Genetic polymorphisms in arginase I and II and childhood asthma and atopy

Li, Huiling; Romieu, Isabelle; Sienra-Monge, Juan-Jose; Ramírez-Aguilar, Matiana; Río-Navarro, Blanca Estela Del; Kistner, Emily O.; Gjessing, Håkon K.; Lara-Sanchez, Irma del Carmen; Chiu, Grace Y.; London, Stephanie J.

doi:10.1016/j.jaci.2005.09.026

Cited by 89 publications

(90 citation statements)

References 40 publications

(40 reference statements)

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“…Moreover, increased immunoreactivity against arginase I, which could possibly be induced by nicotine, was recently observed in both the epithelium and the smooth muscle layer of smoking asthmatics [129]. Interestingly, single nucleotide polymorphisms of arginase I and II have recently been found to be associated with atopy and risk of childhood asthma, respectively [130].…”

Section: Acute Modulation Of Ahrmentioning

confidence: 99%

Airway hyperresponsiveness in asthma: lessons from in vitro model systems and animal models

Gosens¹,

Zaagsma²

2008

European Respiratory Journal

107

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Airway hyperresponsiveness (AHR) is a hallmark clinical symptom of asthma. At least two components of AHR have been identified: 1) baseline AHR, which is persistent and presumably caused by airway remodelling due to chronic recurrent airway inflammation; and 2) acute and variable AHR, which is associated with an episodic increase in airway inflammation due to environmental factors such as allergen exposure.Despite intensive research, the mechanisms underlying acute and chronic AHR are poorly understood. Owing to the complex variety of interactive processes that may be involved, in vitro model systems and animal models are indispensable to the unravelling of these mechanisms at the cellular and molecular level.The present paper focuses on a number of translational studies addressing the emerging central role of the airway smooth muscle cell, as a multicompetent cell involved in acute airway constriction as well as structural changes in the airways, in the pathophysiology of airway hyperresponsiveness.

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Section: Acute Modulation Of Ahrmentioning

confidence: 99%

Airway hyperresponsiveness in asthma: lessons from in vitro model systems and animal models

Gosens¹,

Zaagsma²

2008

European Respiratory Journal

107

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“…Polymorphisms in TNF and lipoteichoic acid have been associated with respiratory effects of O 3 in humans [128]. Arginase II has been associated with an increased risk of asthma in children, and the association appeared stronger among children with a smoking parent [131] suggesting that air pollutants could also play a role.…”

Section: Other Genesmentioning

confidence: 99%

Air pollution, oxidative stress and dietary supplementation: a review

Romieu

Castro-Giner²,

Künzli³

et al. 2008

European Respiratory Journal

219

157

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The aim of the present review was to provide an up-to-date overview of the biological and epidemiological evidence of the role of oxidative stress as a major underlying feature of the toxic effect of air pollutants, and the potential role of dietary supplementation in enhancing antioxidant defences.A bibliographic search was conducted through PubMed. The keywords used in the search were ''air pollutant'', ''oxidative stress'', ''inflammation'', ''antioxidant polyunsaturated fatty acids'' and ''genetics''. In addition, the authors also searched for biomarkers of oxidative stress and nutrients.The review presents the most recent data on: the biological and epidemiological evidence of the oxidative stress response to air pollutants; the role of dietary supplementation as a modulator of these effects; and factors of inter-individual variation in human response. The methodology for further epidemiological studies will be discussed in order to improve the current understanding on how nutritional factors may act.There is substantial evidence that air pollution exposure results in increased oxidative stress and that dietary supplementation may play a modulating role on the acute effect of air pollutants. Further epidemiological studies should address the impact of supplementation strategies in the prevention of air-pollution-related long-term effects in areas where people are destined to be exposed for the distant future.

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“…ARG1 is present exclusively in the cytosol of hepatic cells as part of the urea cycle, but ARG2 is found in mitochondria of many tissues without a functioning complete urea cycle, including the lung (18). Intriguingly, ARG2 gene variants, which lie within an asthma linkage region on chromosome 14q24, are some of the earliest and most consistent SNPs discovered in GWAS of asthma, and are strongly linked to origins and severity of asthma (20)(21)(22). ARG2 is composed of 354 amino acid residues, including an NH 2 -terminal presequence for mitochondrial targeting and import (23).…”

Section: Introductionmentioning

confidence: 99%