ArticleInfection and immunity2008
Mycoplasma pneumoniae infection and environmental tobacco smoke inhibit lung glutathione adaptive responses and increase oxidative stress.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Kukoamine A ImprovesBioMed research international · 2022Article
- Role of Mycoplasma Chaperone DnaK in Cellular Transformation.International journal of molecular sciences · 2020Review
- Assessing the Efficacy of Dietary Selenomethionine Supplementation in the Setting of Cardiac Ischemia/Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2019Article
- Association between the oral microbiome and brain resting state connectivity in smokers.NeuroImage · 2019Article
- Mycoplasma infection of cultured cells induces oxidative stress and attenuates cellular base excision repair activity.Mutation research. Genetic toxicology and environmental mutagenesis · 2019Article
- Trends of Lipophilic, Antioxidant and Hematological Parameters Associated with Conventional and Electronic Smoking Habits in Middle-Age Romanians.Journal of clinical medicine · 2019Article
- Infectious mononucleosis and hepatic function.Experimental and therapeutic medicine · 2018Article
- Low uric acid level increases the risk of infectious mononucleosis and this effect is more pronounced in women.Molecular and clinical oncology · 2017Article
- A disrupted transsulphuration pathway results in accumulation of redox metabolites and induction of gametocytogenesis in malaria.Scientific reports · 2017Article
- Insights into the pathogenesis of Mycoplasma pneumoniae (Review).Molecular medicine reports · 2016Review
- Biomass Smoke Exposure Enhances Rhinovirus-Induced Inflammation in Primary Lung Fibroblasts.International journal of molecular sciences · 2016Article
- An ERp57-mediated disulphide exchange promotes the interaction between Burkholderia cenocepacia and epithelial respiratory cells.Scientific reports · 2016Article
- Glutathione Depletion Accelerates Cigarette Smoke-Induced Inflammation and Airspace Enlargement.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
- Global secretome characterization of A549 human alveolar epithelial carcinoma cells during Mycoplasma pneumoniae infection.BMC microbiology · 2014Article
- Nebulized thiocyanate improves lung infection outcomes in mice.British journal of pharmacology · 2013Article
- Selective metabolism of hypothiocyanous acid by mammalian thioredoxin reductase promotes lung innate immunity and antioxidant defense.The Journal of biological chemistry · 2013Article
- Reactive oxygen species mediate Jak2/Stat3 activation and IL-8 expression in pulmonary epithelial cells stimulated with lipid-associated membrane proteins from Mycoplasma pneumoniae.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2012Article
- CFTR is the primary known apical glutathione transporter involved in cigarette smoke-induced adaptive responses in the lung.Free radical biology & medicine · 2012Article
- Lung glutathione adaptive responses to cigarette smoke exposure.Respiratory research · 2011Article
- Mycoplasma gallisepticum infection in the grey partridge Perdix perdix: outbreak description, histopathology, biochemistry and antioxidant parameters.BMC veterinary research · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
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Abstract
Chronic cigarette smoking evokes a lung glutathione (GSH) adaptive response that results in elevated GSH levels in the lung epithelial lining fluid (ELF). Currently, little is known about how the lung regulates or maintains steady-state levels of ELF GSH. Pathogens such as Mycoplasma pneumoniae can exacerbate airway inflammation and oxidative stress. The present study examined whether M. pneumoniae infections synergize with environmental tobacco smoke (ETS) to disrupt lung GSH adaptive responses. Mice were exposed separately and in combination to ETS and M. pneumoniae for 16 weeks. ETS exposure resulted in a doubling of ELF GSH levels, which was blocked in the M. pneumoniae-exposed mice. In addition, the ETS-plus-M. pneumoniae-exposed mice had elevated levels of oxidized glutathione (GSSG), resulting in a dramatic change in the ELF redox state that corresponded with an increase in lung tissue DNA oxidation. Similar findings were observed in human lung epithelial cells in vitro. Cells exposed separately or in combination to cigarette smoke extract and M. pneumoniae for 48 h had elevated apical levels of GSH compared to control cells, and these increases were blocked by M. pneumoniae and were also associated with increased cellular DNA oxidation. Further studies showed that M. pneumoniae exposure blocked ETS-induced increases in GSH reductase, an enzyme that recycles GSSG back to GSH, both in vitro and in vivo. These studies suggest that M. pneumoniae infection synergizes with ETS and suppresses the lung's ability to respond appropriately to environmental challenges leading to enhanced oxidative stress.
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