A hydrolase of trehalose dimycolate induces nutrient influx and stress sensitivity to balance intracellular growth of Mycobacterium tuberculosis.
Identifieur interne : 003A47 ( PubMed/Corpus ); précédent : 003A46; suivant : 003A48A hydrolase of trehalose dimycolate induces nutrient influx and stress sensitivity to balance intracellular growth of Mycobacterium tuberculosis.
Auteurs : Yong Yang ; Kathleen Kulka ; Ronald C. Montelaro ; Todd A. Reinhart ; James Sissons ; Alan Aderem ; Anil K. OjhaSource :
- Cell host & microbe [ 1934-6069 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Cord Factors (metabolism), Cytosol (microbiology), Gene Deletion, Hydrolases (genetics), Hydrolases (metabolism), Hydrolysis, Mice, Mice, Knockout, Mycobacterium tuberculosis (enzymology), Mycobacterium tuberculosis (genetics), Mycobacterium tuberculosis (growth & development), Mycobacterium tuberculosis (physiology).
- MESH :
- chemical , genetics : Hydrolases.
- chemical , metabolism : Cord Factors, Hydrolases.
- enzymology : Mycobacterium tuberculosis.
- genetics : Mycobacterium tuberculosis.
- growth & development : Mycobacterium tuberculosis.
- microbiology : Cytosol.
- physiology : Mycobacterium tuberculosis.
- Animals, Gene Deletion, Hydrolysis, Mice, Mice, Knockout.
Abstract
Chronic tuberculosis in an immunocompetent host is a consequence of the delicately balanced growth of Mycobacterium tuberculosis (Mtb) in the face of host defense mechanisms. We identify an Mtb enzyme (TdmhMtb) that hydrolyzes the mycobacterial glycolipid trehalose dimycolate and plays a critical role in balancing the intracellular growth of the pathogen. TdmhMtb is induced under nutrient-limiting conditions and remodels the Mtb envelope to increase nutrient influx but concomitantly sensitizes Mtb to stresses encountered in the host. Consistent with this, a ΔtdmhMtb mutant is more resilient to stress and grows to levels higher than those of wild-type in immunocompetent mice. By contrast, mutant growth is retarded in MyD88(-/-) mice, indicating that TdmhMtb provides a growth advantage to intracellular Mtb in an immunocompromised host. Thus, the effects and countereffects of TdmhMtb play an important role in balancing intracellular growth of Mtb in a manner that is directly responsive to host innate immunity.
DOI: 10.1016/j.chom.2014.01.008
PubMed: 24528862
Links to Exploration step
pubmed:24528862Le document en format XML
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Montelaro</name><affiliation><nlm:affiliation>Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, PA 15261, USA; Department of Microbiology and Molecular Genetics, University of Pittsburgh, Pittsburgh, PA 15261, USA; Center for Vaccine Research, University of Pittsburgh, Pittsburgh, PA 15261, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Reinhart, Todd A" sort="Reinhart, Todd A" uniqKey="Reinhart T" first="Todd A" last="Reinhart">Todd A. Reinhart</name><affiliation><nlm:affiliation>Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, PA 15261, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Sissons, James" sort="Sissons, James" uniqKey="Sissons J" first="James" last="Sissons">James Sissons</name><affiliation><nlm:affiliation>Seattle Biomedical Research Institute, 307 Westlake Avenue North, Seattle, WA 98109, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Aderem, Alan" sort="Aderem, Alan" uniqKey="Aderem A" first="Alan" last="Aderem">Alan Aderem</name><affiliation><nlm:affiliation>Seattle Biomedical Research Institute, 307 Westlake Avenue North, Seattle, WA 98109, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Ojha, Anil K" sort="Ojha, Anil K" uniqKey="Ojha A" first="Anil K" last="Ojha">Anil K. 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Montelaro</name><affiliation><nlm:affiliation>Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, PA 15261, USA; Department of Microbiology and Molecular Genetics, University of Pittsburgh, Pittsburgh, PA 15261, USA; Center for Vaccine Research, University of Pittsburgh, Pittsburgh, PA 15261, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Reinhart, Todd A" sort="Reinhart, Todd A" uniqKey="Reinhart T" first="Todd A" last="Reinhart">Todd A. Reinhart</name><affiliation><nlm:affiliation>Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, PA 15261, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Sissons, James" sort="Sissons, James" uniqKey="Sissons J" first="James" last="Sissons">James Sissons</name><affiliation><nlm:affiliation>Seattle Biomedical Research Institute, 307 Westlake Avenue North, Seattle, WA 98109, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Aderem, Alan" sort="Aderem, Alan" uniqKey="Aderem A" first="Alan" last="Aderem">Alan Aderem</name><affiliation><nlm:affiliation>Seattle Biomedical Research Institute, 307 Westlake Avenue North, Seattle, WA 98109, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Ojha, Anil K" sort="Ojha, Anil K" uniqKey="Ojha A" first="Anil K" last="Ojha">Anil K. Ojha</name><affiliation><nlm:affiliation>Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, PA 15261, USA. Electronic address: ano7@pitt.edu.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Cell host & microbe</title><idno type="eISSN">1934-6069</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cord Factors (metabolism)</term><term>Cytosol (microbiology)</term><term>Gene Deletion</term><term>Hydrolases (genetics)</term><term>Hydrolases (metabolism)</term><term>Hydrolysis</term><term>Mice</term><term>Mice, Knockout</term><term>Mycobacterium tuberculosis (enzymology)</term><term>Mycobacterium tuberculosis (genetics)</term><term>Mycobacterium tuberculosis (growth & development)</term><term>Mycobacterium tuberculosis (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Hydrolases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cord Factors</term><term>Hydrolases</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Mycobacterium tuberculosis</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mycobacterium tuberculosis</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Mycobacterium tuberculosis</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Cytosol</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Mycobacterium tuberculosis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Gene Deletion</term><term>Hydrolysis</term><term>Mice</term><term>Mice, Knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Chronic tuberculosis in an immunocompetent host is a consequence of the delicately balanced growth of Mycobacterium tuberculosis (Mtb) in the face of host defense mechanisms. We identify an Mtb enzyme (TdmhMtb) that hydrolyzes the mycobacterial glycolipid trehalose dimycolate and plays a critical role in balancing the intracellular growth of the pathogen. TdmhMtb is induced under nutrient-limiting conditions and remodels the Mtb envelope to increase nutrient influx but concomitantly sensitizes Mtb to stresses encountered in the host. Consistent with this, a ΔtdmhMtb mutant is more resilient to stress and grows to levels higher than those of wild-type in immunocompetent mice. By contrast, mutant growth is retarded in MyD88(-/-) mice, indicating that TdmhMtb provides a growth advantage to intracellular Mtb in an immunocompromised host. Thus, the effects and countereffects of TdmhMtb play an important role in balancing intracellular growth of Mtb in a manner that is directly responsive to host innate immunity.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24528862</PMID><DateCreated><Year>2014</Year><Month>02</Month><Day>17</Day></DateCreated><DateCompleted><Year>2014</Year><Month>10</Month><Day>08</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1934-6069</ISSN><JournalIssue CitedMedium="Internet"><Volume>15</Volume><Issue>2</Issue><PubDate><Year>2014</Year><Month>Feb</Month><Day>12</Day></PubDate></JournalIssue><Title>Cell host & microbe</Title><ISOAbbreviation>Cell Host Microbe</ISOAbbreviation></Journal><ArticleTitle>A hydrolase of trehalose dimycolate induces nutrient influx and stress sensitivity to balance intracellular growth of Mycobacterium tuberculosis.</ArticleTitle><Pagination><MedlinePgn>153-63</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.chom.2014.01.008</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1931-3128(14)00031-6</ELocationID><Abstract><AbstractText>Chronic tuberculosis in an immunocompetent host is a consequence of the delicately balanced growth of Mycobacterium tuberculosis (Mtb) in the face of host defense mechanisms. We identify an Mtb enzyme (TdmhMtb) that hydrolyzes the mycobacterial glycolipid trehalose dimycolate and plays a critical role in balancing the intracellular growth of the pathogen. TdmhMtb is induced under nutrient-limiting conditions and remodels the Mtb envelope to increase nutrient influx but concomitantly sensitizes Mtb to stresses encountered in the host. Consistent with this, a ΔtdmhMtb mutant is more resilient to stress and grows to levels higher than those of wild-type in immunocompetent mice. By contrast, mutant growth is retarded in MyD88(-/-) mice, indicating that TdmhMtb provides a growth advantage to intracellular Mtb in an immunocompromised host. Thus, the effects and countereffects of TdmhMtb play an important role in balancing intracellular growth of Mtb in a manner that is directly responsive to host innate immunity.</AbstractText><CopyrightInformation>Copyright © 2014 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Yong</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, PA 15261, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kulka</LastName><ForeName>Kathleen</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, PA 15261, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Montelaro</LastName><ForeName>Ronald C</ForeName><Initials>RC</Initials><AffiliationInfo><Affiliation>Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, PA 15261, USA; Department of Microbiology and Molecular Genetics, University of Pittsburgh, Pittsburgh, PA 15261, USA; Center for Vaccine Research, University of Pittsburgh, Pittsburgh, PA 15261, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Reinhart</LastName><ForeName>Todd A</ForeName><Initials>TA</Initials><AffiliationInfo><Affiliation>Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, PA 15261, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sissons</LastName><ForeName>James</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Seattle Biomedical Research Institute, 307 Westlake Avenue North, Seattle, WA 98109, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aderem</LastName><ForeName>Alan</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Seattle Biomedical Research Institute, 307 Westlake Avenue North, Seattle, WA 98109, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ojha</LastName><ForeName>Anil K</ForeName><Initials>AK</Initials><AffiliationInfo><Affiliation>Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, PA 15261, USA. Electronic address: ano7@pitt.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>UL1 TR000005</GrantID><Acronym>TR</Acronym><Agency>NCATS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>UL1 RR024153</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 AI079288</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U19 AI100627</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI79288</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., 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HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:24528862" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a PittsburghV1
| This area was generated with Dilib version V0.6.38. |  |