FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2116569673> ?p ?o ?g. }

• W2116569673 endingPage "301" @default.
• W2116569673 startingPage "290" @default.
• W2116569673 abstract "Neutrophil depleted mice are protected from concanavalin A-mediated hepatitis, showing that neutrophils are critical for cellular liver damage. Interleukin-6 has pro- and anti-inflammatory properties and mediates neutrophil recruitment in diseases such as rheumatoid arthritis. In classic signaling, interleukin-6 binds to the membrane-bound interleukin-6-receptor and initiates signaling via gp130. In interleukin-6 trans-signaling, the agonistic soluble interleukin-6-receptor can form a soluble interleukin-6/interleukin-6-receptor complex and stimulate cells which only express gp130 but no interleukin-6-receptor. Interleukin-6 trans-signaling was shown to be important for liver regeneration and development of liver adenomas. Here, we show that blocking classic interleukin-6 signaling but not interleukin-6 trans-signaling reduced concanavalin A-induced liver damage in mice, with reduced liver STAT3 phosphorylation and liver neutrophil accumulation. However, the level of neutrophil-attracting chemokine KC is only reduced by inhibition of interleukin-6 trans-signaling. Analysis of circulating neutrophils after concanavalin A challenge revealed that classic interleukin-6 signaling is required for the mobilization of blood neutrophils. Reduced neutrophil infiltration was accompanied by increased levels of hepatoprotective monocyte chemoattractant protein-1 and reduced level of hepatodestructive interleukin-4. Abrogated classic interleukin-6 signaling in concanavalin A-mediated hepatitis exhibited liver-protective effects indicating that interleukin-6 classic but not interleukin-6 trans-signaling is responsible for liver damage. Classic interleukin-6 signaling is required to mount an efficient neutrophilia during concanavalin A-induced immune response, which might have clinical implications in the regard that blocking global interleukin-6 signaling pathways is a treatment option in different chronic inflammatory diseases. ►Blocking classic IL-6 signaling reduced ConA-induced liver damage. ►Blocking IL-6 trans-signaling has no effect on ConA-induced liver damage. ►IL-6 blockade led to reduced liver infiltrating neutrophils. ►Classic IL-6 signaling is required for the mobilization of blood neutrophils. ►IL-6 blockade led to increased MCP-1 and reduced IL-4." @default.
• W2116569673 created "2016-06-24" @default.
• W2116569673 creator A5013428965 @default.
• W2116569673 creator A5025552082 @default.
• W2116569673 creator A5028364627 @default.
• W2116569673 creator A5031353542 @default.
• W2116569673 creator A5035884358 @default.
• W2116569673 creator A5054515511 @default.
• W2116569673 creator A5073346179 @default.
• W2116569673 creator A5088470216 @default.
• W2116569673 creator A5089057275 @default.
• W2116569673 date "2011-03-01" @default.
• W2116569673 modified "2023-09-25" @default.
• W2116569673 title "Essential role of neutrophil mobilization in concanavalin A-induced hepatitis is based on classic IL-6 signaling but not on IL-6 trans-signaling" @default.
• W2116569673 cites W1571743853 @default.
• W2116569673 cites W1597588755 @default.
• W2116569673 cites W1602943807 @default.
• W2116569673 cites W1776476655 @default.
• W2116569673 cites W1877916940 @default.
• W2116569673 cites W1878983031 @default.
• W2116569673 cites W190052799 @default.
• W2116569673 cites W2007268662 @default.
• W2116569673 cites W2020798985 @default.
• W2116569673 cites W2036988498 @default.
• W2116569673 cites W2038479043 @default.
• W2116569673 cites W2045510035 @default.
• W2116569673 cites W2046169019 @default.
• W2116569673 cites W2055253557 @default.
• W2116569673 cites W2055560719 @default.
• W2116569673 cites W2058529396 @default.
• W2116569673 cites W2067761476 @default.
• W2116569673 cites W2101596544 @default.
• W2116569673 cites W2105620133 @default.
• W2116569673 cites W2107682360 @default.
• W2116569673 cites W2110523291 @default.
• W2116569673 cites W2115116869 @default.
• W2116569673 cites W2117521006 @default.
• W2116569673 cites W2128673878 @default.
• W2116569673 cites W2131520834 @default.
• W2116569673 cites W2138453840 @default.
• W2116569673 cites W2150737557 @default.
• W2116569673 cites W2154923159 @default.
• W2116569673 cites W2163712919 @default.
• W2116569673 cites W2165893090 @default.
• W2116569673 cites W2295791300 @default.
• W2116569673 cites W4229751290 @default.
• W2116569673 cites W4238652665 @default.
• W2116569673 doi "https://doi.org/10.1016/j.bbadis.2010.11.009" @default.
• W2116569673 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21130161" @default.
• W2116569673 hasPublicationYear "2011" @default.
• W2116569673 type Work @default.
• W2116569673 sameAs 2116569673 @default.
• W2116569673 citedByCount "28" @default.
• W2116569673 countsByYear W21165696732012 @default.
• W2116569673 countsByYear W21165696732013 @default.
• W2116569673 countsByYear W21165696732014 @default.
• W2116569673 countsByYear W21165696732015 @default.
• W2116569673 countsByYear W21165696732016 @default.
• W2116569673 countsByYear W21165696732017 @default.
• W2116569673 countsByYear W21165696732018 @default.
• W2116569673 countsByYear W21165696732019 @default.
• W2116569673 countsByYear W21165696732020 @default.
• W2116569673 countsByYear W21165696732021 @default.
• W2116569673 countsByYear W21165696732022 @default.
• W2116569673 countsByYear W21165696732023 @default.
• W2116569673 crossrefType "journal-article" @default.
• W2116569673 hasAuthorship W2116569673A5013428965 @default.
• W2116569673 hasAuthorship W2116569673A5025552082 @default.
• W2116569673 hasAuthorship W2116569673A5028364627 @default.
• W2116569673 hasAuthorship W2116569673A5031353542 @default.
• W2116569673 hasAuthorship W2116569673A5035884358 @default.
• W2116569673 hasAuthorship W2116569673A5054515511 @default.
• W2116569673 hasAuthorship W2116569673A5073346179 @default.
• W2116569673 hasAuthorship W2116569673A5088470216 @default.
• W2116569673 hasAuthorship W2116569673A5089057275 @default.
• W2116569673 hasConcept C126037660 @default.
• W2116569673 hasConcept C149892131 @default.
• W2116569673 hasConcept C170493617 @default.
• W2116569673 hasConcept C19869320 @default.
• W2116569673 hasConcept C202751555 @default.
• W2116569673 hasConcept C203014093 @default.
• W2116569673 hasConcept C2776885963 @default.
• W2116569673 hasConcept C2777977768 @default.
• W2116569673 hasConcept C2778122271 @default.
• W2116569673 hasConcept C2778690821 @default.
• W2116569673 hasConcept C2778923194 @default.
• W2116569673 hasConcept C55493867 @default.
• W2116569673 hasConcept C62478195 @default.
• W2116569673 hasConcept C74172505 @default.
• W2116569673 hasConcept C86803240 @default.
• W2116569673 hasConcept C95444343 @default.
• W2116569673 hasConceptScore W2116569673C126037660 @default.
• W2116569673 hasConceptScore W2116569673C149892131 @default.
• W2116569673 hasConceptScore W2116569673C170493617 @default.
• W2116569673 hasConceptScore W2116569673C19869320 @default.
• W2116569673 hasConceptScore W2116569673C202751555 @default.
• W2116569673 hasConceptScore W2116569673C203014093 @default.
• W2116569673 hasConceptScore W2116569673C2776885963 @default.

• next