Synthesis of IL-6 by Hepatocytes Is a Normal Response to Common Hepatic Stimuli
Identifieur interne : 001077 ( Main/Merge ); précédent : 001076; suivant : 001078Synthesis of IL-6 by Hepatocytes Is a Normal Response to Common Hepatic Stimuli
Auteurs : Callie A. Norris [États-Unis] ; Mu He [États-Unis] ; Liang-I Kang [États-Unis] ; Michael Qi Ding [États-Unis] ; Josiah E. Radder [États-Unis] ; Meagan M. Haynes [États-Unis] ; Yu Yang [États-Unis] ; Shirish Paranjpe [États-Unis] ; William C. Bowen [États-Unis] ; Anne Orr [États-Unis] ; George K. Michalopoulos [États-Unis] ; Donna B. Stolz [États-Unis] ; Wendy M. Mars [États-Unis]Source :
- PLoS ONE [ 1932-6203 ] ; 2014.
Descripteurs français
- KwdFr :
- ARN messager (métabolisme), Animaux, Cellules cultivées, Communication autocrine, Facteur de croissance des hépatocytes (métabolisme), Facteur de croissance des hépatocytes (pharmacologie), Foie (), Foie (immunologie), Foie (métabolisme), Hépatocytes (), Hépatocytes (métabolisme), Interleukine-6 (biosynthèse), Interleukine-6 (génétique), Interleukine-6 (métabolisme), Lipopolysaccharides (pharmacologie), Macrophages (métabolisme), Milieux de culture sans sérum, Rats de lignée F344, Souris de lignée C57BL.
- MESH :
- biosynthèse : Interleukine-6.
- génétique : Interleukine-6.
- immunologie : Foie.
- métabolisme : ARN messager, Facteur de croissance des hépatocytes, Foie, Hépatocytes, Interleukine-6, Macrophages.
- pharmacologie : Facteur de croissance des hépatocytes, Lipopolysaccharides.
- Animaux, Cellules cultivées, Communication autocrine, Foie, Hépatocytes, Milieux de culture sans sérum, Rats de lignée F344, Souris de lignée C57BL.
English descriptors
- KwdEn :
- Animals, Autocrine Communication, Cells, Cultured, Culture Media, Serum-Free, Hepatocyte Growth Factor (metabolism), Hepatocyte Growth Factor (pharmacology), Hepatocytes (drug effects), Hepatocytes (metabolism), Interleukin-6 (biosynthesis), Interleukin-6 (genetics), Interleukin-6 (metabolism), Lipopolysaccharides (pharmacology), Liver (drug effects), Liver (immunology), Liver (metabolism), Macrophages (metabolism), Mice, Inbred C57BL, RNA, Messenger (metabolism), Rats, Inbred F344.
- MESH :
- chemical , biosynthesis : Interleukin-6.
- chemical , genetics : Interleukin-6.
- chemical , metabolism : Hepatocyte Growth Factor, Interleukin-6, RNA, Messenger.
- chemical , pharmacology : Hepatocyte Growth Factor, Lipopolysaccharides.
- chemical : Culture Media, Serum-Free.
- drug effects : Hepatocytes, Liver.
- immunology : Liver.
- metabolism : Hepatocytes, Liver, Macrophages.
- Animals, Autocrine Communication, Cells, Cultured, Mice, Inbred C57BL, Rats, Inbred F344.
Abstract
Exogenous interleukin 6 (IL-6), synthesized at the initiation of the acute phase response, is considered responsible for signaling hepatocytes to produce acute phase proteins. It is widely posited that IL-6 is either delivered to the liver in an endocrine fashion from immune cells at the site of injury, or alternatively, in a paracrine manner by hepatic immune cells within the liver. A recent publication showed there was a muted IL-6 response in lipopolysaccharide (LPS)-injured mice when nuclear NFκB was specifically inactivated in the hepatocytes. This indicates hepatocellular signaling is also involved in regulating the acute phase production of IL-6. Herein, we present extensive
Url:
DOI: 10.1371/journal.pone.0096053
PubMed: 24763697
PubMed Central: 3999098
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PMC:3999098Le document en format XML
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<term>Culture Media, Serum-Free</term>
<term>Hepatocyte Growth Factor (metabolism)</term>
<term>Hepatocyte Growth Factor (pharmacology)</term>
<term>Hepatocytes (drug effects)</term>
<term>Hepatocytes (metabolism)</term>
<term>Interleukin-6 (biosynthesis)</term>
<term>Interleukin-6 (genetics)</term>
<term>Interleukin-6 (metabolism)</term>
<term>Lipopolysaccharides (pharmacology)</term>
<term>Liver (drug effects)</term>
<term>Liver (immunology)</term>
<term>Liver (metabolism)</term>
<term>Macrophages (metabolism)</term>
<term>Mice, Inbred C57BL</term>
<term>RNA, Messenger (metabolism)</term>
<term>Rats, Inbred F344</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (métabolisme)</term>
<term>Animaux</term>
<term>Cellules cultivées</term>
<term>Communication autocrine</term>
<term>Facteur de croissance des hépatocytes (métabolisme)</term>
<term>Facteur de croissance des hépatocytes (pharmacologie)</term>
<term>Foie ()</term>
<term>Foie (immunologie)</term>
<term>Foie (métabolisme)</term>
<term>Hépatocytes ()</term>
<term>Hépatocytes (métabolisme)</term>
<term>Interleukine-6 (biosynthèse)</term>
<term>Interleukine-6 (génétique)</term>
<term>Interleukine-6 (métabolisme)</term>
<term>Lipopolysaccharides (pharmacologie)</term>
<term>Macrophages (métabolisme)</term>
<term>Milieux de culture sans sérum</term>
<term>Rats de lignée F344</term>
<term>Souris de lignée C57BL</term>
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</keywords>
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<term>Interleukin-6</term>
<term>RNA, Messenger</term>
</keywords>
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<term>Lipopolysaccharides</term>
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</keywords>
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<term>Liver</term>
</keywords>
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</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Foie</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Liver</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Hepatocytes</term>
<term>Liver</term>
<term>Macrophages</term>
</keywords>
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<term>Facteur de croissance des hépatocytes</term>
<term>Foie</term>
<term>Hépatocytes</term>
<term>Interleukine-6</term>
<term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Facteur de croissance des hépatocytes</term>
<term>Lipopolysaccharides</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Autocrine Communication</term>
<term>Cells, Cultured</term>
<term>Mice, Inbred C57BL</term>
<term>Rats, Inbred F344</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules cultivées</term>
<term>Communication autocrine</term>
<term>Foie</term>
<term>Hépatocytes</term>
<term>Milieux de culture sans sérum</term>
<term>Rats de lignée F344</term>
<term>Souris de lignée C57BL</term>
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<front><div type="abstract" xml:lang="en"><p>Exogenous interleukin 6 (IL-6), synthesized at the initiation of the acute phase response, is considered responsible for signaling hepatocytes to produce acute phase proteins. It is widely posited that IL-6 is either delivered to the liver in an endocrine fashion from immune cells at the site of injury, or alternatively, in a paracrine manner by hepatic immune cells within the liver. A recent publication showed there was a muted IL-6 response in lipopolysaccharide (LPS)-injured mice when nuclear NFκB was specifically inactivated in the hepatocytes. This indicates hepatocellular signaling is also involved in regulating the acute phase production of IL-6. Herein, we present extensive <italic>in vitro</italic>
and <italic>in vivo</italic>
evidence that normal hepatocytes are directly induced to synthesize IL-6 mRNAs and protein by challenge with LPS, a bacterial hepatotoxin, and by HGF, an important regulator of hepatic homeostasis. As the IL-6 receptor is found on the hepatocyte, these results reveal that induction of the acute phase response can be regulated in an autocrine as well as endocrine/paracrine fashion. Further, herein we provide data indicating that following partial hepatectomy (PHx), HGF differentially regulates IL-6 production in hepatocytes (induces) versus immune cells (suppresses), signifying disparate regulation of the cell sources involved in IL-6 production is a biologically relevant mechanism that has previously been overlooked. These findings have wide ranging ramifications regarding how we currently interpret a variety of <italic>in vivo</italic>
and <italic>in vitro</italic>
biological models involving elements of IL-6 signaling and the hepatic acute phase response.</p>
</div>
</front>
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<author><name sortKey="Apte, U" uniqKey="Apte U">U Apte</name>
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<author><name sortKey="Mars, Wm" uniqKey="Mars W">WM Mars</name>
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<author><name sortKey="Bowen, Wc" uniqKey="Bowen W">WC Bowen</name>
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<author><name sortKey="Luo, Jh" uniqKey="Luo J">JH Luo</name>
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