ArticleExperimental and molecular pathology2007
CD8+ T cells contribute to macrophage accumulation and airspace enlargement following repeated irritant exposure.
Article in Experimental and molecular pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- The role of CD8 + T lymphocytes in chronic obstructive pulmonary disease: a systematic review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Pooled it
- Lung CD8+ T cells in COPD have increased expression of bacterial TLRs.Respiratory research · 2013Trial
- Roles for T/B lymphocytes and ILC2s in experimental chronic obstructive pulmonary disease.Journal of leukocyte biology · 2019Article
- AIM2/IL-1α/TGF-β Axis in PBMCs From Exacerbated Chronic Obstructive Pulmonary Disease (COPD) Patients Is Not Related to COX-2-Dependent Inflammatory Pathway.Frontiers in physiology · 2019Article
- SCGB3A2 Inhibits Acrolein-Induced Apoptosis through Decreased p53 Phosphorylation.Acta histochemica et cytochemica · 2015Article
- Enhancement of the acrolein-induced production of reactive oxygen species and lung injury by GADD34.Oxidative medicine and cellular longevity · 2015Article
- Acrolein-exposed normal human lung fibroblasts in vitro: cellular senescence, enhanced telomere erosion, and degradation of Werner's syndrome protein.Environmental health perspectives · 2014Article
- Human CD56+ cytotoxic lung lymphocytes kill autologous lung cells in chronic obstructive pulmonary disease.PloS one · 2014Article
- Probiotics in the management of lung diseases.Mediators of inflammation · 2013Review
- Article
- Current concepts on oxidative/carbonyl stress, inflammation and epigenetics in pathogenesis of chronic obstructive pulmonary disease.Toxicology and applied pharmacology · 2011Review
- Exposure to acrolein by inhalation causes platelet activation.Toxicology and applied pharmacology · 2010Article
- Chronic cigarette smoke exposure generates pathogenic T cells capable of driving COPD-like disease in Rag2-/- mice.American journal of respiratory and critical care medicine · 2010Article
- Sustained CTL activation by murine pulmonary epithelial cells promotes the development of COPD-like disease.The Journal of clinical investigation · 2009Article
- Nonredundant functions of alphabeta and gammadelta T cells in acrolein-induced pulmonary pathology.Toxicological sciences : an official journal of the Society of Toxicology · 2008Article
- Pneumocystis murina infection and cigarette smoke exposure interact to cause increased organism burden, development of airspace enlargement, and pulmonary inflammation in mice.Infection and immunity · 2008Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPersistent macrophage accumulation and alveolar enlargement are hallmark features of chronic obstructive pulmonary disease (COPD). A role for CD8(+) lymphocytes in the development of COPD is suggested based on observations that this T cell subset is increased in the airways and parenchyma of smokers that develop COPD with airflow limitation. In this study, we utilize a mouse model of COPD to examine the contributions of CD8(+) T cells in the persistent macrophage accumulation and airspace enlargement resulting from chronic irritant exposure.
methodsWe analyzed pulmonary inflammation and alveolar destruction in wild-type and Cd8-deficient mice chronically exposed to acrolein, a potent respiratory tract irritant. We further examined cytokine mRNA expression levels by RNase protection assay, matrix metalloproteinase (MMP) activity by gelatin zymography, and epithelial cell apoptosis by active caspase3 immunohistochemistry in wild-type and Cd8-deficient mice exposed chronically to acrolein.
resultsThese studies demonstrate that CD8(+) T cells are important mediators of macrophage accumulation in the lung and the progressive airspace enlargement in response to chronic acrolein exposures. The expression of several inflammatory cytokines (IP-10, IFN-gamma, IL-12, RANTES, and MCP-1), MMP2 and MMP9 gelatinase activity, and caspase3 immunoreactivity in pulmonary epithelial cells were attenuated in the Cd8-deficient mice compared to wild-type.
conclusionsThese results indicate that CD8(+) T cells actively contribute to macrophage accumulation and the development of irritant-induced airspace enlargement.
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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.