Calcitriol [1, 25[OH]2 D3] pre- and post-treatment suppresses inflammatory response to influenza A (H1N1) infection in human lung A549 epithelial cells. (Q39270851)

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English	Calcitriol [1, 25[OH]2 D3] pre- and post-treatment suppresses inflammatory response to influenza A (H1N1) infection in human lung A549 epithelial cells.	scientific article

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9 March 2020

Calcitriol [1, 25[OH]2 D3] pre- and post-treatment suppresses inflammatory response to influenza A (H1N1) infection in human lung A549 epithelial cells (English)

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Europe PubMed Central

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https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:23015061%20AND%20SRC:MED&resulttype=core&format=json

9 March 2020

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Drirh Khare

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9 March 2020

Nachiket M Godbole

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9 March 2020

Shailesh D Pawar

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9 March 2020

Gaurav Pandey

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9 March 2020

Sushil Gupta

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9 March 2020

Deepak Kumar

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9 March 2020

Madan M Godbole

9

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9 March 2020

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27 September 2012

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9 March 2020

European Journal of Nutrition

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9 March 2020

52

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9 March 2020

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9 March 2020

1405-1415

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9 March 2020

Cellular transcriptional profiling in influenza A virus-infected lung epithelial cells: the role of the nonstructural NS1 protein in the evasion of the host innate defense and its potential contribution to pandemic influenza

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Serologic cross-reactivity with pandemic (H1N1) 2009 virus in pigs, Europe.

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Influenza virus coinfection with Bordetella bronchiseptica enhances bacterial colonization and host responses exacerbating pulmonary lesions

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Association between serum 25-hydroxyvitamin D level and upper respiratory tract infection in the Third National Health and Nutrition Examination Survey

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Epidemic influenza and vitamin D

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Association of subclinical vitamin D deficiency with severe acute lower respiratory infection in Indian children under 5 y.

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Influenza virus activates inflammasomes via its intracellular M2 ion channel

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Mechanisms of nutrient modulation of the immune response

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On the epidemiology of influenza

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21 January 2018

Respiratory epithelial cells convert inactive vitamin D to its active form: potential effects on host defense

1 reference

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21 January 2018

Vitamin D decreases respiratory syncytial virus induction of NF-kappaB-linked chemokines and cytokines in airway epithelium while maintaining the antiviral state

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Autophagy, apoptosis, and the influenza virus M2 protein

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Autophagy is involved in influenza A virus replication

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Matrix protein 2 of influenza A virus blocks autophagosome fusion with lysosomes.

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Th17 cells: effector T cells with inflammatory properties

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21 January 2018

Innate immune control and regulation of influenza virus infections

1 reference

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Interleukin-17 and type 17 helper T cells

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21 January 2018

Delayed clearance of viral load and marked cytokine activation in severe cases of pandemic H1N1 2009 influenza virus infection.

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Clinical aspects and cytokine response in severe H1N1 influenza A virus infection

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Key role of regulated upon activation normal T-cell expressed and secreted, nonstructural protein1 and myeloperoxidase in cytokine storm induced by influenza virus PR-8 (A/H1N1) infection in A549 bronchial epithelial cells

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Antioxidant therapy as a potential approach to severe influenza-associated complications

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Inhibition of RANTES expression by indirubin in influenza virus-infected human bronchial epithelial cells

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Interferon targeted genes in host defense

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Parathyroid hormone decreases renal vitamin D receptor expression in vivo

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Vitamin D3 down-regulates monocyte TLR expression and triggers hyporesponsiveness to pathogen-associated molecular patterns.

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Parathyroid hormone down-regulates 1,25-dihydroxyvitamin D receptors (VDR) and VDR messenger ribonucleic acid in vitro and blocks homologous up-regulation of VDR in vivo

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Serum 25-hydroxyvitamin d and the incidence of acute viral respiratory tract infections in healthy adults

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Variations in Vitamin D Production Could Possibly Explain the Seasonality of Childhood Respiratory Infections in Hawaii

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Parathyroid hormone prevents 1,25 (OH)2D3 induced down-regulation of the vitamin D receptor in growth plate chondrocytes in vitro

1 reference

https://pubmed.ncbi.nlm.nih.gov/23015061

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1 reference

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10.1007/S00394-012-0449-7

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9 March 2020

release_y6gu3bgxxfbldfo5xlkwge7gdy

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24 November 2022

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9 March 2020

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