High mobility group box-1 protects against Aflatoxin G1-induced pulmonary epithelial cell damage in the lung inflammatory environment

Kang, Lifei; Guo, Ningfei; Liu, Xiaoyi; Wang, Xiuqing; Guo, Wenli; Xie, Shelly M.; Liu, Chunping; Lv, Ping; Xing, Lingxiao; Zhang, Xianghong; Shen, Haitao

doi:10.1016/j.toxlet.2020.05.013

Cited by 9 publications

(7 citation statements)

References 48 publications

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“…HMGB1 is a nonhistone nuclear protein abundant in lung, liver, kidney and other organs 22 . It acts as a potential target for acute lung injury and inflammation 22,23 . Notably, HMGB1 inhibition exerts effects to repress bacteria dissemination and cytokine storm, consequently alleviating carbapenem‐resistant Kp‐induced pneumonia 24 .…”

Section: Introductionmentioning

confidence: 99%

“…22 It acts as a potential target for acute lung injury and inflammation. 22,23 Notably, HMGB1 inhibition exerts effects to repress bacteria dissemination and cytokine storm, consequently alleviating carbapenem-resistant Kp-induced pneumonia. 24 More importantly, HMGB1 itself increases the level of IL−6 and TNF-α, thus switching the differentiation of M2-like macrophages to the M1 phenotype.…”

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confidence: 99%

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Mechanism of chlorogenic acid in alveolar macrophage polarization in Klebsiella pneumoniae-induced pneumonia

Tan

Yang

et al. 2021

Journal of Leukocyte Biology

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Chlorogenic acid (CA) has been discovered to regulate macrophage polarization in pneumonia. This study aims to analyze the functional mechanism of CA in alveolar macrophage (AM) polarization and provide a theoretical basis for treatment of Klebsiella pneumoniae (Kp)-induced pneumonia. Mice were infected with Kp, and treated with CA and silent information regulator 1 (SIRT1) inhibitor (Selisistat). Mouse survival rate was recorded and bacterial burden was detected. AM polarization and pathologic change of lung tissues were evaluated. Expressions of SIRT1 and HMGB1 and cytokine levels were detected. MH-S cells were infected with Kp to establish the pneumonia cell model, followed by transfection of si-SIRT1 and HMGB1 overexpression vector. The HMGB1 expression in the nucleus and cytoplasm was detected. HMGB1 subcellular localization and HMGB1 acetylation level were detected. Kp led to high death rates, SIRT down-regulation and increases in inflammatory factor level and bacterial burden, and promoted M1 polarization. CA treatment improved mouse survival rate and promoted M2 polarization and SIRT1 expression. SIRT1 decreased HMGB1 acetylation level to inhibit nuclear to the cytoplasm translocation. Silencing SIRT1 or HMGB1 overexpression reversed the effect of CA on Kp-induced pneumonia. Overall, CA activated SIRT1 to inhibit HMGB1 acetylation level and nuclear translocation, thereby promoting M2 polarization in AMs and alleviating Kp-induced pneumonia.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%

Mechanism of chlorogenic acid in alveolar macrophage polarization in Klebsiella pneumoniae-induced pneumonia

Tan

Yang

et al. 2021

Journal of Leukocyte Biology

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“…The lungs and liver are targets of aflatoxin B 1 , following dietary or inhalational exposure [53,54]. Oral administration of aflatoxin G 1 , another member of the carcinogenic aflatoxin family, caused tumor necrosis factor (TNF)α-dependent inflammation that enhanced oxidative DNA damage in alveolar epithelial cells, which in turn may be related to aflatoxin G 1 -induced lung carcinogenesis [55].…”

Section: Carcinogens Used In Rodent Lung Tumor Modelsmentioning

confidence: 99%

Relationship between Lung Carcinogenesis and Chronic Inflammation in Rodents

Nakano‐Narusawa

Yokohira

Yamakawa

et al. 2021

Cancers

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Lung cancer remains the leading cause of cancer-related deaths, with an estimated 1.76 million deaths reported in 2018. Numerous studies have focused on the prevention and treatment of lung cancer using rodent models. Various chemicals, including tobacco-derived agents induce lung cancer and pre-cancerous lesions in rodents. In recent years, transgenic engineered rodents, in particular, those generated with a focus on the well-known gene mutations in human lung cancer (KRAS, EGFR, and p53 mutations) have been widely studied. Animal studies have revealed that chronic inflammation significantly enhances lung carcinogenesis, and inhibition of inflammation suppresses cancer progression. Moreover, the reduction in tumor size by suppression of inflammation in animal experiments suggests that chronic inflammation influences the promotion of tumorigenesis. Here, we review rodent lung tumor models induced by various chemical carcinogens, including tobacco-related carcinogens, and transgenics, and discuss the roles of chronic inflammation in lung carcinogenesis.

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“…HMGB1 is passively released from necrotic cells and can also be actively secreted by immune cells (Figure 1C) such as macrophages [44], microglia [45], neutrophils [46], and natural killer cells [47], and also by non-immune cells, such as fibroblasts [48], epithelial cells [49,50], neurons [33], platelets [51], hepatocytes [52], and cardiomyocytes [53]. The active secretion of HMGB1 is triggered by microbial pathogens such as lipopolysaccharide (LPS) and polyinosinic-polycytidylic acid (poly(I:C)) [44,52,54], or endogenous substances, such as ROS [55], reactive nitrogen species (RNS) [56], hyperglycemia [53], inflammatory cytokines (e.g., TNF-α [49], interferon (IFN)-α [54], INF-γ [57], ATP [19,58], nitric oxide [54], calcium phosphate-based mineralo-organic particles [46], and also by cell-to-cell interaction [47].…”

Section: Release Of Hmgb1mentioning

confidence: 99%

Role of HMGB1 in Chemotherapy-Induced Peripheral Neuropathy

Sekiguchi

Kawabata

2020

IJMS

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Chemotherapy-induced peripheral neuropathy (CIPN), one of major dose-limiting side effects of first-line chemotherapeutic agents such as paclitaxel, oxaliplatin, vincristine, and bortezomib is resistant to most of existing medicines. The molecular mechanisms of CIPN have not been fully understood. High mobility group box 1 (HMGB1), a nuclear protein, is a damage-associated molecular pattern protein now considered to function as a pro-nociceptive mediator once released to the extracellular space. Most interestingly, HMGB1 plays a key role in the development of CIPN. Soluble thrombomodulin (TMα), known to degrade HMGB1 in a thrombin-dependent manner, prevents CIPN in rodents treated with paclitaxel, oxaliplatin, or vincristine and in patients with colorectal cancer undergoing oxaliplatin-based chemotherapy. In this review, we describe the role of HMGB1 and its upstream/downstream mechanisms in the development of CIPN and show drug candidates that inhibit the HMGB1 pathway, possibly useful for prevention of CIPN.

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High mobility group box-1 protects against Aflatoxin G1-induced pulmonary epithelial cell damage in the lung inflammatory environment

Cited by 9 publications

References 48 publications

Mechanism of chlorogenic acid in alveolar macrophage polarization in Klebsiella pneumoniae-induced pneumonia

Mechanism of chlorogenic acid in alveolar macrophage polarization in Klebsiella pneumoniae-induced pneumonia

Relationship between Lung Carcinogenesis and Chronic Inflammation in Rodents

Role of HMGB1 in Chemotherapy-Induced Peripheral Neuropathy

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