Persistence of Serotonergic Enhancement of Airway Response in a Model of Childhood Asthma

Moore, Brian D; Hyde, Dallas M.; Miller, Lisa; Wong, Emily; Schelegle, Edward S.

doi:10.1165/rcmb.2013-0387oc

Cited by 11 publications

(12 citation statements)

References 66 publications

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“…Human and animal studies suggest that adiposity-induced leptin increase and subsequent leptin resistance would affect these transmitters, causing or worsening asthma symptoms. This relates both to orexigenic neuropeptides such as neuropeptide Y (114)(115)(116)(117)(118)(119)(120) , endocannabinoids (121,122) , endogenous opioids (123)(124)(125)(126) ; and anorexigenic neuropeptides such as tachykinins and its most studied members substance P (127)(128)(129)(130)(131)(132) , α-melanocyte-stimulating hormone (133)(134)(135) , corticotropin-releasing factor (136)(137)(138)(139)(140)(141) and serotonin (142)(143)(144)(145)(146)(147)(148)(149)(150) . Altogether, it suggests that these peptides can modulate asthmatic inflammation among obese patients.…”

Section: Possible Linksmentioning

confidence: 99%

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

2016

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Obesity is a risk factor for asthma, and obese asthmatics have lower disease control and increased symptom severity. Several putative links have been proposed, including genetics, mechanical restriction of the chest and the intake of corticosteroids. The most consistent evidence, however, comes from studies of cytokines produced by the adipose tissue called adipokines. Adipokine imbalance is associated with both proinflammatory status and asthma. Although reverse causation has been proposed, it is now acknowledged that obesity precedes asthma symptoms. Nevertheless, prenatal origins of both conditions complicate the search for causality. There is a confirmed role of neuro-immune cross-talk mediating obesityinduced asthma, with leptin playing a key role in these processes. Obesity-induced asthma is now considered a distinct asthma phenotype. In fact, it is one of the most important determinants of asthma phenotypes. Two main subphenotypes have been distinguished. The first phenotype, which affects adult women, is characterised by later onset and is more likely to be non-atopic. The childhood obesity-induced asthma phenotype is characterised by primary and predominantly atopic asthma. In obesity-induced asthma, the immune responses are shifted towards T helper (Th) 1 polarisation rather than the typical atopic Th2 immunological profile. Moreover, obese asthmatics might respond differently to environmental triggers. The high cost of treatment of obesity-related asthma, and the burden it causes for the patients and their families call for urgent intervention. Phenotype-specific approaches seem to be crucial for the success of prevention and treatment.

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Section: Possible Linksmentioning

confidence: 99%

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

2016

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“…Average diameter for terminal bronchioles in FA group was 0.79 mm while in the Ozone/HDMA group it was 0.72 m based on the model of a right circular cylinder (V = π*radius 2 *length). Only these two cohorts were examined for length difference of bronchioles because only the Ozone/HDMA showed increased airway hyperresponsiveness compared to the FA cohort 16 .…”

Section: Resultsmentioning

confidence: 99%

“…Rhesus monkeys have been reported to have hyperplastic bronchiolar epithelium and altered smooth muscle bundle orientation in both terminal and respiratory bronchioles after similar cyclic ozone exposure 6 . Chronic exposure to ozone and allergens followed by 30 months recovery in filtered air resulted in structural changes of small airway narrowing that were associated with airway hyperresponsiveness 16 . The driving force behind most features of airway remodeling appears to be inflammation with multiple cytokines, chemokines, and growth factors involved from both structural and inflammatory cells 39 .…”

Section: Discussionmentioning

confidence: 99%

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Early life exposure to allergen and ozone results in altered development in adolescent rhesus macaque lungs

Herring¹,

Putney²,

George³

et al. 2015

Toxicology and Applied Pharmacology

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In rhesus macaques, previous studies have shown that episodic exposure to allergen alone or combined with ozone inhalation during the first 6 months of life results in a condition with many of the hallmarks of asthma. This exposure regimen results in altered development of the distal airways and parenchyma (Avdalovic et al., 2012). We hypothesized that the observed alterations in lung parenchyma would be permanent following a long-term recovery in filtered (FA) housing. Forty-eight infant rhesus macaques (30 days old) sensitized to house dust mite (HDM) were treated with two week cycles of FA, house dust mite allergen (HDMA), ozone (O3) or HDMA/ozone (HDMA + O3) for five months. At the end of the five months, six animals from each group were necropsied. The other six animals in each group were allowed to recover in FA for 30 more months at which time they were necropsied. Design-based stereology was used to estimate volumes of lung components, number of alveoli, size of alveoli, distribution of alveolar volumes, interalveolar capillary density. After 30 months of recovery, monkeys exposed to HDMA, in either group, had significantly more alveoli than filtered air. These alveoli also had higher capillary densities as compare with FA controls. These results indicate that early life exposure to HDMA alone or HDMA + O3 alters the development process in lung alveoli.

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“…These changes were associated with altered serotonin, substance P, and fibroblast growth factor signaling in conducting airways ( Evans et al 2003 ; Moore et al 2012 ; Murphy et al 2012 , 2013 ). The cessation of exposure for 6 months resulted the normalization of fibroblast growth factor signaling and epithelial hyperinnervation, while airway serotonin signaling remained altered for as long as 2.5 following the end of exposure ( Evans et al 2004 ; Kajekar et al 2007 ; Moore et al 2014 ). In total, these studies of early-life episodic ozone exposure provide evidence for prolonged structural and functional airway changes that could increase the risk for chronic lung disease as the animal ages.…”

Section: Role Of Nonhuman Primates In Inhalation Toxicologymentioning

confidence: 99%

Nonhuman Primate Models of Respiratory Disease: Past, Present, and Future

et al. 2017

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The respiratory system consists of an integrated network of organs and structures that primarily function for gas exchange. In mammals, oxygen and carbon dioxide are transmitted through a complex respiratory tract, consisting of the nasal passages, pharynx, larynx, and lung. Exposure to ambient air throughout the lifespan imposes vulnerability of the respiratory system to environmental challenges that can contribute toward development of disease. The importance of the respiratory system to human health is supported by statistics from the Centers for Disease Control and Prevention; in 2015, chronic lower respiratory diseases were the third leading cause of death in the United States. In light of the significant mortality associated with respiratory conditions that afflict all ages of the human population, this review will focus on basic and preclinical research conducted in nonhuman primate models of respiratory disease. In comparison with other laboratory animals, the nonhuman primate lung most closely resembles the human lung in structure, physiology, and mucosal immune mechanisms. Studies defining the influence of inhaled microbes, pollutants, or allergens on the nonhuman primate lung have provided insight on disease pathogenesis, with the potential for elucidation of molecular targets leading to new treatment modalities. Vaccine trials in nonhuman primates have been crucial for confirmation of safety and protective efficacy against infectious diseases of the lung in a laboratory animal model that recapitulates pathology observed in humans. In looking to the future, nonhuman primate models of respiratory diseases will continue to be instrumental for translating biomedical research for improvement of human health.

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Persistence of Serotonergic Enhancement of Airway Response in a Model of Childhood Asthma

Cited by 11 publications

References 66 publications

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

Early life exposure to allergen and ozone results in altered development in adolescent rhesus macaque lungs

Nonhuman Primate Models of Respiratory Disease: Past, Present, and Future

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