The role of nitric oxide in the epigenetic regulation of THP-1 induced by lipopolysaccharide

Rios, Ester Correia Sarmento; Lima, Thaís Martins de; Moretti, Ana Iochabel Soares; Soriano, Francisco

doi:10.1016/j.lfs.2016.01.041

Cited by 14 publications

(12 citation statements)

References 33 publications

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“…Moreover, TSA reduced neutrophil infiltration, ICAM-1, and E-selectin expression [80], and reduced liver-damage markers, IL-10 expression, and MPO [81]. Interestingly, TSA blocks endotoxin tolerance induction as well [82]. Other pan-HDAC inhibitors, such as valproic acid [83] or butyric acid [80,84] were similarly effective in improving septic outcomes by reducing pro-inflammatory gene expression and concomitant reduced organ damage.…”

Section: Hdac Inhibitors (Hdaci) As Anti-inflammatory Agentsmentioning

confidence: 99%

Histone Deacetylation Inhibitors as Therapy Concept in Sepsis

Knethen

Brüne

2019

IJMS

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Sepsis is characterized by dysregulated gene expression, provoking a hyper-inflammatory response occurring in parallel to a hypo-inflammatory reaction. This is often associated with multi-organ failure, leading to the patient’s death. Therefore, reprogramming of these pro- and anti-inflammatory, as well as immune-response genes which are involved in acute systemic inflammation, is a therapy approach to prevent organ failure and to improve sepsis outcomes. Considering epigenetic, i.e., reversible, modifications of chromatin, not altering the DNA sequence as one tool to adapt the expression profile, inhibition of factors mediating these changes is important. Acetylation of histones by histone acetyltransferases (HATs) and initiating an open-chromatin structure leading to its active transcription is counteracted by histone deacetylases (HDACs). Histone deacetylation triggers a compact nucleosome structure preventing active transcription. Hence, inhibiting the activity of HDACs by specific inhibitors can be used to restore the expression profile of the cells. It can be assumed that HDAC inhibitors will reduce the expression of pro-, as well as anti-inflammatory mediators, which blocks sepsis progression. However, decreased cytokine expression might also be unfavorable, because it can be associated with decreased bacterial clearance.

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Section: Hdac Inhibitors (Hdaci) As Anti-inflammatory Agentsmentioning

confidence: 99%

Histone Deacetylation Inhibitors as Therapy Concept in Sepsis

Knethen

Brüne

2019

IJMS

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“…Another study found that when the LPS concentration was 40 µg/mL, LO2 cell expression of proinflammatory factors peaked . While some studies used 500 ng/mL LPS to stimulate immune cells, even used 100 ng/mL LPS . Therefore, optimizing the concentration and action time of LPS‐stimulated cells is very helpful for subsequent studies.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis B core antigen can regulate NLRP3 inflammasome pathway in HepG2 cells

Xiao-lin

Lei

et al. 2019

Journal of Medical Virology

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Hepatitis B virus (HBV)has four open reading frames (ORFs) of which ORF C is consists of the pre Core and Core genes encodes the Hepatitis B core antigen (HBcAg) and Hepatitis B e antigen (HBeAg). Studies have shown that HBeAg significantly inhibits the NLRP3 inflammasome activation and interleukin-1β (IL-1β) production.However, the role of HBcAg and ORF C proteins (in this paper, ORF C proteins = HBcAg + HBeAg) were remain unclear. Our study aims to assess whether HBcAg and ORF C proteins can affect the NLRP3 inflammasome pathway. Vectors expressing ORF C proteins and HBcAg were designed and transfected into HepG2 cells. And then, cells were stimulated with lipopolysaccharide (LPS). Activation of the NLRP3 inflammasome and the levels of IL-1β and IL-18 were evaluated by Western blot analysis, quantitative reverse-transcription polymerase chain reaction, enzyme-linked immunosorbent assay, and immunofluorescence. The expression of NLRP3 and IL-1β peaked when HepG2 cells were stimulated with 1000 ng/mL LPS for 18 to 24 hours.HBcAg, but not ORF C proteins, promoted LPS-induced NLRP3 inflammasome activation and IL-1β production. These findings provide a novel mechanism on how the HBV causes liver inflammation and may provide insights into the search for new therapeutic strategies. K E Y W O R D Shepatitis B core antigen, interleukin-18, interleukin-1β, NLRP3, ORF C proteins

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“…Despite the fact that the clearance of periodontal pathogens through an inflammatory response relies heavily on the recognition of LPS, it has been shown that low doses of LPS can induce ET, leading to reduced production of inflammatory cytokines (Rios et al, 2016;Seeley & Ghosh, 2017). In periodontitis, biofilm can disrupt the gingival tissues, resulting in a compromised epithelial barrier, and periodontal pockets followed by colonization with gram-negative bacteria (Touyz, 2013).…”

Section: The Link Between Endotoxin Tolerance and Periodontal Diseasementioning

confidence: 99%

Understanding the role of endotoxin tolerance in chronic inflammatory conditions and periodontal disease

Larsson

Garaicoa-Pazmiño

Asa’ad

et al. 2022

J Clinic Periodontology

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Objective: This review aims to present the current understanding of endotoxin tolerance (ET) in chronic inflammatory diseases and explores the potential connection with periodontitis.Summary: Subsequent exposure to lipopolysaccharides (LPS) triggers ET, a phenomenon regulated by different mechanisms and pathways, including toll-like receptors (TLRs), nuclear factor kappa-light-chain enhancer of activated B-cells (NFκB), apoptosis of immune cells, epigenetics, and microRNAs (miRNAs). These mechanisms interconnect ET with chronic inflammatory diseases including periodontitis. While the direct correlation between ET and periodontal destruction has not been fully elucidated, emerging reports point towards the potential tolerization of human periodontal ligament cells (hPDLCs) and gingival tissues with a significant reduction of TLR levels.Conclusions: There is a potential link between ET and periodontal diseases. Future studies should explore the crucial role of ET in the pathogenesis of periodontal diseases, as evidence of a tolerized oral mucosa may represent an intrinsic mechanism capable of regulating the oral immune response. A clear understanding of this host immune regulatory mechanism might lead to effective and more predictable therapeutic strategies to treat chronic inflammatory diseases and periodontitis.

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The role of nitric oxide in the epigenetic regulation of THP-1 induced by lipopolysaccharide

Cited by 14 publications

References 33 publications

Histone Deacetylation Inhibitors as Therapy Concept in Sepsis

Histone Deacetylation Inhibitors as Therapy Concept in Sepsis

Hepatitis B core antigen can regulate NLRP3 inflammasome pathway in HepG2 cells

Understanding the role of endotoxin tolerance in chronic inflammatory conditions and periodontal disease

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