A previously uncharacterized two-component signaling system in uropathogenic Escherichia coli coordinates protection against host-derived oxidative stress with activation of hemolysin-mediated host cell pyroptosis
Uropathogenic Escherichia coli (UPEC) deploy an array of virulence factors to successfully establish urinary tract infections. Hemolysin is a pore-forming toxin, and its expression correlates with the severity of UPEC infection. Two-component signaling systems (TCSs) are a major mechanism by which b...
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| Veröffentlicht in: | PLoS pathogens 2021-10, Vol.17 (10), p.e1010005-e1010005 |
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| creator | Gu, Hongwei Cai, Xuwang Zhang, Xinyang Luo, Jie Zhang, Xiaoyang Hu, Xiao Cai, Wentong Li, Ganwu |
| description | Uropathogenic
Escherichia coli
(UPEC) deploy an array of virulence factors to successfully establish urinary tract infections. Hemolysin is a pore-forming toxin, and its expression correlates with the severity of UPEC infection. Two-component signaling systems (TCSs) are a major mechanism by which bacteria sense environmental cues and respond by initiating adaptive responses. Here, we began this study by characterizing a novel TCS (C3564/C3565, herein renamed
orhK
/
orhR
for
o
xidative
r
esistance and
h
emolysis
k
inase/
r
egulator) that is encoded on a UPEC pathogenicity island, using bioinformatic and biochemical approaches. A prevalence analysis indicates that
orhK
/
orhR
is highly associated with the UPEC pathotype, and it rarely occurs in other
E
.
coli
pathotypes tested. We then demonstrated that OrhK/OrhR directly activates the expression of a putative methionine sulfoxide reductase system (C3566/C3567) and hemolysin (HlyA) in response to host-derived hydrogen peroxide (H
2
O
2
) exposure. OrhK/OrhR increases UPEC resistance to H
2
O
2
in vitro
and survival in macrophages in cell culture via C3566/C3567. Additionally, OrhK/OrhR mediates hemolysin-induced renal epithelial cell and macrophage death via a pyroptosis pathway. Reducing intracellular H
2
O
2
production by a chemical inhibitor impaired OrhK/OrhR-mediated activation of
c3566-c3567
and
hlyA
. We also uncovered that UPEC links the two key virulence traits by cotranscribing the
c3566-c3567
and
hlyCABD
operons. Taken together, our data suggest a paradigm in which a signal transduction system coordinates both bacterial pathogen defensive and offensive traits in the presence of host-derived signals; and this exquisite mechanism likely contributes to hemolysin-induced severe pathological outcomes. |
| doi_str_mv | 10.1371/journal.ppat.1010005 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_2598100927</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A681018429</galeid><doaj_id>oai_doaj_org_article_285a749719fb4ae688f73a7c5d0b8d88</doaj_id><sourcerecordid>A681018429</sourcerecordid><originalsourceid>FETCH-LOGICAL-c638t-940975e0d67f2b2a0bd8c798b8c75719a56221168f1c76518e12c8d2005e9aeb3</originalsourceid><addsrcrecordid>eNqVk9uK1TAUhosozjj6BoIBb_Si26RtmvRGGIZRBwYFD9chTdI2Q5vUJN0z2_f0fVz7oLhlbqSQhuRb_79WkpVlzwlekZKRNzd-CU6Oq3mWaUUwwRjTB9kpobTMWcmqh3_NT7InMd5gXJGS1I-zk7KqaVkQfpr9PEdzMGvrlzhu0OLUIINUyQT7w2iUbn2u_DR7Z1xC0fZgaF2P4iYmMyHr0BI8-A--N84qdBnVAKFqsBIpP1oYfNDWyWQi-PhkVLLeIdlL62JCg48p1xCxBjN_Z7VMMEUxBRMjurVpQJCMXctdlO_QYCY_bqJ1-WS0BVm900DKjCOaN5BM8tHGp9mjTo7RPDv8z7Jv7y6_XnzIrz-9v7o4v85VXfKUNxVuGDVY16wr2kLiVnPFGt7CSBlpJK2LgpCad0SxmhJuSKG4LuCkTSNNW55lL_a68-ijONxIFAVtONxHUzAgrvaE9vJGzMFOMmyEl1bsFnzohQzJqtGIglPJqgZ8u7aSpua8Y6Vkimrccs05aL09uC0tlK_gToIcj0SPd5wdRO_XglOKS1aDwKuDQPDfFxOTmGzcHp10Bh4A5M2LbeKEAPryH_T-6g5UL6EA6zoPvmorKs5rgAivigao1T0UfNpMVsHb6iysHwW8PgoAJpm71MslRnH15fN_sB-P2WrPquBjDKb7c3YEi21T_S5SbJtKHJqq_AXZZxpx</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2598100927</pqid></control><display><type>article</type><title>A previously uncharacterized two-component signaling system in uropathogenic Escherichia coli coordinates protection against host-derived oxidative stress with activation of hemolysin-mediated host cell pyroptosis</title><source>DOAJ Directory of Open Access Journals</source><source>PubMed Central Open Access</source><source>Public Library of Science (PLoS)</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Gu, Hongwei ; Cai, Xuwang ; Zhang, Xinyang ; Luo, Jie ; Zhang, Xiaoyang ; Hu, Xiao ; Cai, Wentong ; Li, Ganwu</creator><contributor>Mecsas, Joan</contributor><creatorcontrib>Gu, Hongwei ; Cai, Xuwang ; Zhang, Xinyang ; Luo, Jie ; Zhang, Xiaoyang ; Hu, Xiao ; Cai, Wentong ; Li, Ganwu ; Mecsas, Joan</creatorcontrib><description>Uropathogenic
Escherichia coli
(UPEC) deploy an array of virulence factors to successfully establish urinary tract infections. Hemolysin is a pore-forming toxin, and its expression correlates with the severity of UPEC infection. Two-component signaling systems (TCSs) are a major mechanism by which bacteria sense environmental cues and respond by initiating adaptive responses. Here, we began this study by characterizing a novel TCS (C3564/C3565, herein renamed
orhK
/
orhR
for
o
xidative
r
esistance and
h
emolysis
k
inase/
r
egulator) that is encoded on a UPEC pathogenicity island, using bioinformatic and biochemical approaches. A prevalence analysis indicates that
orhK
/
orhR
is highly associated with the UPEC pathotype, and it rarely occurs in other
E
.
coli
pathotypes tested. We then demonstrated that OrhK/OrhR directly activates the expression of a putative methionine sulfoxide reductase system (C3566/C3567) and hemolysin (HlyA) in response to host-derived hydrogen peroxide (H
2
O
2
) exposure. OrhK/OrhR increases UPEC resistance to H
2
O
2
in vitro
and survival in macrophages in cell culture via C3566/C3567. Additionally, OrhK/OrhR mediates hemolysin-induced renal epithelial cell and macrophage death via a pyroptosis pathway. Reducing intracellular H
2
O
2
production by a chemical inhibitor impaired OrhK/OrhR-mediated activation of
c3566-c3567
and
hlyA
. We also uncovered that UPEC links the two key virulence traits by cotranscribing the
c3566-c3567
and
hlyCABD
operons. Taken together, our data suggest a paradigm in which a signal transduction system coordinates both bacterial pathogen defensive and offensive traits in the presence of host-derived signals; and this exquisite mechanism likely contributes to hemolysin-induced severe pathological outcomes.</description><identifier>ISSN: 1553-7374</identifier><identifier>ISSN: 1553-7366</identifier><identifier>EISSN: 1553-7374</identifier><identifier>DOI: 10.1371/journal.ppat.1010005</identifier><identifier>PMID: 34653218</identifier><language>eng</language><publisher>San Francisco: Public Library of Science</publisher><subject>Apoptosis ; Bacteria ; Biology and Life Sciences ; Causes of ; Cell activation ; Cell culture ; Cell death ; Cell survival ; Cellular signal transduction ; Development and progression ; E coli ; Epithelial cells ; Epithelium ; Escherichia coli ; Gene expression ; Genetic aspects ; Hemolysis and hemolysins ; Host-bacteria relationships ; Hydrogen peroxide ; Infections ; Kinases ; Macrophages ; Medicine and Health Sciences ; Methionine ; Mutation ; Neutrophils ; Operons ; Oxidation resistance ; Oxidative stress ; Pathogenicity ; Pathogens ; Phosphorylation ; Physiological aspects ; Pore formation ; Proteins ; Pyroptosis ; Reductases ; Signal transduction ; Signalling systems ; Toxins ; Urinary tract ; Urinary tract infections ; Virulence ; Virulence factors</subject><ispartof>PLoS pathogens, 2021-10, Vol.17 (10), p.e1010005-e1010005</ispartof><rights>COPYRIGHT 2021 Public Library of Science</rights><rights>2021 Gu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 Gu et al 2021 Gu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c638t-940975e0d67f2b2a0bd8c798b8c75719a56221168f1c76518e12c8d2005e9aeb3</citedby><cites>FETCH-LOGICAL-c638t-940975e0d67f2b2a0bd8c798b8c75719a56221168f1c76518e12c8d2005e9aeb3</cites><orcidid>0000-0002-2282-302X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8550376/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8550376/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27903,27904,53769,53771,79346,79347</link.rule.ids></links><search><contributor>Mecsas, Joan</contributor><creatorcontrib>Gu, Hongwei</creatorcontrib><creatorcontrib>Cai, Xuwang</creatorcontrib><creatorcontrib>Zhang, Xinyang</creatorcontrib><creatorcontrib>Luo, Jie</creatorcontrib><creatorcontrib>Zhang, Xiaoyang</creatorcontrib><creatorcontrib>Hu, Xiao</creatorcontrib><creatorcontrib>Cai, Wentong</creatorcontrib><creatorcontrib>Li, Ganwu</creatorcontrib><title>A previously uncharacterized two-component signaling system in uropathogenic Escherichia coli coordinates protection against host-derived oxidative stress with activation of hemolysin-mediated host cell pyroptosis</title><title>PLoS pathogens</title><description>Uropathogenic
Escherichia coli
(UPEC) deploy an array of virulence factors to successfully establish urinary tract infections. Hemolysin is a pore-forming toxin, and its expression correlates with the severity of UPEC infection. Two-component signaling systems (TCSs) are a major mechanism by which bacteria sense environmental cues and respond by initiating adaptive responses. Here, we began this study by characterizing a novel TCS (C3564/C3565, herein renamed
orhK
/
orhR
for
o
xidative
r
esistance and
h
emolysis
k
inase/
r
egulator) that is encoded on a UPEC pathogenicity island, using bioinformatic and biochemical approaches. A prevalence analysis indicates that
orhK
/
orhR
is highly associated with the UPEC pathotype, and it rarely occurs in other
E
.
coli
pathotypes tested. We then demonstrated that OrhK/OrhR directly activates the expression of a putative methionine sulfoxide reductase system (C3566/C3567) and hemolysin (HlyA) in response to host-derived hydrogen peroxide (H
2
O
2
) exposure. OrhK/OrhR increases UPEC resistance to H
2
O
2
in vitro
and survival in macrophages in cell culture via C3566/C3567. Additionally, OrhK/OrhR mediates hemolysin-induced renal epithelial cell and macrophage death via a pyroptosis pathway. Reducing intracellular H
2
O
2
production by a chemical inhibitor impaired OrhK/OrhR-mediated activation of
c3566-c3567
and
hlyA
. We also uncovered that UPEC links the two key virulence traits by cotranscribing the
c3566-c3567
and
hlyCABD
operons. Taken together, our data suggest a paradigm in which a signal transduction system coordinates both bacterial pathogen defensive and offensive traits in the presence of host-derived signals; and this exquisite mechanism likely contributes to hemolysin-induced severe pathological outcomes.</description><subject>Apoptosis</subject><subject>Bacteria</subject><subject>Biology and Life Sciences</subject><subject>Causes of</subject><subject>Cell activation</subject><subject>Cell culture</subject><subject>Cell death</subject><subject>Cell survival</subject><subject>Cellular signal transduction</subject><subject>Development and progression</subject><subject>E coli</subject><subject>Epithelial cells</subject><subject>Epithelium</subject><subject>Escherichia coli</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Hemolysis and hemolysins</subject><subject>Host-bacteria relationships</subject><subject>Hydrogen peroxide</subject><subject>Infections</subject><subject>Kinases</subject><subject>Macrophages</subject><subject>Medicine and Health Sciences</subject><subject>Methionine</subject><subject>Mutation</subject><subject>Neutrophils</subject><subject>Operons</subject><subject>Oxidation resistance</subject><subject>Oxidative stress</subject><subject>Pathogenicity</subject><subject>Pathogens</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Pore formation</subject><subject>Proteins</subject><subject>Pyroptosis</subject><subject>Reductases</subject><subject>Signal transduction</subject><subject>Signalling systems</subject><subject>Toxins</subject><subject>Urinary tract</subject><subject>Urinary tract infections</subject><subject>Virulence</subject><subject>Virulence factors</subject><issn>1553-7374</issn><issn>1553-7366</issn><issn>1553-7374</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqVk9uK1TAUhosozjj6BoIBb_Si26RtmvRGGIZRBwYFD9chTdI2Q5vUJN0z2_f0fVz7oLhlbqSQhuRb_79WkpVlzwlekZKRNzd-CU6Oq3mWaUUwwRjTB9kpobTMWcmqh3_NT7InMd5gXJGS1I-zk7KqaVkQfpr9PEdzMGvrlzhu0OLUIINUyQT7w2iUbn2u_DR7Z1xC0fZgaF2P4iYmMyHr0BI8-A--N84qdBnVAKFqsBIpP1oYfNDWyWQi-PhkVLLeIdlL62JCg48p1xCxBjN_Z7VMMEUxBRMjurVpQJCMXctdlO_QYCY_bqJ1-WS0BVm900DKjCOaN5BM8tHGp9mjTo7RPDv8z7Jv7y6_XnzIrz-9v7o4v85VXfKUNxVuGDVY16wr2kLiVnPFGt7CSBlpJK2LgpCad0SxmhJuSKG4LuCkTSNNW55lL_a68-ijONxIFAVtONxHUzAgrvaE9vJGzMFOMmyEl1bsFnzohQzJqtGIglPJqgZ8u7aSpua8Y6Vkimrccs05aL09uC0tlK_gToIcj0SPd5wdRO_XglOKS1aDwKuDQPDfFxOTmGzcHp10Bh4A5M2LbeKEAPryH_T-6g5UL6EA6zoPvmorKs5rgAivigao1T0UfNpMVsHb6iysHwW8PgoAJpm71MslRnH15fN_sB-P2WrPquBjDKb7c3YEi21T_S5SbJtKHJqq_AXZZxpx</recordid><startdate>20211015</startdate><enddate>20211015</enddate><creator>Gu, 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(PLoS)</general><scope>AAYXX</scope><scope>CITATION</scope><scope>ISN</scope><scope>ISR</scope><scope>3V.</scope><scope>7QL</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-2282-302X</orcidid></search><sort><creationdate>20211015</creationdate><title>A previously uncharacterized two-component signaling system in uropathogenic Escherichia coli coordinates protection against host-derived oxidative stress with activation of hemolysin-mediated host cell pyroptosis</title><author>Gu, Hongwei ; Cai, Xuwang ; Zhang, Xinyang ; Luo, Jie ; Zhang, Xiaoyang ; Hu, Xiao ; Cai, Wentong ; Li, Ganwu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c638t-940975e0d67f2b2a0bd8c798b8c75719a56221168f1c76518e12c8d2005e9aeb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Apoptosis</topic><topic>Bacteria</topic><topic>Biology and Life Sciences</topic><topic>Causes of</topic><topic>Cell activation</topic><topic>Cell culture</topic><topic>Cell death</topic><topic>Cell survival</topic><topic>Cellular signal transduction</topic><topic>Development and progression</topic><topic>E coli</topic><topic>Epithelial cells</topic><topic>Epithelium</topic><topic>Escherichia coli</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Hemolysis and hemolysins</topic><topic>Host-bacteria relationships</topic><topic>Hydrogen peroxide</topic><topic>Infections</topic><topic>Kinases</topic><topic>Macrophages</topic><topic>Medicine and Health Sciences</topic><topic>Methionine</topic><topic>Mutation</topic><topic>Neutrophils</topic><topic>Operons</topic><topic>Oxidation resistance</topic><topic>Oxidative stress</topic><topic>Pathogenicity</topic><topic>Pathogens</topic><topic>Phosphorylation</topic><topic>Physiological aspects</topic><topic>Pore formation</topic><topic>Proteins</topic><topic>Pyroptosis</topic><topic>Reductases</topic><topic>Signal transduction</topic><topic>Signalling systems</topic><topic>Toxins</topic><topic>Urinary tract</topic><topic>Urinary tract infections</topic><topic>Virulence</topic><topic>Virulence factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gu, Hongwei</creatorcontrib><creatorcontrib>Cai, Xuwang</creatorcontrib><creatorcontrib>Zhang, Xinyang</creatorcontrib><creatorcontrib>Luo, Jie</creatorcontrib><creatorcontrib>Zhang, Xiaoyang</creatorcontrib><creatorcontrib>Hu, Xiao</creatorcontrib><creatorcontrib>Cai, Wentong</creatorcontrib><creatorcontrib>Li, Ganwu</creatorcontrib><collection>CrossRef</collection><collection>Gale In Context: Canada</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium 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Ganwu</au><au>Mecsas, Joan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A previously uncharacterized two-component signaling system in uropathogenic Escherichia coli coordinates protection against host-derived oxidative stress with activation of hemolysin-mediated host cell pyroptosis</atitle><jtitle>PLoS pathogens</jtitle><date>2021-10-15</date><risdate>2021</risdate><volume>17</volume><issue>10</issue><spage>e1010005</spage><epage>e1010005</epage><pages>e1010005-e1010005</pages><issn>1553-7374</issn><issn>1553-7366</issn><eissn>1553-7374</eissn><abstract>Uropathogenic
Escherichia coli
(UPEC) deploy an array of virulence factors to successfully establish urinary tract infections. Hemolysin is a pore-forming toxin, and its expression correlates with the severity of UPEC infection. Two-component signaling systems (TCSs) are a major mechanism by which bacteria sense environmental cues and respond by initiating adaptive responses. Here, we began this study by characterizing a novel TCS (C3564/C3565, herein renamed
orhK
/
orhR
for
o
xidative
r
esistance and
h
emolysis
k
inase/
r
egulator) that is encoded on a UPEC pathogenicity island, using bioinformatic and biochemical approaches. A prevalence analysis indicates that
orhK
/
orhR
is highly associated with the UPEC pathotype, and it rarely occurs in other
E
.
coli
pathotypes tested. We then demonstrated that OrhK/OrhR directly activates the expression of a putative methionine sulfoxide reductase system (C3566/C3567) and hemolysin (HlyA) in response to host-derived hydrogen peroxide (H
2
O
2
) exposure. OrhK/OrhR increases UPEC resistance to H
2
O
2
in vitro
and survival in macrophages in cell culture via C3566/C3567. Additionally, OrhK/OrhR mediates hemolysin-induced renal epithelial cell and macrophage death via a pyroptosis pathway. Reducing intracellular H
2
O
2
production by a chemical inhibitor impaired OrhK/OrhR-mediated activation of
c3566-c3567
and
hlyA
. We also uncovered that UPEC links the two key virulence traits by cotranscribing the
c3566-c3567
and
hlyCABD
operons. Taken together, our data suggest a paradigm in which a signal transduction system coordinates both bacterial pathogen defensive and offensive traits in the presence of host-derived signals; and this exquisite mechanism likely contributes to hemolysin-induced severe pathological outcomes.</abstract><cop>San Francisco</cop><pub>Public Library of Science</pub><pmid>34653218</pmid><doi>10.1371/journal.ppat.1010005</doi><orcidid>https://orcid.org/0000-0002-2282-302X</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1553-7374 |
| ispartof | PLoS pathogens, 2021-10, Vol.17 (10), p.e1010005-e1010005 |
| issn | 1553-7374 1553-7366 1553-7374 |
| language | eng |
| recordid | cdi_plos_journals_2598100927 |
| source | DOAJ Directory of Open Access Journals; PubMed Central Open Access; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Apoptosis Bacteria Biology and Life Sciences Causes of Cell activation Cell culture Cell death Cell survival Cellular signal transduction Development and progression E coli Epithelial cells Epithelium Escherichia coli Gene expression Genetic aspects Hemolysis and hemolysins Host-bacteria relationships Hydrogen peroxide Infections Kinases Macrophages Medicine and Health Sciences Methionine Mutation Neutrophils Operons Oxidation resistance Oxidative stress Pathogenicity Pathogens Phosphorylation Physiological aspects Pore formation Proteins Pyroptosis Reductases Signal transduction Signalling systems Toxins Urinary tract Urinary tract infections Virulence Virulence factors |
| title | A previously uncharacterized two-component signaling system in uropathogenic Escherichia coli coordinates protection against host-derived oxidative stress with activation of hemolysin-mediated host cell pyroptosis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-23T20%3A45%3A41IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=A%20previously%20uncharacterized%20two-component%20signaling%20system%20in%20uropathogenic%20Escherichia%20coli%20coordinates%20protection%20against%20host-derived%20oxidative%20stress%20with%20activation%20of%20hemolysin-mediated%20host%20cell%20pyroptosis&rft.jtitle=PLoS%20pathogens&rft.au=Gu,%20Hongwei&rft.date=2021-10-15&rft.volume=17&rft.issue=10&rft.spage=e1010005&rft.epage=e1010005&rft.pages=e1010005-e1010005&rft.issn=1553-7374&rft.eissn=1553-7374&rft_id=info:doi/10.1371/journal.ppat.1010005&rft_dat=%3Cgale_plos_%3EA681018429%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2598100927&rft_id=info:pmid/34653218&rft_galeid=A681018429&rft_doaj_id=oai_doaj_org_article_285a749719fb4ae688f73a7c5d0b8d88&rfr_iscdi=true |