Linoleic acid metabolite drives severe asthma by causing airway epithelial injury
Mabalirajan U, Rehman R, Ahmad T, Kumar S, Singh S, Leishangthem GD, Aich J, Kumar M, Khanna K, Singh VP, Dinda AK, Biswal S, Agrawal A, Ghosh B
Scientific reports · 99 citas
Cómo se estudió
- Diseño
- Estudio en animales (clasificado por nuestro filtro de IA)
- Estudiado en
- Personas, más trabajo en animales o laboratorio
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- Council of Scientific and Industrial Research, India
- Subvenciones
- Council of Scientific and Industrial Research, India (MLP5502)
Según 1 financiador declarado y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2013-02-27 · Sci Rep · vol. 3 · número 1 · pág. 1349
- Editorial
- Nature Portfolio
- Citado
- 116 citas · más que el 96% de estudios similares · 5.3× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 47 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY-NC-ND
- Áreas de investigación
- Asthma and respiratory diseases · Ion Channels and Receptors · Respiratory and Cough-Related Research
- Palabras clave
- Proinflammatory cytokine, Airway, Medicine, Neutrophilia, Asthma, Inflammation, Immunology, TRPV1, Respiratory epithelium, Lung, Bronchoconstriction, Pathogenesis, Transient receptor potential channel, Receptor, Anesthesia, Internal medicine
- MeSH
- respiratory mucosa, neutrophils, extracellular space, mitochondria, animals, mice, inbred balb c, humans, mice, asthma, disease models, animal, calcium, fatty acids, unsaturated, linoleic acid, species specificity, trpv cation channels, gene knockdown techniques
14 autores
- Ulaganathan Mabalirajan🇮🇳Institute of Genomics and Integrative Biology
- Rakhshinda Rehman🇮🇳Institute of Genomics and Integrative Biology
- Tanveer Ahmad🇮🇳Institute of Genomics and Integrative Biology
- Sarvesh Kumar🇺🇸Johns Hopkins University
- Suchita Singh🇮🇳Institute of Genomics and Integrative Biology
- Geeta Devi Leishangthem🇮🇳All India Institute of Medical Sciences
- Jyotirmoi Aich🇮🇳Institute of Genomics and Integrative Biology
- Manish Kumar🇮🇳Institute of Genomics and Integrative Biology
- Kritika Khanna🇮🇳Institute of Genomics and Integrative Biology
- Vijay Pal Singh🇮🇳Institute of Genomics and Integrative Biology
- Amit Kumar Dinda🇮🇳All India Institute of Medical Sciences
- Shyam S. Biswal🇺🇸Johns Hopkins University
- Anurag Agrawal🇮🇳Institute of Genomics and Integrative Biology
- Balaram Ghosh🇮🇳Institute of Genomics and Integrative Biology
Resumen
El texto original del estudio, en el idioma en que se publicó.
Airway epithelial injury is the hallmark of various respiratory diseases, but its mechanisms remain poorly understood. While 13-S-hydroxyoctadecadienoic acid (13-S-HODE) is produced in high concentration during mitochondrial degradation in reticulocytes little is known about its role in asthma pathogenesis. Here, we show that extracellular 13-S-HODE induces mitochondrial dysfunction and airway epithelial apoptosis. This is associated with features of severe airway obstruction, lung remodeling, increase in epithelial stress related proinflammatory cytokines and drastic airway neutrophilia in mouse. Further, 13-S-HODE induced features are attenuated by inhibiting Transient Receptor Potential Cation Channel, Vanilloid-type 1 (TRPV1) both in mouse model and human bronchial epithelial cells. These findings are relevant to human asthma, as 13-S-HODE levels are increased in human asthmatic airways. Blocking of 13-S-HODE activity or disruption of TRPV1 activity attenuated airway injury and asthma mimicking features in murine allergic airway inflammation. These findings indicate that 13-S-HODE induces mitochondrial dysfunction and airway epithelial injury.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY-NC-ND).
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