Estudio temporal de diabetes mellitus tipo 1 en Chile: asociación con factores ambientales durante el período 2000-2007

R, Nelly González; Torres-Avilés, Francisco; P, Elena Carrasco; P, Francisca Salas; B, Francisco Pérez

doi:10.4067/s0034-98872013000500007

Cited by 15 publications

(4 citation statements)

References 30 publications

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“…Epidemiologic studies strongly suggest that exposure to air pollution can increase both the incidence and severity of autoimmune disease (Farhat et al, 2011; Gawda et al, 2017). Specifically, exposure to PM 1 in the atmosphere aggravates type 1 diabetes, rheumatoid arthritis, and multiple sclerosis, among others (Angelici et al, 2016; Beyerlein et al, 2015; Brook et al, 2013; Chang et al, 2016; Di Ciaula, 2016; Gonzalez et al, 2013; Gregory et al, 2008; Hathout et al, 2002; Malmqvist et al, 2015; Oikonen et al, 2003; Roux et al, 2017; Vojinovic et al, 2015). Although strong correlations exist connecting PM exposure to autoimmune disease, identifying mechanisms leading to this disease process has proven particularly difficult.…”

Section: Introductionmentioning

confidence: 99%

Ambient urban dust particulate matter reduces pathologic T cells in the CNS and severity of EAE

O’Driscoll

Owens

Hoffmann

et al. 2019

Environmental Research

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Background: Autoimmune diseases have increased in incidence and prevalence worldwide. While genetic predispositions play a role, environmental factors are a major contributor. Atmospheric particulate matter (PM) is a complex mixture composed of metals, nitrates, sulfates and diverse adsorbed organic compounds like polycyclic aromatic hydrocarbons (PAHs) and dioxins. Exposure to atmospheric PM aggravates autoimmune diseases such as type 1 diabetes, rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus, among others. PAHs and dioxins are known aryl hydrocarbon receptor (AHR) ligands. The AHR modulates T cell differentiation and directs the balance between effector and regulatory T cells in vitro and in experimental autoimmune encephalomyelitis (EAE), a murine model of autoimmune disease. This study aims to identify pathways that contribute to autoimmune disease and their potential use as therapeutic targets to alleviate symptoms and the need for global immunosuppression. This study tests the hypothesis that atmospheric PM enhances effector T cell differentiation and aggravates autoimmune disease. Results: An atmospheric ambient urban dust PM sample, standard reference material (SRM)1649b, was tested for its effects on autoimmunity. SRM1649b PM enhanced Th17 differentiation in an AHR-dependent manner in vitro, however intranasal treatment of SRM1649b PM delayed onset of EAE and reduced cumulative and peak clinical scores. Chronic and acute intranasal exposure of SRM1649b PM delayed onset of EAE. Chronic intranasal exposure did not reduce severity of EAE while acute intranasal exposure significantly reduced severity of disease. Acute intranasal treatment of low dose SRM1649b PM had no effect on clinical score or day of onset in EAE. Delayed onset of EAE by intranasal SRM1649b PM was AHR-dependent in vivo. Oral gavage of SRM1649b PM, in the absence of AHR ligands in the diet, had no effect on day of disease onset or severity of EAE. Day 10 analysis of T cells in the CNS after intranasal treatment of SRM1649b PM showed a reduction of pathologic T cell subsets in vivo. Moreover, MOG-specific splenocytes require AHR to generate or maintain IL-10 producing cells and reduce IFNγ producing cells in vitro. Conclusions: These results identify the AHR pathway as a potential target for driving targeted immunosuppression in the CNS in the context of atmospheric PM-mediated autoimmune disease. The effects of SRM1649b PM on EAE are dependent on route of exposure, with intranasal treatment reducing severity of EAE and delaying disease onset while oral gavage has no effect. Intranasal SRM1649b PM reduces pathologic T cells in the CNS, specifically Th1 cells and Th1Th17 double positive cells, leading to reduced severity of EAE and AHR-dependent delayed disease onset. Additionally, SRM1649b PM treatment of antigen-specific T cells leads to AHR-dependent increase in percent IL-10 positive cells in vitro. These findings may shed light on the known increase of infection after exposure to atmospheric PM and serve...

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Section: Introductionmentioning

confidence: 99%

Ambient urban dust particulate matter reduces pathologic T cells in the CNS and severity of EAE

O’Driscoll

Owens

Hoffmann

et al. 2019

Environmental Research

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“…Hathout et al (20) found pre-diagnosis PM 10 exposure was significantly higher in children diagnosed before 5 years of age compared to healthy controls. Likewise, a study from Chile found that PM 2.5 levels were associated with the onset of T1D in children (19). Beyerlein et al (16) analyzed data from a population-based register monitoring incidence of diabetes in children and youths in Germany since 2009 and found that high exposure to the traffic-related air pollutants PM 10 , NO 2 , and possibly PM 2.5 accelerated the manifestation of T1D, but only in very young children.…”

Section: Particulate Mattermentioning

confidence: 94%

The Aryl Hydrocarbon Receptor as an Immune-Modulator of Atmospheric Particulate Matter-Mediated Autoimmunity

O’Driscoll

Mezrich

2018

Front. Immunol.

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This review examines the current literature on the effects of atmospheric particulate matter (PM) on autoimmune disease and proposes a new role for the aryl hydrocarbon receptor (AHR) as a modulator of T cells in PM-mediated autoimmune disease. There is a significant body of literature regarding the strong epidemiologic correlations between PM exposures and worsened autoimmune diseases. Genetic predispositions account for 30% of all autoimmune disease leaving environmental factors as major contributors. Increases in incidence and prevalence of autoimmune disease have occurred concurrently with an increase in air pollution. Currently, atmospheric PM is considered to be the greatest environmental health risk worldwide. Atmospheric PM is a complex heterogeneous mixture composed of diverse adsorbed organic compounds such as polycyclic aromatic hydrocarbons (PAHs) and dioxins, among others. Exposure to atmospheric PM has been shown to aggravate several autoimmune diseases. Despite strong correlations between exposure to atmospheric PM and worsened autoimmune disease, the mechanisms underlying aggravated disease are largely unknown. The AHR is a ligand activated transcription factor that responds to endogenous and exogenous ligands including toxicants present in PM, such as PAHs and dioxins. A few studies have investigated the effects of atmospheric PM on AHR activation and immune function and demonstrated that atmospheric PM can activate the AHR, change cytokine expression, and alter T cell differentiation. Several studies have found that the AHR modulates the balance between regulatory and effector T cell functions and drives T cell differentiation in vitro and in vivo using murine models of autoimmune disease. However, there are very few studies on the role of AHR in PM-mediated autoimmune disease. The AHR plays a critical role in the balance of effector and regulatory T cells and in autoimmune disease. With increased incidence and prevalence of autoimmune disease occurring concurrently with increases in air pollution, potential mechanisms that drive inflammatory and exacerbated disease need to be elucidated. This review focuses on the AHR as a potential mechanistic target for modulating T cell responses associated with PM-mediated autoimmune disease providing the most up-to-date literature on the role of AHR in autoreactive T cell function and autoimmune disease.

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“…To evaluate the impact of PM2.5 on the occurrence of T1D Gonzáles et al [96] reviewed data of children and adolescents with T1D at onset who received their first insulin injection between 2000 and 2007. Comparing these data with the PM rates obtained from Environmental Services they demonstrated a significant increase of relative risk related to PM2.5 showing that air pollution factors could be related to peaks of T1D incidence.…”

Section: Human Studiesmentioning

confidence: 99%

Endocrine Disrupting Chemicals and Type 1 Diabetes

Predieri

Bruzzi

Bigi

et al. 2020

IJMS

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Type 1 diabetes (T1D) is the most common chronic metabolic disease in children and adolescents. The etiology of T1D is not fully understood but it seems multifactorial. The genetic background determines the predisposition to develop T1D, while the autoimmune process against β-cells seems to be also determined by environmental triggers, such as endocrine disrupting chemicals (EDCs). Environmental EDCs may act throughout different temporal windows as single chemical agent or as chemical mixtures. They could affect the development and the function of the immune system or of the β-cells function, promoting autoimmunity and increasing the susceptibility to autoimmune attack. Human studies evaluating the potential role of exposure to EDCs on the pathogenesis of T1D are few and demonstrated contradictory results. The aim of this narrative review is to summarize experimental and epidemiological studies on the potential role of exposure to EDCs in the development of T1D. We highlight what we know by animals about EDCs’ effects on mechanisms leading to T1D development and progression. Studies evaluating the EDC levels in patients with T1D were also reported. Moreover, we discussed why further studies are needed and how they should be designed to better understand the causal mechanisms and the next prevention interventions.

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Estudio temporal de diabetes mellitus tipo 1 en Chile: asociación con factores ambientales durante el período 2000-2007

Abstract: (Rev Med Chile 2013; 141: 595-601).

Cited by 15 publications

References 30 publications

Ambient urban dust particulate matter reduces pathologic T cells in the CNS and severity of EAE

Ambient urban dust particulate matter reduces pathologic T cells in the CNS and severity of EAE

The Aryl Hydrocarbon Receptor as an Immune-Modulator of Atmospheric Particulate Matter-Mediated Autoimmunity

Endocrine Disrupting Chemicals and Type 1 Diabetes

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