ArticleThe Journal of biological chemistry2011
Elevated inflammatory response in caveolin-1-deficient mice with Pseudomonas aeruginosa infection is mediated by STAT3 protein and nuclear factor kappaB (NF-kappaB).
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 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.
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Who cites it
71 citing papers in PubMed, 89 citations in OpenAlex.
- Cellular signaling meets bacterial infection: the integrative role of STAT3.Frontiers in cellular and infection microbiology · 2026Review
- Characterization of Corneal Defects in ATG7-Deficient Mice.International journal of molecular sciences · 2025Article
- Revolutionizing Autoimmune Research: The Role of Caveolin-1.Immunity, inflammation and disease · 2025Review
- NF-Journal of immunology research · 2025Article
- Caveolin-Mediated Endocytosis: Bacterial Pathogen Exploitation and Host-Pathogen Interaction.Cells · 2024Review
- The critical roles of caveolin-1 in lung diseases.Frontiers in pharmacology · 2024Review
- An integrated multi-omics analysis of identifies distinct molecular characteristics in pulmonary infections of Pseudomonas aeruginosa.PLoS pathogens · 2023Article
- Review
- Physiological and pathophysiological mechanisms of the molecular and cellular biology of angiogenesis and inflammation in moyamoya angiopathy and related vascular diseases.Frontiers in neurology · 2023Review
- Advances in the role of STAT3 in macrophage polarization.Frontiers in immunology · 2023Review
- TurboID Screening of the OmpP2 Protein Reveals Host Proteins Involved in Recognition and Phagocytosis ofMicrobiology spectrum · 2022Article
- Molecular Mechanisms of Lipid Metabolism Disorders in Infectious Exacerbations of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2021Review
- Quorum Sensing and NF-κB Inhibition of Synthetic Coumaperine Derivatives fromMolecules (Basel, Switzerland) · 2021Article
- Role of Lipid Rafts in Pathogen-Host Interaction - A Mini Review.Frontiers in immunology · 2021Review
- Caveolae and lipid sorting: Shaping the cellular response to stress.The Journal of cell biology · 2020Review
- Article
- The role of SOCS3 in the hypothalamic paraventricular nucleus in rat model of inflammatory pain.Journal of inflammation (London, England) · 2020Article
- Influence of Inflammatory Disease on the Pathophysiology of Moyamoya Disease and Quasi-moyamoya Disease.Neurologia medico-chirurgica · 2019Review
- Article
- Penehyclidine hydrochloride alleviates lipopolysaccharide‑induced acute lung injury in rats: Potential role of caveolin‑1 expression upregulation.International journal of molecular medicine · 2019Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Caveolin-1 (Cav-1), an important composition protein within the flask-shaped membrane invaginations termed caveolae, may play a role in host defense against infections. However, the phenotype in Pseudomonas aeruginosa-infected cav1 knock-out (KO) mice is still unresolved, and the mechanism involved is almost entirely unknown. Using a respiratory infection model, we confirmed a crucial role played by Cav-1 in host defense against this pathogen because Cav-1 KO mice showed increased mortality, severe lung injury, and systemic dissemination as compared with wild-type (WT) littermates. In addition, cav1 KO mice exhibited elevated inflammatory cytokines (IL-6, TNF-α, and IL-12a), decreased phagocytic ability of macrophages, and increased superoxide release in the lung, liver, and kidney. We further studied relevant cellular signaling processes and found that STAT3 and NF-κB are markedly activated. Our data revealed that the Cav-1/STAT3/NF-κB axis is responsible for a dysregulated cytokine response, which contributes to increased mortality and disease progression. Moreover, down-regulating Cav-1 in cell culture with a dominant negative strategy demonstrated that STAT3 activation was essential for the translocation of NF-κB into the nucleus, confirming the observations from cav1 KO mice. Collectively, our studies indicate that Cav-1 is critical for inflammatory responses regulating the STAT3/NF-κB pathway and thereby impacting P. aeruginosa infection.
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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.