ArticleThe American journal of pathology2012
Elastase/LPS-exposed mice exhibit impaired innate immune responses to bacterial challenge: role of scavenger receptor A.
Article in The American journal of pathology, 2012. 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, 44 citations in OpenAlex.
- The evolving role of the immune microenvironment of tumor draining lymph nodes in the development of biomarkers of non-small cell lung cancer.Frontiers in oncology · 2026Review
- Animal models: An essential tool to dissect the heterogeneity of chronic obstructive pulmonary disease.Journal of translational internal medicine · 2023Article
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- The EGFR/ErbB inhibitor neratinib modifies the neutrophil phosphoproteome and promotes apoptosis and clearance by airway macrophages.Frontiers in immunology · 2022Article
- Microvesicle-Mediated Communication Within the Alveolar Space: Mechanisms of Uptake by Epithelial Cells and Alveolar Macrophages.Frontiers in immunology · 2022Article
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- Animal Models Reflecting Chronic Obstructive Pulmonary Disease and Related Respiratory Disorders: Translating Pre-Clinical Data into Clinical Relevance.Journal of innate immunity · 2020Review
- MyD88 controls airway epithelial Muc5ac expression during TLR activation conditions from agricultural organic dust exposure.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Pellino-1 Regulates Immune Responses toFrontiers in immunology · 2019Article
- Endotoxin-Induced Emphysema Exacerbation: A Novel Model of Chronic Obstructive Pulmonary Disease Exacerbations Causing Cardiopulmonary Impairment and Diaphragm Dysfunction.Frontiers in physiology · 2019Article
- Article
- Review
- Changes in Expression of the Membrane Receptors CD14, MHC-II, SR-A, and TLR4 in Tissue-Specific Monocytes/Macrophages Following Porphyromonas gingivalis-LPS Stimulation.Inflammation · 2018Article
- World Trade Center (WTC) dust exposure in mice is associated with inflammation, oxidative stress and epigenetic changes in the lung.Experimental and molecular pathology · 2017Article
- Treatment with intranasal iloprost reduces disease manifestations in a murine model of previously established COPD.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Intra-tracheal Administration of Haemophilus influenzae in Mouse Models to Study Airway Inflammation.Journal of visualized experiments : JoVE · 2016Article
- A short-term mouse model that reproduces the immunopathological features of rhinovirus-induced exacerbation of COPD.Clinical science (London, England : 1979) · 2015Article
- Why do we need a nonhuman primate model of smoking-induced COPD?The American journal of pathology · 2015Article
- Effects of Chung-Pae Inhalation Therapy on a Mouse Model of Chronic Obstructive Pulmonary Disease.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Housing conditions modulate the severity of Mycoplasma pulmonis infection in mice deficient in class A scavenger receptor.Comparative medicine · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Nontypeable Haemophilus influenzae (NTHi) is an important bacterial pathogen associated with lower respiratory tract colonization and with acute exacerbations and disease progression in chronic obstructive pulmonary disease (COPD). Why the immune system fails to eliminate NTHi and the exact contribution of the organism to COPD progression are not well understood, in part because we lack an animal model that mimics all aspects of COPD. For this study, we used an established murine model that exhibits typical features of COPD. Elastase/LPS-exposed mice infected with NTHi showed persistence of bacteria up to 5 days after infection, whereas mice exposed to elastase, LPS, or PBS cleared all bacteria by 3 days. Elastase/LPS-exposed mice also showed sustained lung neutrophilic inflammation, goblet cell metaplasia, airway hyperresponsiveness, and progression of emphysema at 15 days after infection. Alveolar macrophages isolated from elastase/LPS-exposed mice showed impaired bacterial phagocytosis, reduced expression of MARCO and of mannose receptor, and absent expression of scavenger receptor-A (SR-A). Neutralization of SR-A significantly decreased phagocytosis of NTHi by normal alveolar macrophages. Our results suggest that elastase/LPS-exposed mice show impaired bacterial clearance and sustained lung inflammation. Lack of SR-A expression may, in part, be responsible for impaired phagocytosis of bacteria by alveolar macrophages of elastase/LPS-exposed mice. These data validate the suitability of elastase/LPS model for investigating NTHi pathogenesis and progression of disease in COPD.
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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.