FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2325834977> ?p ?o ?g. }

• W2325834977 endingPage "5" @default.
• W2325834977 startingPage "5" @default.
• W2325834977 abstract "Pneumococcal infections are the leading cause of community-acquired pneumonia. Although the type 1 interferon-α (IFN-α) is a well-known antiviral cytokine, the role of IFN-α in antipneumococcal host defense and its therapeutic potential remain poorly understood. We have investigated these issues by using a murine transgene expression model. We found that in control animals, Streptococcus pneumoniae infection caused severe weight loss and excessive lung inflammation, associated with rapid bacterial outgrowth. In contrast, the animals that received a single dose of an adenoviral vector expressing IFN-α prior to pneumococcal infection demonstrated rapid and effective control of bacterial replication and lung inflammation and improved clinical outcome. Enhanced protection by IFN-α was due to increased activation of neutrophils and macrophages with increased release of reactive oxygen and nitrogen species and bacterial killing. Furthermore, we found that raised levels of IFN-α in the lung remained immune protective even when the gene transfer vector was given at a time postpneumococcal infection. Our study thus shows that the classically antiviral type 1 IFN can be exploited for enhancing immunity against pneumococcal infection via its activating effects on innate immune cells. Our findings hold implications for the therapeutic use of IFN-α gene transfer strategies to combat pneumococcal infections. Pneumococcal infections are the leading cause of community-acquired pneumonia. Although the type 1 interferon-α (IFN-α) is a well-known antiviral cytokine, the role of IFN-α in antipneumococcal host defense and its therapeutic potential remain poorly understood. We have investigated these issues by using a murine transgene expression model. We found that in control animals, Streptococcus pneumoniae infection caused severe weight loss and excessive lung inflammation, associated with rapid bacterial outgrowth. In contrast, the animals that received a single dose of an adenoviral vector expressing IFN-α prior to pneumococcal infection demonstrated rapid and effective control of bacterial replication and lung inflammation and improved clinical outcome. Enhanced protection by IFN-α was due to increased activation of neutrophils and macrophages with increased release of reactive oxygen and nitrogen species and bacterial killing. Furthermore, we found that raised levels of IFN-α in the lung remained immune protective even when the gene transfer vector was given at a time postpneumococcal infection. Our study thus shows that the classically antiviral type 1 IFN can be exploited for enhancing immunity against pneumococcal infection via its activating effects on innate immune cells. Our findings hold implications for the therapeutic use of IFN-α gene transfer strategies to combat pneumococcal infections." @default.
• W2325834977 created "2016-06-24" @default.
• W2325834977 creator A5005295653 @default.
• W2325834977 creator A5010566259 @default.
• W2325834977 creator A5061306534 @default.
• W2325834977 creator A5072686480 @default.
• W2325834977 creator A5078020142 @default.
• W2325834977 creator A5086485401 @default.
• W2325834977 creator A5087826169 @default.
• W2325834977 date "2014-01-01" @default.
• W2325834977 modified "2023-10-01" @default.
• W2325834977 title "Type 1 interferon gene transfer enhances host defense against pulmonary Streptococcus pneumoniae infection via activating innate leukocytes" @default.
• W2325834977 cites W1661717153 @default.
• W2325834977 cites W1957173764 @default.
• W2325834977 cites W1966683713 @default.
• W2325834977 cites W1978151323 @default.
• W2325834977 cites W1988872232 @default.
• W2325834977 cites W2010288671 @default.
• W2325834977 cites W2031120873 @default.
• W2325834977 cites W2042166646 @default.
• W2325834977 cites W2055752749 @default.
• W2325834977 cites W2059359470 @default.
• W2325834977 cites W2068678093 @default.
• W2325834977 cites W2082889122 @default.
• W2325834977 cites W2108162055 @default.
• W2325834977 cites W2113075037 @default.
• W2325834977 cites W2118519438 @default.
• W2325834977 cites W2121369371 @default.
• W2325834977 cites W2122758441 @default.
• W2325834977 cites W2123710681 @default.
• W2325834977 cites W2130419890 @default.
• W2325834977 cites W2145435157 @default.
• W2325834977 cites W2146769688 @default.
• W2325834977 cites W80494079 @default.
• W2325834977 doi "https://doi.org/10.1038/mtm.2014.5" @default.
• W2325834977 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4378291" @default.
• W2325834977 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26015944" @default.
• W2325834977 hasPublicationYear "2014" @default.
• W2325834977 type Work @default.
• W2325834977 sameAs 2325834977 @default.
• W2325834977 citedByCount "20" @default.
• W2325834977 countsByYear W23258349772014 @default.
• W2325834977 countsByYear W23258349772015 @default.
• W2325834977 countsByYear W23258349772016 @default.
• W2325834977 countsByYear W23258349772017 @default.
• W2325834977 countsByYear W23258349772018 @default.
• W2325834977 countsByYear W23258349772019 @default.
• W2325834977 countsByYear W23258349772020 @default.
• W2325834977 countsByYear W23258349772021 @default.
• W2325834977 countsByYear W23258349772022 @default.
• W2325834977 countsByYear W23258349772023 @default.
• W2325834977 crossrefType "journal-article" @default.
• W2325834977 hasAuthorship W2325834977A5005295653 @default.
• W2325834977 hasAuthorship W2325834977A5010566259 @default.
• W2325834977 hasAuthorship W2325834977A5061306534 @default.
• W2325834977 hasAuthorship W2325834977A5072686480 @default.
• W2325834977 hasAuthorship W2325834977A5078020142 @default.
• W2325834977 hasAuthorship W2325834977A5086485401 @default.
• W2325834977 hasAuthorship W2325834977A5087826169 @default.
• W2325834977 hasBestOaLocation W23258349771 @default.
• W2325834977 hasConcept C126322002 @default.
• W2325834977 hasConcept C136449434 @default.
• W2325834977 hasConcept C159047783 @default.
• W2325834977 hasConcept C203014093 @default.
• W2325834977 hasConcept C2776152631 @default.
• W2325834977 hasConcept C2776178377 @default.
• W2325834977 hasConcept C2777914695 @default.
• W2325834977 hasConcept C2779892413 @default.
• W2325834977 hasConcept C2780841837 @default.
• W2325834977 hasConcept C2781253189 @default.
• W2325834977 hasConcept C501593827 @default.
• W2325834977 hasConcept C71924100 @default.
• W2325834977 hasConcept C86803240 @default.
• W2325834977 hasConcept C8891405 @default.
• W2325834977 hasConcept C89423630 @default.
• W2325834977 hasConceptScore W2325834977C126322002 @default.
• W2325834977 hasConceptScore W2325834977C136449434 @default.
• W2325834977 hasConceptScore W2325834977C159047783 @default.
• W2325834977 hasConceptScore W2325834977C203014093 @default.
• W2325834977 hasConceptScore W2325834977C2776152631 @default.
• W2325834977 hasConceptScore W2325834977C2776178377 @default.
• W2325834977 hasConceptScore W2325834977C2777914695 @default.
• W2325834977 hasConceptScore W2325834977C2779892413 @default.
• W2325834977 hasConceptScore W2325834977C2780841837 @default.
• W2325834977 hasConceptScore W2325834977C2781253189 @default.
• W2325834977 hasConceptScore W2325834977C501593827 @default.
• W2325834977 hasConceptScore W2325834977C71924100 @default.
• W2325834977 hasConceptScore W2325834977C86803240 @default.
• W2325834977 hasConceptScore W2325834977C8891405 @default.
• W2325834977 hasConceptScore W2325834977C89423630 @default.
• W2325834977 hasLocation W23258349771 @default.
• W2325834977 hasLocation W23258349772 @default.
• W2325834977 hasLocation W23258349773 @default.
• W2325834977 hasOpenAccess W2325834977 @default.
• W2325834977 hasPrimaryLocation W23258349771 @default.
• W2325834977 hasRelatedWork W1556863319 @default.
• W2325834977 hasRelatedWork W1905511256 @default.
• W2325834977 hasRelatedWork W1975031531 @default.

• next