₂S for 24h and cytokine concentrations were measured. Results: Subgingival plaque from periodontitis patients had more H₂S producing bacteria and produced more H₂S, than healthy controls. PBMCs exposed to H₂S secreted significantly more IL-1ß and IL-18 (p<0.0001) than untreated control PBMCs from both groups. PBMCs from the periodontitis patients secreted higher levels of the cytokines, both spontaneously (IL-1ß p=0.0001; IL-18 p=0.09) and after exposure to H₂S (IL-1ß p=0.03; IL-18 p=0.04), which is a new finding not previously reported. Conclusions: H₂S, from the subgingival microbiota, can contribute to a host inflammatory response through secretion of the pro-inflammatory cytokines IL-1? and IL-18. Since this response differs between individuals, it may also reflect the susceptibility of the host to develop periodontitis.

SUBMITTER: Basic A

PROVIDER: S-EPMC6534246 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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H2S mediates increased interleukin (IL)-1β and IL-18 production in leukocytes from patients with periodontitis.

Basic Amina A Serino Giovanni G Leonhardt Åsa Å Dahlén Gunnar G

Journal of oral microbiology 20190520 1

Background: The mechanisms involved in the interplay between the bacteria and the host cells in periodontitis are not fully understood. Aim: To investigate the effect of the bacterial metabolite H2S on the pro-inflammatory cytokines interleukin (IL)-1β and IL-18 from periodontitis patients and healthy controls, and to evaluate the composition of the subgingival microbiota with its capacity to produce H2S. Methods: Subgingival bacterial samples from pati ...[more]

PMID: 31164964

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Project description:BackgroundThe presence of a polymicrobial dysbiotic film in direct and constant contact with periodontal tissues initiates the host immune response. Interleukin 18 (IL-18) triggers up-regulates the production of other proinflammatory cytokines (TNF-α, IL-1β, IL-6), creating a vicious cycle that expands the inflammatory and destructive process in the periodontal tissue. A systematic review and meta-analysis was carried out with the main propose to investigate IL-18 expression in different biological samples from subjects with chronic periodontitis.MethodsThe protocol followed PRISMA guidelines and was registered in Open Science Framework (OSF): https://doi.org/10.17605/OSF.IO/BS9GM . A digital search was conducted in the databases PubMed, ScienceDirect, Google Scholar, Web of Science and Dentistry & Oral Sciences Source databases were consulted from March 15th, 2005 to February 10th, 2023. Study quality was assessed using the JBI tool for cross-sectional studies and clinical trials. A meta-analysis was performed using a random/fixed effects model to evaluate the concentration of IL-18 in serum, plasma, saliva, gingival tissue and GCF of exposure group compared to control group.ResultsThe search strategy provided a total of 3,156 articles, of which 18 investigations met the inclusion criteria and 15 articles were quantitatively analyzed. The total number of patients studied was 1,275 (682 cases and 593 controls). The meta-analysis revealed significantly elevated IL-18 levels of serum, saliva and GCF of subjects with chronic periodontitis compared to healthy subjects (Serum: SMD = 62.73, 95%CI: 25.43-100.03, Z = 3.29, p = 0.001*; Saliva: SMD = 243.63, 95%CI: 8.68-478.59, Z = 2.03, p = 0.042*; GCF: SMD = 150.26, 95%CI: 56.86-243.66, Z = 3.15, p = 0.02*).ConclusionIL-18 levels in serum, saliva and GCF could have the potential to be used as complementary diagnostic tools to the clinical and radiographic parameters in subjects with periodontitis.

Project description:Interleukin-1β (IL-1β), a major pro-inflammatory cytokine, is a leaderless cytosolic protein whose secretion does not follow the classical endoplasmic reticulum-to-Golgi pathway, and for which a canonical mechanism of secretion remains to be established. Neutrophils are essential players against bacterial and fungi infections. These cells are rapidly and massively recruited from the circulation into infected tissues and, beyond of displaying an impressive arsenal of toxic weapons effective to kill pathogens, are also an important source of IL-1β in infectious conditions. Here, we analyzed if an unconventional secretory autophagy mechanism is involved in the exportation of IL-1β by these cells. Our findings indicated that inhibition of autophagy with 3-methyladenine and Wortmannin markedly reduced IL-1β secretion induced by LPS + ATP, as did the disruption of the autophagic flux with Bafilomycin A1 and E64d. These compounds did not noticeable affect neutrophil viability ruling out that the effects on IL-1β secretion were due to cell death. Furthermore, VPS34IN-1, a specific autophagy inhibitor, was still able to reduce IL-1β secretion when added after it was synthesized. Moreover, siRNA-mediated knockdown of ATG5 markedly reduced IL-1β secretion in neutrophil-differentiated PLB985 cells. Upon LPS + ATP stimulation, IL-1β was incorporated to an autophagic compartment, as was revealed by its colocalization with LC3B by confocal microscopy. Overlapping of IL-1β-LC3B in a vesicular compartment peaked before IL-1β increased in culture supernatants. On the other hand, stimulation of autophagy by cell starvation augmented the colocalization of IL-1β and LC3B and then promoted neutrophil IL-1β secretion. In addition, specific ELISAs indicated that although both IL-1β and pro-IL-1β are released to culture supernatants upon neutrophil stimulation, autophagy only promotes IL-1β secretion. Furthermore, the serine proteases inhibitor AEBSF reduced IL-1β secretion. Moreover, IL-1β could be also found colocalizing with elastase, suggesting both some vesicles containing IL-1β intersect azurophil granules content and that serine proteases also regulate IL-1β secretion. Altogether, our findings indicate that an unconventional autophagy-mediated secretory pathway mediates IL-1β secretion in human neutrophils.

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H₂S mediates increased interleukin (IL)-1? and IL-18 production in leukocytes from patients with periodontitis.

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H<sub>2</sub>S mediates increased interleukin (IL)-1β and IL-18 production in leukocytes from patients with periodontitis.

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Dataset Information

H2S mediates increased interleukin (IL)-1? and IL-18 production in leukocytes from patients with periodontitis.

Publications

H<sub>2</sub>S mediates increased interleukin (IL)-1β and IL-18 production in leukocytes from patients with periodontitis.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

H₂S mediates increased interleukin (IL)-1? and IL-18 production in leukocytes from patients with periodontitis.