Cigarette smoke extract promotes DNA methyltransferase <scp>3a</scp> expression in dendritic cells, inducing Th‐17/Treg imbalance via the <scp>c‐Jun</scp>/allograft inflammatory factor 1 axis

Huang, Dan; Zhou, Bin; Luo, Zhiqiang; Yu, Shuchun; Tang, Bin

doi:10.1002/kjm2.12367

Cited by 6 publications

(6 citation statements)

References 36 publications

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“…The inhibitions of DNMTs and Notch pathway suppressed inflammatory response and cellular apoptosis in a cell model of COPD ( Qiu et al, 2018 ). Cigarette smoke extract treatment also promoted the expression of DNMT3A in dendritic cells of COPD mouse models, and DNMT3A regulated Th17/Treg cell balance via c-Jun/AIF1 axis ( Huang et al, 2021 ). Our study further illustrated that DNMT1 was significantly increased in the lung tissue of COPD rats, which may generate novel mechanistic insight into therapeutic targets for the treatment of COPD.…”

Section: Discussionmentioning

confidence: 99%

Shema Oral Liquid Ameliorates the Severity of LPS-Induced COPD via Regulating DNMT1

et al. 2022

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Background: Chronic obstructive pulmonary disease (COPD) is the most common respiratory disease with high morbidity and mortality. Shema oral liquid (Shema) is a traditional Chinese medicine (TCM) approved for the treatment of respiratory diseases. Clinical applications have shown that Shema has antitussive, expectorant, and anti-asthmatic effects, but its definite efficacy to COPD is still unclear. This study aimed to explore the therapeutic capacity and potential mechanism of Shema in treatment of COPD.Methods: Network pharmacology was used to investigated the possible pharmacological mechanism of Shema against COPD. A rat model of lipopolysaccharide (LPS)-induced COPD was established to determine pulmonary ventilatory function, serum inflammatory cytokines, and pulmonary pathological change. Subsequently, tandem mass tag (TMT)-based quantitative proteomics was used to further reveal the therapeutic targets related with Shema against COPD. Western blot was finally performed to validate the expression of targeted proteins screened by proteomics research.Results: Network pharmacology analysis indicated that Shema against COPD mainly inhibited the inflammation and affected the immune system. The animal experiment demonstrated that Shema treatment protected the lung tissue from LPS induced injury, inhibited the levels of serum inflammatory cytokines such as interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α, and improved the respiratory ventilatory function by upregulating forced expiratory volume in 0.1 s (FEV0.1), FEV0.3, forced vital capacity (FVC), and the ratios of FEV0.1 (0.3)/FVC. Proteomic analysis and western blot both proved that Shema inhibited the expression of DNA methyltransferase 1 (DNMT1) in the lung tissue.Conclusion: The therapeutic mechanism of Shema in treatment of COPD may involve inhibiting inflammatory response, improving pulmonary ventilatory function, and alleviating LPS-induced lung injury through regulating the expression of DNMT1. This study also shed light on the development of therapeutic strategies in treating COPD by intervening DNMT-related pathways.

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Section: Discussionmentioning

confidence: 99%

Shema Oral Liquid Ameliorates the Severity of LPS-Induced COPD via Regulating DNMT1

et al. 2022

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“…Liver and colon proteins were extracted using a radioimmunoprecipitation assay kit (Thermo Fisher Scientific, Waltham, MA, USA). Western blot was performed as previously described (Huang et al, 2021). Membrane protein bands were visualized using an electrochemiluminescence detection system (Tianneng, Shanghai, China) and grey‐scale quantification of the protein bands was performed using ImageJ.…”

Section: Methodsmentioning

confidence: 99%

Section: Protein Extraction and Western Blotmentioning

confidence: 99%

Porphyromonas gingivalis exacerbates alcoholic liver disease by altering gut microbiota composition and host immune response in mice

Gao

Zhang

Wei

et al. 2023

J Clinic Periodontology

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AimPorphyromonas gingivalis (P. gingivalis), a major periodontal pathogen, increases the risk of systemic diseases. P. gingivalis infection is closely associated with alcoholic liver disease (ALD), but the underlying mechanism remains unclear. We aimed to investigate the role of P. gingivalis in the pathogenesis of ALD.Materials and MethodsAn ALD mouse model was established using a Lieber‐DeCarli liquid diet, and C57BL/6 mice were treated with P. gingivalis to detect the pathological indicators of ALD.ResultsOral administration of P. gingivalis exacerbated alcohol‐induced alterations in the gut microbiota, leading to gut barrier dysfunction and inflammatory response and disruption of the T‐helper 17 cell/T‐regulatory cell ratio in the colon of ALD mice. Furthermore, P. gingivalis worsened liver inflammation in ALD mice by increasing the protein expression of toll‐like receptor 4 (TLR4) and p65, increasing the mRNA expression of interleukins‐6 (IL‐6) and tumour necrosis factor‐alpha (TNF‐α) and up‐regulating the transforming growth factor‐beta 1 (TGF‐β1) and galectin‐3 (Gal‐3) production.ConclusionsThese results indicate that P. gingivalis accelerates the pathogenesis of ALD via the oral–gut–liver axis, necessitating a new treatment strategy for patients with ALD complicated by periodontitis.

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“…Additionally, AIF1 inhibition can inhibit antigen-specific CD8+ T-cell activation, limiting CXCR3, IFN-γ and granzyme B expression and proliferation and, in turn, expanding IL-10-producing CD8+ CD122+ PD-1+ regulatory T cells [69]. Moreover, DNA methyltransferase 3a expression in DCs is involved in the regulation of T H17 /T reg cells polarization through the c-Jun/AIF1 axis, because c-Jun can bind to the promoter of AIF1 [70]. Finally, AIF1 modulates interferon regulatory factor 8 (IRF8) and transcription factor RelB (by interaction with protein kinase C (PKC) to promote NF-κB and MAPK signaling and drive hematopoietic stem cell differentiation into classical DC type 1 (cDC1) subsets and monocyte-derived DC (Mo-DC) under Fms-related tyrosine kinase 3-ligand (Flt3-L) and granulocyte macrophage-colony stimulatory factor (GM-CSF) stimuli, respectively [71].…”

Section: Functions In Immunity: Macrophages T Lymphocytes and Dendrit...mentioning

confidence: 99%

AIF1: Function and Connection with Inflammatory Diseases

De Leon-Oliva,

Garcia-Montero,

Fraile-Martinez

et al. 2023

Biology

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Macrophages are a type of immune cell distributed throughout all tissues of an organism. Allograft inflammatory factor 1 (AIF1) is a calcium-binding protein linked to the activation of macrophages. AIF1 is a key intracellular signaling molecule that participates in phagocytosis, membrane ruffling and F-actin polymerization. Moreover, it has several cell type-specific functions. AIF1 plays important roles in the development of several diseases: kidney disease, rheumatoid arthritis, cancer, cardiovascular diseases, metabolic diseases and neurological disorders, and in transplants. In this review, we present a comprehensive review of the known structure, functions and role of AIF1 in inflammatory diseases.

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Cigarette smoke extract promotes DNA methyltransferase 3a expression in dendritic cells, inducing Th‐17/Treg imbalance via the c‐Jun/allograft inflammatory factor 1 axis

Cited by 6 publications

References 36 publications

Shema Oral Liquid Ameliorates the Severity of LPS-Induced COPD via Regulating DNMT1

Shema Oral Liquid Ameliorates the Severity of LPS-Induced COPD via Regulating DNMT1

Porphyromonas gingivalis exacerbates alcoholic liver disease by altering gut microbiota composition and host immune response in mice

AIF1: Function and Connection with Inflammatory Diseases

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