ArticleOccupational and environmental medicine2011
Enhancement of systemic and sputum granulocyte response to inhaled endotoxin in people with the GSTM1 null genotype.
Article in Occupational and environmental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Gamma tocopherol effect on LPS-induced sputum neutrophilia is not modified by BMI or GSTM1 genotype.The Journal of allergy and clinical immunology · 2019Trial
- Endotoxin and β-1,3-d-Glucan in Concentrated Ambient Particles Induce Rapid Increase in Blood Pressure in Controlled Human Exposures.Hypertension (Dallas, Tex. : 1979) · 2015Trial
- A Review of theInternational journal of genomics · 2023Review
- Liver-Metabolizing Genes and Their Relationship to the Performance of Elite Spanish Male Endurance Athletes; a Prospective Transversal Study.Sports medicine - open · 2019Article
- Systemic inflammatory response to inhaled endotoxin does not correlate with airway response.Respiratory research · 2019Article
- The glutathione-S-transferase mu-1 null genotype increases wood smoke-induced airway inflammation.The Journal of allergy and clinical immunology · 2019Article
- Assessing the impact of air pollution on childhood asthma morbidity: how, when, and what to do.Current opinion in allergy and clinical immunology · 2018Review
- House Dust Endotoxin and Peripheral Leukocyte Counts: Results from Two Large Epidemiologic Studies.Environmental health perspectives · 2017Article
- Reproducibility of the inflammatory response to inhaled endotoxin in healthy volunteers.The Journal of allergy and clinical immunology · 2016Article
- Human experimental endotoxemia in modeling the pathophysiology, genomics, and therapeutics of innate immunity in complex cardiometabolic diseases.Arteriosclerosis, thrombosis, and vascular biology · 2015Review
- Glutathione S-transferase M1 modulates allergen-induced NF-κB activation in asthmatic airway epithelium.Allergy · 2014Article
- Effect of inhaled endotoxin on mucociliary clearance and airway inflammation in mild smokers and nonsmokers.Journal of aerosol medicine and pulmonary drug delivery · 2014Article
- Sputum neutrophil count after bronchial allergen challenge is related to peripheral blood neutrophil chemotaxis in asthma patients.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
- Supplementation with γ-tocopherol attenuates endotoxin-induced airway neutrophil and mucous cell responses in rats.Free radical biology & medicine · 2014Article
- Asthmatic airway neutrophilia after allergen challenge is associated with the glutathione S-transferase M1 genotype.American journal of respiratory and critical care medicine · 2013Article
- Role of GSTM1 in resistance to lung inflammation.Free radical biology & medicine · 2012Review
- Glutathione-S-transferase M1 regulation of diesel exhaust particle-induced pro-inflammatory mediator expression in normal human bronchial epithelial cells.Particle and fibre toxicology · 2012Article
- The effect of environmental oxidative stress on airway inflammation.Current opinion in allergy and clinical immunology · 2012Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveTo determine if the GSTM1 null genotype is a risk factor for increased inflammatory response to inhaled endotoxin.
methods35 volunteers who had undergone inhalation challenge with a 20 000 endotoxin unit dose of Clinical Center Reference Endotoxin (CCRE) were genotyped for the GSTM1 null polymorphism. Parameters of airway and systemic inflammation observed before and after challenge were compared in GSTM1 null (n=17) and GSTM1 (n=18) sufficient volunteers.
resultsGSTM1 null volunteers had significantly increased circulating white blood cells (WBCs), polymorphonuclear neutrophils (PMNs), platelets and sputum PMNs (% sputum PMNs and PMNs/mg sputum) after CCRE challenge. GSTM1 sufficient volunteers had significant, but lower increases in circulating WBCs, PMNs and % sputum PMNs, and no increase in platelets or PMNs/mg sputum. Linear regression analysis adjusted for baseline values of the entire cohort revealed that the GSTM1 null genotype significantly increased circulating WBCs, platelets and % sputum PMNs after challenge.
conclusionThese data support the hypothesis that the GSTM1 null genotype is a risk factor for increased acute respiratory and systemic inflammatory response to inhaled CCRE. These data are consistent with other observations that the GSTM1 null genotype is associated with increased respiratory, systemic and cardiovascular effects linked to ambient air particulate matter exposure and indicate that the GSTM1 null genotype should be considered a risk factor for adverse health effects associated with exposure to environmental endotoxin.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.