About: Streptococcus pneumoniae induced c-Jun-N-terminal kinase- and AP-1 -dependent IL-8 release by lung epithelial BEAS-2B cells

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About: Streptococcus pneumoniae induced c-Jun-N-terminal kinase- and AP-1 -dependent IL-8 release by lung epithelial BEAS-2B cells Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Streptococcus pneumoniae induced c-Jun-N-terminal kinase- and AP-1 -dependent IL-8 release by lung epithelial BEAS-2B cells
Creator	Hippenstiel, Stefan Opitz, Bastian Suttorp, Norbert Schmeck, Bernd Moog, Kerstin Rosseau, Simone Zahlten, Janine De, De;, De;, Janine De;, Kerstin De;, Philippe De;, Vincent Dje N', Guessan -Dje_Philippe Dje N'guessan, Philippe Hippenstiel@charite, Stefan Moog, Moog@charite, Kerstin Nguessan@charite, Schmeck@charite, Bernd Van Laak, Vincent Van, Laak -Vincent Zahlten, Zahlten@charite, Janine
Source	Medline; PMC
abstract	BACKGROUND: Although pneumococcal pneumonia is one of the most common causes of death due to infectious diseases, little is known about pneumococci-lung cell interaction. Herein we tested the hypothesis that pneumococci activated pulmonary epithelial cell cytokine release by c-Jun-NH(2)-terminal kinase (JNK) METHODS: Human bronchial epithelial cells (BEAS-2B) or epithelial HEK293 cells were infected with S. pneumoniae R6x and cytokine induction was measured by RT-PCR, ELISA and Bioplex assay. JNK-phosphorylation was detected by Western blot and nuclear signaling was assessed by electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP). JNK was modulated by the small molecule inhibitor SP600125 and AP1 by transfection of a dominant negative mutant. RESULTS: S. pneumoniae induced the release of distinct CC and CXC, as well as Th1 and Th2 cytokines and growth factors by human lung epithelial cell line BEAS-2B. Furthermore, pneumococci infection resulted in JNK phosphorylation in BEAS-2B cells. Inhibition of JNK by small molecule inhibitor SP600125 reduced pneumococci-induced IL-8 mRNA expression and release of IL-8 and IL-6. One regulator of the il8 promoter is JNK-phosphorylated activator protein 1 (AP-1). We showed that S. pneumoniae time-dependently induced DNA binding of AP-1 and its phosphorylated subunit c-Jun with a maximum at 3 to 5 h after infection. Recruitment of Ser(63/73)-phosphorylated c-Jun and RNA polymerase II to the endogenous il8 promoter was found 2 h after S. pneumoniae infection by chromatin immunoprecipitation. AP-1 repressor A-Fos reduced IL-8 release by TLR2-overexpressing HEK293 cells induced by pneumococci but not by TNFα. Antisense-constructs targeting the AP-1 subunits Fra1 and Fra2 had no inhibitory effect on pneumococci-induced IL-8 release. CONCLUSION: S. pneumoniae-induced IL-8 expression by human epithelial BEAS-2B cells depended on activation of JNK and recruitment of phosphorylated c-Jun to the il8 promoter.
has issue date	2006-07-12(xsd:dateTime)
bibo:doi	10.1186/1465-9921-7-98
bibo:pmid	16834785
has license	cc-by
sha1sum (hex)	104a23fead757f1b8272ae0813db98b413375ae0
schema:url	https://doi.org/10.1186/1465-9921-7-98
resource representing a document's title	Streptococcus pneumoniae induced c-Jun-N-terminal kinase- and AP-1 -dependent IL-8 release by lung epithelial BEAS-2B cells
has PubMed Central identifier	PMC1533820
has PubMed identifier	16834785
schema:publication	Respir Res
resource representing a document's body	covid:104a23fead757f1b8272ae0813db98b413375ae0#body_text
is schema:about of	named entity 'EMSA' named entity 'epithelial cell' named entity 'cytokine' named entity 'ChIP' named entity 'mutant' named entity 'pneumococcal pneumonia' named entity 'RESPIRATORY' named entity 'C-JUN' named entity 'DETECTED' named entity 'CYTOKINE RELEASE' named entity 'KINASE' named entity 'AP-1' named entity 'CELLS' named entity 'LUNG' named entity 'CYTOKINE ' named entity 'ASSESSED' named entity 'CHROMATIN IMMUNOPRECIPITATION' named entity 'LUNG' named entity 'TERMINAL' named entity 'EPITHELIAL' named entity 'BRONCHIAL' named entity 'ACTIVATED' named entity 'SMALL MOLECULE INHIBITOR' named entity 'C-JUN' named entity 'N-TERMINAL ' named entity 'TRANSFECTION' named entity 'ABOUT' named entity 'INTERACTION' named entity 'ELISA' named entity 'HUMAN' named entity 'INDUCED' named entity 'EPITHELIAL' named entity 'DEPENDENT' named entity 'STREPTOCOCCUS PNEUMONIAE' named entity 'LITTLE' named entity 'CELL' named entity 'WESTERN BLOT' named entity 'MODULATED' named entity 'HEK293 CELLS' named entity 'METHODS' named entity 'INFECTIOUS DISEASES' named entity 'ASSAY' named entity 'MEASURED' named entity 'ELECTROPHORETIC MOBILITY SHIFT ASSAY ' named entity 'BIOPLEX' named entity 'AP1' named entity 'INDUCTION' named entity 'PNEUMOCOCCAL PNEUMONIA' named entity 'NUCLEAR SIGNALING' named entity 'JNK' named entity 'CAUSES OF DEATH' named entity 'INFECTED' named entity 'RT-PCR' named entity 'KNOWN' named entity 'HYPOTHESIS' named entity 'DUE TO' named entity 'DOMINANT NEGATIVE MUTANT' named entity 'COMMON'

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