Oral administration of aflatoxin G1 induces chronic alveolar inflammation associated with lung tumorigenesis

Liu, Chunping; Shen, Haitao; Li, Yi; Shao, Peilu; Soulika, Athena M.; Meng, Xinxing; Xing, Lingxiao; Xia, Yan; Zhang, Xianghong

doi:10.1016/j.toxlet.2014.11.002

Cited by 34 publications

(45 citation statements)

References 41 publications

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“…Findings that it remained elevated for at least 21 d are in accord with the persistent inflammatory response observed in exposed humans (Yoon et al, 2013; Liu et al, 2015). The fact that COX-2 was mainly expressed by Type II cells provides support for the notion that these cells participate in inflammatory responses to tissue injury (Cheng et al, 2016).…”

Section: Discussionsupporting

confidence: 79%

World Trade Center (WTC) dust exposure in mice is associated with inflammation, oxidative stress and epigenetic changes in the lung

Sunil

Vayas

Fang

et al. 2017

Experimental and Molecular Pathology

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Exposure to World Trade Center (WTC) dust has been linked to respiratory disease in humans. In the present studies we developed a rodent model of WTC dust exposure to analyze lung oxidative stress and inflammation, with the goal of elucidating potential epigenetic mechanisms underlying these responses. Exposure of mice to WTC dust (20 μg, i.t.) was associated with upregulation of heme oxygenase-1 and cyclooxygenase-2 within 3 days, a response which persisted for at least 21 days. Whereas matrix metalloproteinase was upregulated 7 days post-WTC dust exposure, IL-6RA1 was increased at 21 days; conversely, expression of mannose receptor, a scavenger receptor important in particle clearance, decreased. After WTC dust exposure, increases in methylation of histone H3 lysine K4 at 3 days, lysine K27 at 7 days and lysine K36, were observed in the lung, along with hypermethylation of Line-1 element at 21 days. Alterations in pulmonary mechanics were also observed following WTC dust exposure. Thus, 3 days post-exposure, lung resistance and tissue damping were decreased. In contrast at 21 days, lung resistance, central airway resistance, tissue damping and tissue elastance were increased. These data demonstrate that WTC dust-induced inflammation and oxidative stress are associated with epigenetic modifications in the lung and altered pulmonary mechanics. These changes may contribute to the development of WTC dust pathologies.

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Section: Discussionsupporting

confidence: 79%

World Trade Center (WTC) dust exposure in mice is associated with inflammation, oxidative stress and epigenetic changes in the lung

Sunil

Vayas

Fang

et al. 2017

Experimental and Molecular Pathology

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“…The mice were randomly divided into different groups, and 3 or 8 mice were in one experimental group according to our previous studies. 28,29 The mice assigned to the urethane exposure group were injected intraperitoneally (i.p) with urethane (1 g/kg body weight in 200 µL PBS) once per week for 8 weeks. Mice in the TNF-α blockade group were treated with 1 g/kg body weight urethane once per week, and with a soluble TNF receptor sTNFR:Fc (i.p.…”

Section: Animal Treatmentmentioning

confidence: 99%

“…Total RNA was prepared from frozen lung tissue using TRIzol reagent (Invitrogen), according to the protocol supplied by the manufacturer. 28 cDNA was synthesized using GoScript Reverse Transcription System (Promega, USA) with random primers. Transcription levels were evaluated via real-time PCR using a GoTaq qPCR Master Mix (Promega, USA) and a Stratagene Mx3005P (Agilent Technologies, USA).…”

Section: Quantitative Real-time Pcrmentioning

confidence: 99%

Lung adenocarcinoma‐related TNF‐α‐dependent inflammation upregulates MHC‐II on alveolar type II cells through CXCR‐2 to contribute to Treg expansion

et al. 2020

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MHC‐II on alveolar type‐II (AT‐II) cells is associated with immune tolerance in an inflammatory microenvironment. Recently, we found TNF‐α upregulated MHC‐II in AT‐II in vitro. In this study, we explored whether TNF‐α‐mediated inflammation upregulates MHC‐II on AT‐II cells to trigger Treg expansion in inflammation‐driven lung adenocarcinoma (IDLA). Using urethane‐induced mice IDLA model, we found that IDLA cells mainly arise from AT‐II cells, which are the major source of MHC‐II. Blocking urethane‐induced inflammation by TNF‐α neutralization inhibited tumorigenesis and reversed MHC‐II upregulation on tumor cells of AT‐II cellular origin in IDLA. MHC‐II‐dependent AT‐II cells were isolated from IDLA‐induced Treg expansion. In human LA samples, we found high expression of MHC‐II in tumor cells of AT‐II cellular origin, which was correlated with increased Foxp3+ T cells infiltration as well as CXCR‐2 expression. CXCR‐2 and MHC‐II colocalization was observed in inflamed lung tissue and IDLA cells of AT‐II cellular origin. Furthermore, at the pro‐IDLA inflammatory stage, TNF‐α‐neutralization or CXCR‐2 deficiency inhibited the upregulation of MHC‐II on AT‐II cells in inflamed lung tissue. Thus, tumor cells of AT‐II cellular origin contribute to Treg expansion in an MHC‐II‐dependent manner in TNF‐α‐mediated IDLA. At the pro‐tumor inflammatory stage, TNF‐α‐dependent lung inflammation plays an important role in MHC‐II upregulation on AT‐II cells.

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“…Estos resultados ayudan a establecer un vínculo entre la presencia en el aire de AFB1 y carcinoma respiratorio humano. (16) Trabajos realizados por Liu et al 2015 (17) demostraron que una sola administración intratraqueal de Aflatoxina G1 (AFG1) produjo cambios inflamatorios crónicos en el tabique alveolar de ratas. Basándose en este hallazgo, posteriormente administraron AFG1en ratones BALB /c con una sonda oral observando doce meses más tarde hiperplasia epitelial alveolar y adenocarcinoma.…”

Section: Exposición a Aflatoxinas Por Ingestión Toxicidadunclassified

Affections in animals and humans due to ingestion or exposure to aflatoxins. Preventive measures to avoid toxic effects

Toso

Toribio

Diesser

et al. 2018

cienvet

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Oral administration of aflatoxin G1 induces chronic alveolar inflammation associated with lung tumorigenesis

Cited by 34 publications

References 41 publications

World Trade Center (WTC) dust exposure in mice is associated with inflammation, oxidative stress and epigenetic changes in the lung

World Trade Center (WTC) dust exposure in mice is associated with inflammation, oxidative stress and epigenetic changes in the lung

Lung adenocarcinoma‐related TNF‐α‐dependent inflammation upregulates MHC‐II on alveolar type II cells through CXCR‐2 to contribute to Treg expansion

Affections in animals and humans due to ingestion or exposure to aflatoxins. Preventive measures to avoid toxic effects

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