Imbalance of Th17/Tregs in rats with smoke inhalation-induced acute lung injury

Zhang, Fan; Li, Mian-Yang; Lan, Ya-ting; Wang, Chengbin

doi:10.1038/srep21348

Cited by 43 publications

(36 citation statements)

References 57 publications

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“…However, the molecular mechanisms involved in the pathogenesis of smoke-inhalation-induced acute lung injury are poorly defined [3,4]. In the pathological process of SI-ALI, it is generally believed that inflammatory cells and release of inflammatory mediators, especially neutrophils and macrophages, are mandatory [3][4][5]. The accumulation of neutrophils in the lung microvasculature, interstitium and alveolar space is a key feature of SI-ALI/ARDS [3,5].…”

Section: Introductionmentioning

confidence: 99%

“…In the pathological process of SI-ALI, it is generally believed that inflammatory cells and release of inflammatory mediators, especially neutrophils and macrophages, are mandatory [3][4][5]. The accumulation of neutrophils in the lung microvasculature, interstitium and alveolar space is a key feature of SI-ALI/ARDS [3,5]. Neutrophils are the first leukocytes to be recruited to sites of inflammation in response to chemotactic factors released by activated macrophages and pulmonary epithelial and endothelial cells.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-155 Participates in Smoke-Inhalation-Induced Acute Lung Injury through Inhibition of SOCS-1

et al. 2020

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Smoke inhalation causes acute lung injury (ALI), a severe clinical disease with high mortality. Accumulating evidence indicates that microRNA-155 (miR-155) and suppressor of cytokine signaling 1 (SOCS-1), as mediators of inflammatory response, are involved in the pathogenesis of ALI. In this paper, we explored the proinflammatory mechanism of miR-155 in smoke-inhalation-induced ALI. Our data revealed that smoke inhalation induces miR-155 expression, and miR-155 knockout (KO) significantly ameliorates smoke-inhalation-induced lung injury in mice. Neutrophil infiltration and myeloperoxidase (MPO), macrophage inflammatory protein 2 (MIP-2) and keratinocyte chemoattractant (KC) expressions were decreased in miR-155–/– mice after smoke inhalation as well. Real-time RT-PCR and immunoblotting results showed that SOCS-1 level was remarkably increased in miR-155–/– mice after smoke exposure. Furthermore, the experiments performed in isolated miR-155 KO pulmonary neutrophils demonstrated that the lack of SOCS-1 enhanced inflammatory cytokines (MIP-2 and KC) secretion in response to smoke stimulation. In conclusion, smoke induces increased expression of miR-155, and miR-155 is involved in inflammatory response to smoke-inhalation-induced lung injury by inhibiting the expression of SOCS-1.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA-155 Participates in Smoke-Inhalation-Induced Acute Lung Injury through Inhibition of SOCS-1

et al. 2020

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“…In keeping, it was documented, that the exposition of mice to ultrafine particles (less than 0.1 µm) elevates the frequency of Th1 cells in circulation and reduces the level of Treg cells in the lungs [33]. Moreover, Zhang et al described the increased ratio of Th17/Treg after the exposition of rats to smoke, suggesting its potential role in pathogenesis of smoke inhalation-induced acute lung injury [34], while the results from similar study in mice link Th17/Treg cells imbalance with pathogenesis of cigarette induced emphysema [35].…”

Section: Discussionmentioning

confidence: 96%

Transition Metal Containing Particulate Matter Promotes Th1 and Th17 Inflammatory Response by Monocyte Activation in Organic and Inorganic Compounds Dependent Manner

Gałuszka

Stec

Węglarczyk

et al. 2020

IJERPH

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In recent years, a significant increase in the frequency of disorders caused by air pollutants has been observed. Here we asked whether transition metal-containing particulate matter (TMCPM), a component of air pollution, has an effect on the activity of human CD4+ T cell subsets (Th1, Th2, Th17, and Treg). Peripheral blood mononuclear cells (PBMC) from healthy donors were cultured with or without NIST (SRM 1648a—standard urban particulate matter purchased from the National Institute for Standards and Technology) and LAP (SRM 1648a particulate matter treated within 120 min with cold oxygen plasma) preparations of TMCPM, differing in organic compounds content. Data show that TMCPM treatment increased the level of CD4+ cells positive for IFN-γ and IL-17A, specific for Th1 and Th17 cells, respectively. Moreover, a substantial decrease in frequency of Foxp3 positive CD4+ cells was observed in parallel. This effect was more pronounced for NIST particles, containing more organic components, including endotoxin (LPS - lipopolysaccharide) and required the presence of monocytes. Inactivation of LPS by treatment of TMCPM with polymyxin B reduced the inflammatory response of monocytes and Th subsets but did not abolish this activity, suggesting a role of their inorganic components. In conclusion, treatment of human PBMC with TMCPM skews the balance of Th1/Th2 and Treg/Th17 cells, promoting polarization of CD4+ T cells into Th1 and Th17 subsets. This phenomenon requires activation of monocytes and depends on the organic and inorganic fractions, including endotoxin content in TMCPM, as significantly higher inflammatory response was observed for the NIST comparing to LAP. This observation may shed a new light on the role of TMCPM in development and exacerbation of allergies, inflammatory, and autoimmune disorders.

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“…Another publication demonstrated that gut-derived T h 17 cells increase immune injury after NTN induction (15). The imbalance of T h 17 and T reg cells was also shown to correlate with the activities of diseases, such as acute lung injury (32), lupus erythematosus (33), and chronic pulmonary disease (34). T h 17 cells lacking multidrug resistance protein (MDR)-1 (35) or G-protein coupled receptor (Gpr)-65 and Toso (36) have been shown not to be pathogenic in inflammatory diseases.…”

Section: Discussionmentioning

confidence: 99%

T‐lymphocyte–specific knockout of IKK‐2 or NEMO induces T _h 17 cells in an experimental nephrotoxic nephritis mouse model

et al. 2018

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Experimental nephrotoxic serum nephritis (NTN) is a model for T‐cell–mediated human rapid progressive glomerulonephritis. T‐cell receptor stimulation involves intracellular signaling events that ultimately lead to the activation of transcription factors, such as NF‐κB. We explored the involvement of the NF‐κB components IKK‐2 and NEMO in NTN, by using cell‐specific knockouts of IKK‐2 and NEMO in CD4+ T lymphocytes. Our results demonstrate that although the course of disease was not grossly altered in CD4xIKK2Δ and CD4xNEMOΔ animals, renal regulatory T cells were significantly reduced and T helper (Th)1 and Th17 cells significantly increased in both knockout mouse groups. The expression of the renal cytokines and chemokines IL‐1β, CCL‐2, and CCL‐20 was also significantly altered in both knockout mice. Lymphocyte transcriptome analysis confirmed the increased expression of Th17‐related cytokines in spleen CD4+ T cells. Moreover, our array data demonstrate an interrupted canonical NF‐κB pathway and an increased expression of noncanonical NF‐κB pathway–related genes in nephritic CD4xNEMOΔ mice, highlighting different downstream effects of deletion of IKK‐2 or NEMO in T lymphocytes. We propose that better understanding of the role of IKK‐2 and NEMO in nephritis is essential for the clinical application of kinase inhibitors in patients with glomerulonephritis.—Guo, L., Huang, J., Chen, M., Piotrowski, E., Song, N., Zahner, G., Paust, H.‐J., Alawi, M., Geffers, R., Thaiss, F. T‐lymphocyte–specific knockout of IKK‐2 or NEMO induces Th17 cells in an experimental nephrotoxic nephritis mouse model. FASEB J. 33, 2359–2371 (2019). http://www.fasebj.org

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Imbalance of Th17/Tregs in rats with smoke inhalation-induced acute lung injury

Cited by 43 publications

References 57 publications

MicroRNA-155 Participates in Smoke-Inhalation-Induced Acute Lung Injury through Inhibition of SOCS-1

MicroRNA-155 Participates in Smoke-Inhalation-Induced Acute Lung Injury through Inhibition of SOCS-1

Transition Metal Containing Particulate Matter Promotes Th1 and Th17 Inflammatory Response by Monocyte Activation in Organic and Inorganic Compounds Dependent Manner

T‐lymphocyte–specific knockout of IKK‐2 or NEMO induces T _h 17 cells in an experimental nephrotoxic nephritis mouse model

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Imbalance of Th17/Tregs in rats with smoke inhalation-induced acute lung injury

Cited by 43 publications

References 57 publications

MicroRNA-155 Participates in Smoke-Inhalation-Induced Acute Lung Injury through Inhibition of SOCS-1

MicroRNA-155 Participates in Smoke-Inhalation-Induced Acute Lung Injury through Inhibition of SOCS-1

Transition Metal Containing Particulate Matter Promotes Th1 and Th17 Inflammatory Response by Monocyte Activation in Organic and Inorganic Compounds Dependent Manner

T‐lymphocyte–specific knockout of IKK‐2 or NEMO induces T h 17 cells in an experimental nephrotoxic nephritis mouse model

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T‐lymphocyte–specific knockout of IKK‐2 or NEMO induces T _h 17 cells in an experimental nephrotoxic nephritis mouse model