ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
Adaptation to chronic hypoxia involves immune cell invasion and increased expression of inflammatory cytokines in rat carotid body.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 96 citations in OpenAlex.
- Trial
- Dexamethasone mimics aspects of physiological acclimatization to 8 hours of hypoxia but suppresses plasma erythropoietin.Journal of applied physiology (Bethesda, Md. : 1985) · 2013Trial
- Translating physiology of the arterial chemoreflex into novel therapeutic interventions targeting carotid bodies in cardiometabolic disorders.The Journal of physiology · 2025Review
- Interleukins expression by rat Lymphocytes exposed to chronic intermittent normobaric hypoxia.Frontiers in physiology · 2025Article
- Altered control of breathing in a rat model of allergic lower airway inflammation.Journal of neurophysiology · 2024Article
- Molecular signaling and clinical implications in the human aging-cancer cycle.Seminars in cancer biology · 2024Review
- Hypoxic Signaling Pathways in Carotid Body Tumors.Cancers · 2024Review
- Article
- Neurochemical Plasticity of the Carotid Body.Advances in anatomy, embryology, and cell biology · 2023Article
- Causes of Hypoxemia in COVID-19.Journal of evolutionary biochemistry and physiology · 2022Article
- Cellular basis of learning and memory in the carotid body.Frontiers in synaptic neuroscience · 2022Review
- Adaptive cardiorespiratory changes to chronic continuous and intermittent hypoxia.Handbook of clinical neurology · 2022Review
- The Role of Pharmacological Treatment in the Chemoreflex Modulation.Frontiers in physiology · 2022Review
- A Comparative Assessment of Effects of Major Mediators of Acute Phase Response (IL-1, TNF-α, IL-6) on Breathing Pattern and Survival Rate in Rats with Acute Progressive Hypoxia.Journal of evolutionary biochemistry and physiology · 2021Article
- Immunity and the carotid body: implications for metabolic diseases.Bioelectronic medicine · 2020Review
- Growth Factors in the Carotid Body-An Update.International journal of molecular sciences · 2020Review
- Exploring the Mediators that Promote Carotid Body Dysfunction in Type 2 Diabetes and Obesity Related Syndromes.International journal of molecular sciences · 2020Review
- Ventilatory and carotid body responses to acute hypoxia in rats exposed to chronic hypoxia during the first and second postnatal weeks.Respiratory physiology & neurobiology · 2020Article
- Carotid bodies contribute to sympathoexcitation induced by acute salt overload.Experimental physiology · 2019Article
- Cancer stem cells as key drivers of tumour progression.Journal of biomedical science · 2018Review
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5 authors at 1 institution in 1 country.
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Abstract
Exposure to chronic hypoxia (CH; 3-28 days at 380 Torr) induces adaptation in mammalian carotid body such that following CH an acute hypoxic challenge elicits an abnormally large increase in carotid sinus nerve impulse activity. The current study examines the hypothesis that CH initiates an immune response in the carotid body and that chemoreceptor hyperexcitability is dependent on the expression and action of inflammatory cytokines. CH resulted in a robust invasion of ED1(+) macrophages, which peaked on day 3 of exposure. Gene expression of proinflammatory cytokines, IL-1beta, TNFalpha, and the chemokine, monocyte chemoattractant protein-1, was increased >2-fold after 1 day of hypoxia followed by a >2-fold increase in IL-6 on day 3. After 28 days of CH, IL-6 remained elevated >5-fold, whereas expression of other cytokines recovered to normal levels. Cytokine expression was not restricted to immune cells. Studies of cultured type I cells harvested following 1 day of in vivo hypoxia showed elevated transcript levels of inflammatory cytokines. In situ hybridization studies confirmed expression of IL-6 in type I cells and also showed that CH induces IL-6 expression in supporting type II cells. Concurrent treatment of CH rats with anti-inflammatory drugs (ibuprofen or dexamethasone) blocked immune cell invasion and severely reduced CH-induced cytokine expression in carotid body. Drug treatment also blocked the development of chemoreceptor hypersensitivity in CH animals. Our findings indicate that chemoreceptor adaptation involves novel neuroimmune mechanisms, which may alter the functional phenotypes of type I cells and chemoafferent neurons.
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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.