ArticleMucosal immunology2015
Key role for scavenger receptor B-I in the integrative physiology of host defense during bacterial pneumonia.
Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Gammaherpesvirus infection unveils exaggerated germinal center responses in an SR-BI-deficient host.Journal of virology · 2025Article
- The Role of SR-BI in sepsis: leveraging mechanistic insights to advance precision steroid therapy.Frontiers in immunology · 2025Review
- Article
- Scavenger receptor BI attenuates oxidized phospholipid-induced pulmonary inflammation.Toxicology and applied pharmacology · 2023Article
- Innate immune responses in pneumonia.Pneumonia (Nathan Qld.) · 2023Review
- Scavenger receptor B1 facilitates the endocytosis of Escherichia coli via TLR4 signaling in mammary gland infection.Cell communication and signaling : CCS · 2023Article
- Class B Scavenger Receptors BI and BII Protect against LPS-Induced Acute Lung Injury in Mice by Mediating LPS.Infection and immunity · 2021Article
- Scavenger Hunt: SR-B1, Adrenal Insufficiency, IL-17A, and Neutrophilic Airway Inflammation in Asthma.American journal of respiratory cell and molecular biology · 2021Article
- Scavenger Receptor BI Attenuates IL-17A-Dependent Neutrophilic Inflammation in Asthma.American journal of respiratory cell and molecular biology · 2021Article
- Novel Mechanisms of Ozone-Induced Pulmonary Inflammation and Resolution, and the Potential Protective Role of Scavenger Receptor BI.Research report (Health Effects Institute) · 2021Article
- High-Density Lipoprotein Therapy in Stroke: Evaluation of Endothelial SR-BI-Dependent Neuroprotective Effects.International journal of molecular sciences · 2020Article
- Euthanasia- and Lavage-mediated Effects on Bronchoalveolar Measures of Lung Injury and Inflammation.American journal of respiratory cell and molecular biology · 2018Article
- A New Frontier in Immunometabolism. Cholesterol in Lung Health and Disease.Annals of the American Thoracic Society · 2017Review
- Roles of the Mevalonate Pathway and Cholesterol Trafficking in Pulmonary Host Defense.Current molecular pharmacology · 2017Article
- A Non-invasive and Technically Non-intensive Method for Induction and Phenotyping of Experimental Bacterial Pneumonia in Mice.Journal of visualized experiments : JoVE · 2016Article
- Interferon alpha bioactivity critically depends on Scavenger receptor class B type I function.Oncoimmunology · 2016Article
- Scavenger receptor class B, type I-mediated uptake of A1AT by pulmonary endothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Scavenger receptor B-I (SR-BI) is a multirecognition receptor that regulates cholesterol trafficking and cardiovascular inflammation. Although it is expressed by neutrophils (PMNs) and lung-resident cells, no role for SR-BI has been defined in pulmonary immunity. Herein, we report that, compared with SR-BI(+/+) counterparts, SR-BI(-/-) mice suffer markedly increased mortality during bacterial pneumonia associated with higher bacterial burden in the lung and blood, deficient induction of the stress glucocorticoid corticosterone, higher serum cytokines, and increased organ injury. SR-BI(-/-) mice had significantly increased PMN recruitment and cytokine production in the infected airspace. This was associated with defective hematopoietic cell-dependent clearance of lipopolysaccharide from the airspace and increased cytokine production by SR-BI(-/-) macrophages. Corticosterone replacement normalized alveolar neutrophilia but not alveolar cytokines, bacterial burden, or mortality, suggesting that adrenal insufficiency derepresses PMN trafficking to the SR-BI(-/-) airway in a cytokine-independent manner. Despite enhanced alveolar neutrophilia, SR-BI(-/-) mice displayed impaired phagocytic killing. Bone marrow chimeras revealed this defect to be independent of the dyslipidemia and adrenal insufficiency of SR-BI(-/-) mice. During infection, SR-BI(-/-) PMNs displayed deficient oxidant production and CD11b externalization, and increased surface L-selectin, suggesting defective activation. Taken together, SR-BI coordinates several steps in the integrated neutrophilic host defense response to pneumonia.
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Registered trials
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.