Zinc Status Modulates Bronchopulmonary Eosinophil Infiltration in a Murine Model of Allergic Inflammation

Richter, Martin; Bonneau, Richard; Girard, Marie-Andrée; Beaulieu, Claudia; Larivée, Pierre

doi:10.1378/chest.123.3_suppl.446s

Cited by 49 publications

(31 citation statements)

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“…36 These nutrients have been hypothesized to influence lung growth 42,43 and airway development, 44,45 improving the T H 1/T H 2 ratio by altering cytokine secretions, 39,46-48 influencing eicosanoid production, 49 and reducing eosinophilia. 50 From this study, we are unable to determine which of these nutrients might be acting either independently or in concert, producing synergistic effects on immune system development, maturation, or function in the growing fetus. However, they stress the importance of consuming whole foods during pregnancy and might be more relevant for future recommendations on pregnancy diet.…”

Section: Discussionmentioning

confidence: 89%

Peanut and tree nut consumption during pregnancy and allergic disease in children—should mothers decrease their intake? Longitudinal evidence from the Danish National Birth Cohort

Maslova

Granström

Hansen

et al. 2012

Journal of Allergy and Clinical Immunology

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Section: Discussionmentioning

confidence: 89%

Peanut and tree nut consumption during pregnancy and allergic disease in children—should mothers decrease their intake? Longitudinal evidence from the Danish National Birth Cohort

Maslova

Granström

Hansen

et al. 2012

Journal of Allergy and Clinical Immunology

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“…It was shown that nutritional Zn deficiency worsens allergic inflammation. In addition, Zn supplementation led to significant improvement in acute and chronic asthma mouse models (35,36).…”

Section: Discussionmentioning

confidence: 99%

Protection of Zinc against Tumor Necrosis Factor–Induced Lethal Inflammation Depends on Heat Shock Protein 70 and Allows Safe Antitumor Therapy

Molle¹,

Roy²,

Bogaert³

et al. 2007

Cancer Research

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Tumor necrosis factor (TNF)-induced inflammation prevents its broad application as an antitumor agent. We here report that addition of ZnSO 4 to the drinking water of mice induces expression of heat shock protein 70 (HSP70) in several organs, notably the gastrointestinal track. Zinc conferred doseresponsive protection against TNF-induced hypothermia, systemic induction of interleukin-6 and NO x , as well as against TNF-induced bowel cell death and death of the organism. The protective effect of zinc was completely absent in mice deficient in the major HSP70-inducible gene, hsp70.1, whereas transgenic mice constitutively expressing the human HSP70.A gene, under control of a B-actin promoter, was also protected against TNF, indicating that an increase in HSP70 is necessary and sufficient to confer protection. The therapeutic potential of the protection induced by ZnSO 4 was clearly shown in a TNF/IFN;-based antitumor therapy using three different tumor models. In hsp70.1 wild-type mice, but not in hsp70.1-deficient mice, zinc very significantly protected against lethality but left the antitumor effect intact. We conclude that zinc protects against TNF in a HSP70-dependent way and that protection by zinc could be helpful in developing a safer anticancer therapy with TNF/IFN;. [Cancer Res 2007;67(15):7301-7]

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“…In mouse models of asthma, Zn deficiency correlated very strongly with high levels of eosinophilia and increased Th2 responses [158,159]. That may be especially relevant to the CF population, where there is often a large Th2 response.…”

Section: Zincmentioning

confidence: 99%

Antioxidants in cystic fibrosis☆Conclusions from the CF Antioxidant Workshop, Bethesda, Maryland, November 11-12, 2003

Cantin

White

Cross

et al. 2007

Free Radical Biology and Medicine

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Although great strides are being made in the care of individuals with cystic fibrosis (CF), this condition remains the most common fatal hereditary disease in North America. Numerous links exist between progression of CF lung disease and oxidative stress. The defect in CF is the loss of function of the transmembrane conductance regulator (CFTR) protein; recent evidence that CFTR expression and function are modulated by oxidative stress suggests that the loss may result in a poor adaptive response to oxidants. Pancreatic insufficiency in CF also increases susceptibility to deficiencies in lipophilic antioxidants. Finally the airway infection and inflammatory processes in the CF lung are potential sources of oxidants that can affect normal airway physiology and contribute to the mechanisms causing characteristic changes associated with bronchiectasis and loss of lung function. These multiple abnormalities in the oxidant/antioxidant balance raise several possibilities for therapeutic interventions that must be carefully assessed. IntroductionCystic fibrosis (CF) is the most common fatal disease caused by a single gene defect in Europe and North America [1,2]. The defective gene was identified in 1989 [3][4][5] and shown to encode the cystic fibrosis trans-membrane conductance regulator protein (CFTR). CFTR is a cyclic AMP-regulated anion channel with greatest selectivity for chloride, and bicarbonate [6][7][8]. Furthermore, CFTR regulates sodium transport across epithelial membranes through interactions with the epithelial sodium channel ENaC [9], and facilitates the trans-membrane export of the small organic anionic peptide glutathione [10]. The expression of CFTR is located in the apical membrane of epithelial cells that line mucous membranes and submucosal glands ☆ A list of participants may be found in the Acknowledgments.

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Zinc Status Modulates Bronchopulmonary Eosinophil Infiltration in a Murine Model of Allergic Inflammation

Cited by 49 publications

References 0 publications

Peanut and tree nut consumption during pregnancy and allergic disease in children—should mothers decrease their intake? Longitudinal evidence from the Danish National Birth Cohort

Peanut and tree nut consumption during pregnancy and allergic disease in children—should mothers decrease their intake? Longitudinal evidence from the Danish National Birth Cohort

Protection of Zinc against Tumor Necrosis Factor–Induced Lethal Inflammation Depends on Heat Shock Protein 70 and Allows Safe Antitumor Therapy

Antioxidants in cystic fibrosis☆Conclusions from the CF Antioxidant Workshop, Bethesda, Maryland, November 11-12, 2003

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