A common environmental pollutant, 4‐nonylphenol, promotes allergic lung inflammation in a murine model of asthma

Suen, Jau‐Ling; Hsu, Sung‐Chi; Hung, Chih‐Hsing; Chao, Yu Shen; Lee, C. L.; Lin, Chia-I; Weng, Tingkun; Yu, Hsin Su; Huang, Shau Ku

doi:10.1111/all.12156

Cited by 28 publications

(23 citation statements)

References 31 publications

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“…AhR expression is increased in peripheral blood mononuclear cells from patients with allergic asthma 87 . The putative AhR ligand, 4-nonylphenol, enhances allergic inflammation in the lung 88 . The inflammation is reduced in mice carrying the AhR d allele, which is defective in ligand binding.…”

Section: Discussionmentioning

confidence: 99%

A mouse model links asthma susceptibility to prenatal exposure to diesel exhaust

Manners¹,

Alam²,

Schwartz³

et al. 2014

Journal of Allergy and Clinical Immunology

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Background Most asthma begins in the first years of life. This early onset cannot be merely attributed to genetic factors, because the prevalence of asthma is increasing. Epidemiological studies have indicated roles for prenatal and early childhood exposures, including exposure to diesel exhaust. However, little is known about the mechanisms. This is largely due to paucity of animal models. Objective We aimed to develop a mouse model of asthma susceptibility through prenatal exposure to diesel exhaust. Methods Pregnant C57BL/6 female mice were given repeated intranasal applications of diesel exhaust particles (DEP) or phosphate-buffered saline (PBS). Offspring underwent suboptimal immunization and challenge with ovalbumin (OVA) or received PBS. Pups were examined for features of asthma; lung and liver tissues were analyzed for transcription of DEP-regulated genes. Results Offspring of mice exposed to DEP were hypersensitive to OVA, indicated by airway inflammation and hyperresponsiveness, increased serum levels of OVA-specific IgE, and increased levels of pulmonary and systemic T-helper (Th)2 and Th17 cytokines. These cytokines were primarily produced by natural killer (NK) cells. Antibody-mediated depletion of NK cells prevented airway inflammation. Asthma susceptibility was associated with increased transcription of genes known to be specifically regulated by the aryl hydrocarbon receptor (AhR) and oxidative stress. Features of asthma were either marginal or absent in OVA-treated pups of PBS-exposed mice. Conclusion We created a mouse model that linked maternal exposure to DEP with asthma susceptibility in offspring. Development of asthma was dependent on NK cells and associated with increased transcription from AhR- and oxidative stress-regulated genes.

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Section: Discussionmentioning

confidence: 99%

A mouse model links asthma susceptibility to prenatal exposure to diesel exhaust

Manners¹,

Alam²,

Schwartz³

et al. 2014

Journal of Allergy and Clinical Immunology

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“…Some in vitro or ex vivo studies suggest that NP skews T cells towards Th2 responses through its influence on dendritic cells (DCs). For example, splenic conventional DCs from NP-exposed mice have shown a potent Th2-skewing ability and express increased levels of IL-6 and TNF-α, but not IL-10 and IL-12, in response to LPS stimulation 15. Further, bone marrow-derived DCs in the presence of NP can influence antigen-specific T cells to secrete significantly less IFN-γ 15.…”

Section: Introductionmentioning

confidence: 99%

“…For example, splenic conventional DCs from NP-exposed mice have shown a potent Th2-skewing ability and express increased levels of IL-6 and TNF-α, but not IL-10 and IL-12, in response to LPS stimulation 15. Further, bone marrow-derived DCs in the presence of NP can influence antigen-specific T cells to secrete significantly less IFN-γ 15. Importantly, NP-exposed mice developed relatively more severe OVA-induced allergic lung inflammation 15.…”

Section: Introductionmentioning

confidence: 99%

“…Further, bone marrow-derived DCs in the presence of NP can influence antigen-specific T cells to secrete significantly less IFN-γ 15. Importantly, NP-exposed mice developed relatively more severe OVA-induced allergic lung inflammation 15. Plasmacytoid DCs (pDCs) are the predominant cells that secrete type I IFN during infection.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, splenic pDCs from NP-exposed mice showed similar cytokine changes upon CpG stimulation under conditions relevant to routing levels of exposure in humans. The exposure to NP promoted allergic lung inflammation in a murine model of asthma 15,18…”

Section: Introductionmentioning

confidence: 99%

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The Effects of Environmental Toxins on Allergic Inflammation

Yang

Hsieh

Kuo

et al. 2014

Allergy Asthma Immunol Res

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The prevalence of asthma and allergic disease has increased worldwide over the last few decades. Many common environmental factors are associated with this increase. Several theories have been proposed to account for this trend, especially those concerning the impact of environmental toxicants. The development of the immune system, particularly in the prenatal period, has far-reaching consequences for health during early childhood, and throughout adult life. One underlying mechanism for the increased levels of allergic responses, secondary to exposure, appears to be an imbalance in the T-helper function caused by exposure to the toxicants. Exposure to environmental endocrine-disrupting chemicals can result in dramatic changes in cytokine production, the activity of the immune system, the overall Th1 and Th2 balance, and in mediators of type 1 hypersensitivity mediators, such as IgE. Passive exposure to tobacco smoke is a common risk factor for wheezing and asthma in children. People living in urban areas and close to roads with a high volume of traffic, and high levels of diesel exhaust fumes, have the highest exposure to environmental compounds, and these people are strongly linked with type 1 hypersensitivity disorders and enhanced Th2 responses. These data are consistent with epidemiological research that has consistently detected increased incidences of allergies and asthma in people living in these locations. During recent decades more than 100,000 new chemicals have been used in common consumer products and are released into the everyday environment. Therefore, in this review, we discuss the environmental effects on allergies of indoor and outside exposure.

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Tumor-Promoting/Associated Inflammation and the Microenvironment: A State of the Science and New Horizons

Bisson

Amedei

Memeo³

et al. 2017

Translational Toxicology and Therapeutics: Windows of Developmental Susceptibility in Reproduction and Cancer

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A common environmental pollutant, 4‐nonylphenol, promotes allergic lung inflammation in a murine model of asthma

Abstract: These results suggested that NP may disturb physiologic function of DCs through, in part, AhR-dependent mechanisms, supporting the importance of NP exposure on the regulation of DC functions and allergic inflammation.

Cited by 28 publications

References 31 publications

A mouse model links asthma susceptibility to prenatal exposure to diesel exhaust

A mouse model links asthma susceptibility to prenatal exposure to diesel exhaust

The Effects of Environmental Toxins on Allergic Inflammation

Tumor-Promoting/Associated Inflammation and the Microenvironment: A State of the Science and New Horizons

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