Patients with Asthma Demonstrate Airway Inflammation after Exposure to Concentrated Ambient Particulate Matter

Alexis, Neil E.; Huang, Y.-C. T.; Rappold, Ana G.; Kehrl, Howard; Devlin, Robert B.; Peden, David B.

doi:10.1164/rccm.201401-0126le

Cited by 22 publications

(11 citation statements)

References 12 publications

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“…Epidemiologic studies have revealed that PM 2.5 pollution correlates with respiratory diseases including asthma and COPD (Dominici et al, ; Yang et al, ; Atkinson et al, ). Lung inflammation is a central feature of many pulmonary diseases, which can be induced by PM 2.5 exposure (Grootendorst et al, ; Alexis et al, ; Janssen et al, ). However, the mechanisms underlying adverse respiratory effects induced by PM 2.5 exposure have not been fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…It has been showed that short‐term exposure to ambient PM 2.5 caused lung function decrement (Rice et al, ). The studies on healthy and asthmatic volunteers have demonstrated that exposure to PM could induce or aggravate airway inflammation (Alexis et al, ; Janssen et al, ). Furthermore, documented evidence from animal studies also indicated that PM 2.5 could result in lung inflammation and fibrosis (Farina et al, ; Ogino et al, ).…”

Section: Introductionmentioning

confidence: 99%

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Involvement of EGF receptor signaling and NLRP12 inflammasome in fine particulate matter‐induced lung inflammation in mice

Jin

Zhang

et al. 2016

Environmental Toxicology

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Epidemiological studies have shown that exposure to ambient fine particulate matter (PM ) is associated with respiratory diseases. Lung inflammation is a central feature of many pulmonary diseases, which can be induced by PM exposure. However, the mechanisms underlying PM -induced lung inflammation remain unclear. To characterize the role of epidermal growth factor receptor (EGFR) and inflammasome in PM -induced lung inflammation in mice, 30 BALB/c mice were intrabroncheally instilled with saline and PM suspension (4.0 mg/kg b.w.) for 5 consecutive days, respectively. Bronchoalveolar lavage (BAL) was conducted and BAL fluid (BALF) was collected. The levels of reactive oxygen species (ROS), inducible nitric oxide synthase (iNOS), epidermal growth factor (EGF), CXCL1, interleukin (IL)-1β, and IL-18 in BALF were determined using ELISA. mRNA levels of IL-6, IL-1β, IL-18, CXCL1, IL-10, NLRP3, Caspase-1, and NLRP12 in lung tissues were determined by RT-PCR. Phospho-EGFR (Tyr1068) and phospho-Akt (Thr308) in lung tissues were examined using immunohistochemical staining and Western blotting, respectively. Protein levels of Caspase-1, NLRP3, NF-κB-p52/p100, and NF-κB-p65 in bronchial epithelium were examined using immunohistochemical staining. It was shown that PM exposure induced lung inflammation. Levels of total protein, ROS, iNOS, EGF, and CXCL1 and cell number in the BALF of mice exposed to PM were markedly elevated relative to the control. mRNA levels of CXCL1, IL-1β, and IL-18 in lung tissues of PM -exposed mice were increased in comparison with the control. However, level of NLRP12 mRNA in lung tissues of PM -exposed mice was reduced. Phospho-EGFR (Tyr1068) and phospho-Akt (Thr308) levels in the lungs of PM -instilled mice were higher than those in the lungs of the control. The protein levels of NF-κB-p52/p100 and NF-κB-p65 in bronchial epithelium of PM -exposed mice were also increased compared with the control. This study suggests that EGF-EGFR-Akt-NF-κB signaling and NLRP12 inflammasome may be associated with PM -induced lung inflammation in mice. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1121-1134, 2017.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Involvement of EGF receptor signaling and NLRP12 inflammasome in fine particulate matter‐induced lung inflammation in mice

Jin

Zhang

et al. 2016

Environmental Toxicology

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“…Clinical studies that investigate the impact of air pollution on allergic sensitization and exacerbations are limited by ethical considerations on de novo allergic sensitization, the requirement for specialized controlled human exposure systems, and the reduced level of mechanistic interrogation possible in human systems. Despite these limitations, controlled exposures to diesel exhaust, ozone, and particulate matter have been performed in healthy subjects and those with asthma. As real‐world exposures are likely to be complex, clinical studies have also examined co‐exposures to multiple environmental insults including combinations of diesel exhaust and ozone, diesel exhaust and allergen, and particulate matter and allergen …”

Section: Potential Roles For Obesity and High‐fat Diet And Air Pollutmentioning

confidence: 99%

Mechanisms and treatments for severe, steroid‐resistant allergic airway disease and asthma

Hansbro

Kim

Starkey

et al. 2017

Immunological Reviews

115

114

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Severe, steroid-resistant asthma is clinically and economically important since affected individuals do not respond to mainstay corticosteroid treatments for asthma. Patients with this disease experience more frequent exacerbations of asthma, are more likely to be hospitalized, and have a poorer quality of life. Effective therapies are urgently required, however, their development has been hampered by a lack of understanding of the pathological processes that underpin disease. A major obstacle to understanding the processes that drive severe, steroid-resistant asthma is that the several endotypes of the disease have been described that are characterized by different inflammatory and immunological phenotypes. This heterogeneity makes pinpointing processes that drive disease difficult in humans. Clinical studies strongly associate specific respiratory infections with severe, steroid-resistant asthma. In this review, we discuss key findings from our studies where we describe the development of representative experimental models to improve our understanding of the links between infection and severe, steroid-resistant forms of this disease. We also discuss their use in elucidating the mechanisms, and their potential for developing effective therapeutic strategies, for severe, steroid-resistant asthma. Finally, we highlight how the immune mechanisms and therapeutic targets we have identified may be applicable to obesity-or pollution-associated asthma.

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“…In particular, adolescents reported more severe asthma symptoms when they were outdoors as compared with other physical contexts. Being outdoors may increase exposure to respiratory irritants such as PM 2.5 and ozone, particularly among this sample of low-income adolescents living in urban Los Angeles, which has some of the most polluted air in the United States (Alexis et al, 2014; Jerrett et al, 2005). Adolescents and other children in disadvantaged minority and low-income groups are disproportionately exposed to multiple environmental chemicals in California.…”

Section: Discussionmentioning

confidence: 94%

Momentary Assessment of Psychosocial Stressors, Context, and Asthma Symptoms in Hispanic Adolescents

Dunton

Dzubur

et al. 2015

Behav Modif

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Objective The current study used a novel real-time data capture strategy, Ecological Momentary Assessment (EMA), to examine whether within-day variability in stress and context leads to exacerbations in asthma symptomatology in the everyday lives of ethnic minority adolescents. Methods Low-income, Hispanic adolescents (N = 20) (7th–12th grade) (54% male) with chronic asthma completed seven days of EMA on smartphones, with an average of five assessments per day during non-school time. EMA surveys queried about where (e.g., home, outdoors) and with whom (e.g., alone, with friends) participants were at the time of the prompt. EMA surveys also assessed over the past few hours whether participants had experienced specific stressors (e.g., being teased, arguing with anyone), asthma symptoms (e.g., wheezing, coughing), or used an asthma inhaler. Multilevel models tested the independent relations of specific stressors, and context to subsequent asthma symptoms adjusting for age, gender, and chronological day in the study. Results Being outdoors and experiencing disagreements with parents, teasing, or arguing were associated with more severe self-reported asthma symptoms in the next few hours (p’s < .05). Being alone and having too much to do were unrelated to the experience of subsequent self-reported asthma symptoms. Conclusions Using a novel real-time data capture strategy, results provide preliminary evidence that being outdoors and experiencing social stressors may induce asthma symptoms in low-income Hispanic children and adolescents with chronic asthma. The results of this preliminary study can serve as the basis for larger epidemiological and intervention studies.

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Patients with Asthma Demonstrate Airway Inflammation after Exposure to Concentrated Ambient Particulate Matter

Cited by 22 publications

References 12 publications

Involvement of EGF receptor signaling and NLRP12 inflammasome in fine particulate matter‐induced lung inflammation in mice

Involvement of EGF receptor signaling and NLRP12 inflammasome in fine particulate matter‐induced lung inflammation in mice

Mechanisms and treatments for severe, steroid‐resistant allergic airway disease and asthma

Momentary Assessment of Psychosocial Stressors, Context, and Asthma Symptoms in Hispanic Adolescents

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