Legionella pneumophila infection-mediated regulation of RICTOR via miR-218 in U937 macrophage cells.
Identifieur interne : 000396 ( Main/Corpus ); précédent : 000395; suivant : 000397Legionella pneumophila infection-mediated regulation of RICTOR via miR-218 in U937 macrophage cells.
Auteurs : Toyoyasu Koriyama ; Munekazu Yamakuchi ; Kazunori Takenouchi ; Yoko Oyama ; Hiroyoshi Takenaka ; Takumi Nagakura ; Izumi Masamoto ; Teruto HashiguchiSource :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2019.
English descriptors
- KwdEn :
- Cytokines (MeSH), Host-Pathogen Interactions (MeSH), Humans (MeSH), Inflammation (MeSH), Legionella pneumophila (MeSH), Legionnaires' Disease (metabolism), Legionnaires' Disease (pathology), Legionnaires' Disease (virology), Macrophages (metabolism), Macrophages (microbiology), Macrophages (pathology), MicroRNAs (analysis), MicroRNAs (metabolism), RNA, Messenger (analysis), Rapamycin-Insensitive Companion of mTOR Protein (metabolism), U937 Cells (MeSH).
- MESH :
- chemical , analysis : MicroRNAs, RNA, Messenger.
- chemical , metabolism : MicroRNAs, Rapamycin-Insensitive Companion of mTOR Protein.
- chemical : Cytokines.
- metabolism : Legionnaires' Disease, Macrophages.
- microbiology : Macrophages.
- pathology : Legionnaires' Disease, Macrophages.
- virology : Legionnaires' Disease.
- Host-Pathogen Interactions, Humans, Inflammation, Legionella pneumophila, U937 Cells.
Abstract
BACKGROUND
Inhalation of aerosolized Legionella pneumophila, a Gram-negative bacterium, can cause severe pneumonia. During infection, L. pneumophila replicates intracellularly in macrophages. The involvement of host microRNAs (miRNAs) in L. pneumophila infection is not fully understood.
METHODS
The human macrophage-like cell line U937 was infected with L. pneumophila. The levels of miRNA and messenger RNA (mRNA) were measured using reverse transcriptase polymerase chain reaction. Release of lactate dehydrogenase was used to evaluate cytotoxicity. The expression of RICTOR and related proteins was examined by western blotting of cell lysates.
RESULTS
L. pneumophila infection upregulated the expression of miR-218 and the host genes SLIT2 and SLIT3 in U937 cells. The expression of RICTOR, a component of the mechanistic target of rapamycin complex 2 (mTORC2), decreased during L. pneumophila infection. RICTOR protein expression was inhibited by the overexpression of miR-218, whereas knockdown of miR-218 restored the downregulation of RICTOR by L. pneumophila. L. pneumophila infection induced the expression of the proinflammatory cytokines IL-6 and TNF-alpha, which was modulated by knockdown of miR-218 or RICTOR.
CONCLUSIONS
Our study revealed the involvement of miR-218 in regulating the inflammatory response of macrophages against L. pneumophila infection. These findings suggest potential novel roles for miR-218 and RICTOR as therapeutic targets of L. pneumophila infection.
DOI: 10.1016/j.bbrc.2018.11.093
PubMed: 30509489
Links to Exploration step
pubmed:30509489Le document en format XML
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<author><name sortKey="Yamakuchi, Munekazu" sort="Yamakuchi, Munekazu" uniqKey="Yamakuchi M" first="Munekazu" last="Yamakuchi">Munekazu Yamakuchi</name>
<affiliation><nlm:affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan. Electronic address: munekazu@m.kufm.kagoshima-u.ac.jp.</nlm:affiliation>
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<author><name sortKey="Takenouchi, Kazunori" sort="Takenouchi, Kazunori" uniqKey="Takenouchi K" first="Kazunori" last="Takenouchi">Kazunori Takenouchi</name>
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<author><name sortKey="Takenaka, Hiroyoshi" sort="Takenaka, Hiroyoshi" uniqKey="Takenaka H" first="Hiroyoshi" last="Takenaka">Hiroyoshi Takenaka</name>
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<author><name sortKey="Nagakura, Takumi" sort="Nagakura, Takumi" uniqKey="Nagakura T" first="Takumi" last="Nagakura">Takumi Nagakura</name>
<affiliation><nlm:affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.</nlm:affiliation>
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<author><name sortKey="Masamoto, Izumi" sort="Masamoto, Izumi" uniqKey="Masamoto I" first="Izumi" last="Masamoto">Izumi Masamoto</name>
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<author><name sortKey="Hashiguchi, Teruto" sort="Hashiguchi, Teruto" uniqKey="Hashiguchi T" first="Teruto" last="Hashiguchi">Teruto Hashiguchi</name>
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<author><name sortKey="Yamakuchi, Munekazu" sort="Yamakuchi, Munekazu" uniqKey="Yamakuchi M" first="Munekazu" last="Yamakuchi">Munekazu Yamakuchi</name>
<affiliation><nlm:affiliation>Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan. Electronic address: munekazu@m.kufm.kagoshima-u.ac.jp.</nlm:affiliation>
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<author><name sortKey="Takenouchi, Kazunori" sort="Takenouchi, Kazunori" uniqKey="Takenouchi K" first="Kazunori" last="Takenouchi">Kazunori Takenouchi</name>
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<author><name sortKey="Oyama, Yoko" sort="Oyama, Yoko" uniqKey="Oyama Y" first="Yoko" last="Oyama">Yoko Oyama</name>
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<author><name sortKey="Nagakura, Takumi" sort="Nagakura, Takumi" uniqKey="Nagakura T" first="Takumi" last="Nagakura">Takumi Nagakura</name>
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<author><name sortKey="Masamoto, Izumi" sort="Masamoto, Izumi" uniqKey="Masamoto I" first="Izumi" last="Masamoto">Izumi Masamoto</name>
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<series><title level="j">Biochemical and biophysical research communications</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cytokines (MeSH)</term>
<term>Host-Pathogen Interactions (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Inflammation (MeSH)</term>
<term>Legionella pneumophila (MeSH)</term>
<term>Legionnaires' Disease (metabolism)</term>
<term>Legionnaires' Disease (pathology)</term>
<term>Legionnaires' Disease (virology)</term>
<term>Macrophages (metabolism)</term>
<term>Macrophages (microbiology)</term>
<term>Macrophages (pathology)</term>
<term>MicroRNAs (analysis)</term>
<term>MicroRNAs (metabolism)</term>
<term>RNA, Messenger (analysis)</term>
<term>Rapamycin-Insensitive Companion of mTOR Protein (metabolism)</term>
<term>U937 Cells (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>MicroRNAs</term>
<term>RNA, Messenger</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>MicroRNAs</term>
<term>Rapamycin-Insensitive Companion of mTOR Protein</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Cytokines</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Legionnaires' Disease</term>
<term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Legionnaires' Disease</term>
<term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Legionnaires' Disease</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Host-Pathogen Interactions</term>
<term>Humans</term>
<term>Inflammation</term>
<term>Legionella pneumophila</term>
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<front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b>
</p>
<p>Inhalation of aerosolized Legionella pneumophila, a Gram-negative bacterium, can cause severe pneumonia. During infection, L. pneumophila replicates intracellularly in macrophages. The involvement of host microRNAs (miRNAs) in L. pneumophila infection is not fully understood.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS</b>
</p>
<p>The human macrophage-like cell line U937 was infected with L. pneumophila. The levels of miRNA and messenger RNA (mRNA) were measured using reverse transcriptase polymerase chain reaction. Release of lactate dehydrogenase was used to evaluate cytotoxicity. The expression of RICTOR and related proteins was examined by western blotting of cell lysates.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS</b>
</p>
<p>L. pneumophila infection upregulated the expression of miR-218 and the host genes SLIT2 and SLIT3 in U937 cells. The expression of RICTOR, a component of the mechanistic target of rapamycin complex 2 (mTORC2), decreased during L. pneumophila infection. RICTOR protein expression was inhibited by the overexpression of miR-218, whereas knockdown of miR-218 restored the downregulation of RICTOR by L. pneumophila. L. pneumophila infection induced the expression of the proinflammatory cytokines IL-6 and TNF-alpha, which was modulated by knockdown of miR-218 or RICTOR.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b>
</p>
<p>Our study revealed the involvement of miR-218 in regulating the inflammatory response of macrophages against L. pneumophila infection. These findings suggest potential novel roles for miR-218 and RICTOR as therapeutic targets of L. pneumophila infection.</p>
</div>
</front>
</TEI>
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<Abstract><AbstractText Label="BACKGROUND">Inhalation of aerosolized Legionella pneumophila, a Gram-negative bacterium, can cause severe pneumonia. During infection, L. pneumophila replicates intracellularly in macrophages. The involvement of host microRNAs (miRNAs) in L. pneumophila infection is not fully understood.</AbstractText>
<AbstractText Label="METHODS">The human macrophage-like cell line U937 was infected with L. pneumophila. The levels of miRNA and messenger RNA (mRNA) were measured using reverse transcriptase polymerase chain reaction. Release of lactate dehydrogenase was used to evaluate cytotoxicity. The expression of RICTOR and related proteins was examined by western blotting of cell lysates.</AbstractText>
<AbstractText Label="RESULTS">L. pneumophila infection upregulated the expression of miR-218 and the host genes SLIT2 and SLIT3 in U937 cells. The expression of RICTOR, a component of the mechanistic target of rapamycin complex 2 (mTORC2), decreased during L. pneumophila infection. RICTOR protein expression was inhibited by the overexpression of miR-218, whereas knockdown of miR-218 restored the downregulation of RICTOR by L. pneumophila. L. pneumophila infection induced the expression of the proinflammatory cytokines IL-6 and TNF-alpha, which was modulated by knockdown of miR-218 or RICTOR.</AbstractText>
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