Mesenchymal stem cells internalize Mycobacterium tuberculosis through scavenger receptors and restrict bacterial growth through autophagy.
Identifieur interne : 000802 ( Main/Exploration ); précédent : 000801; suivant : 000803Mesenchymal stem cells internalize Mycobacterium tuberculosis through scavenger receptors and restrict bacterial growth through autophagy.
Auteurs : Arshad Khan [États-Unis] ; Lovepreet Mann [États-Unis] ; Ramesha Papanna [États-Unis] ; Mi-Ae Lyu [États-Unis] ; Christopher R. Singh [États-Unis] ; Scott Olson [États-Unis] ; N Tony Eissa [États-Unis] ; Jeffrey Cirillo [États-Unis] ; Gobardhan Das [Inde] ; Robert L. Hunter [États-Unis] ; Chinnaswamy Jagannath [États-Unis]Source :
- Scientific reports [ 2045-2322 ] ; 2017.
Descripteurs français
- KwdFr :
- Autophagie (physiologie), Bécline-1 (génétique), Bécline-1 (métabolisme), Cellules THP-1 (MeSH), Cellules cultivées (MeSH), Cellules souches mésenchymateuses (microbiologie), Cellules souches mésenchymateuses (métabolisme), Humains (MeSH), Interférence par ARN (MeSH), Lipoprotéines LDL (métabolisme), Macrophages (métabolisme), Mycobacterium tuberculosis (croissance et développement), Mycobacterium tuberculosis (physiologie), Phagocytose (physiologie), Phagosomes (métabolisme), Récepteurs éboueurs (génétique), Récepteurs éboueurs (métabolisme), Viabilité microbienne (MeSH).
- MESH :
- croissance et développement : Mycobacterium tuberculosis.
- génétique : Bécline-1, Récepteurs éboueurs.
- microbiologie : Cellules souches mésenchymateuses.
- métabolisme : Bécline-1, Cellules souches mésenchymateuses, Lipoprotéines LDL, Macrophages, Phagosomes, Récepteurs éboueurs.
- physiologie : Autophagie, Mycobacterium tuberculosis, Phagocytose.
- Cellules THP-1, Cellules cultivées, Humains, Interférence par ARN, Viabilité microbienne.
English descriptors
- KwdEn :
- Autophagy (physiology), Beclin-1 (genetics), Beclin-1 (metabolism), Cells, Cultured (MeSH), Humans (MeSH), Lipoproteins, LDL (metabolism), Macrophages (metabolism), Mesenchymal Stem Cells (metabolism), Mesenchymal Stem Cells (microbiology), Microbial Viability (MeSH), Mycobacterium tuberculosis (growth & development), Mycobacterium tuberculosis (physiology), Phagocytosis (physiology), Phagosomes (metabolism), RNA Interference (MeSH), Receptors, Scavenger (genetics), Receptors, Scavenger (metabolism), THP-1 Cells (MeSH).
- MESH :
- chemical , genetics : Beclin-1, Receptors, Scavenger.
- chemical , metabolism : Beclin-1, Lipoproteins, LDL, Receptors, Scavenger.
- growth & development : Mycobacterium tuberculosis.
- metabolism : Macrophages, Mesenchymal Stem Cells, Phagosomes.
- microbiology : Mesenchymal Stem Cells.
- physiology : Autophagy, Mycobacterium tuberculosis, Phagocytosis.
- Cells, Cultured, Humans, Microbial Viability, RNA Interference, THP-1 Cells.
Abstract
Human mesenchymal stem cells (MSCs) express scavenger receptors that internalize lipids, including oxidized low-density lipoprotein (oxLDL). We report that MSCs phagocytose Mycobacterium tuberculosis (Mtb) through two types of scavenger receptors (SRs; MARCO and SR-B1), as blockade of the receptors with antibodies or siRNA knockdown decreased the uptake of Mtb. MSCs also expressed mannose receptor (MR) that was found to endocytose rhodamine-labeled mannosylated BSA (rMBSA), though the receptor was not involved in the uptake of Mtb. Dil-oxLDL and rMBSA taken up into MSC endosomes colocalized with Mtb phagosomes, thus suggesting that the latter were fusion competent. Phagocytosed Mtb did not replicate within MSCs, thus suggesting an intrinsic control of bacterial growth. Indeed, MSCs exhibited intrinsic autophagy, which was up-regulated after activation with rapamycin. SiRNA knockdown of autophagy initiator beclin-1 enhanced Mtb survival, whereas rapamycin-induced autophagy increased intracellular killing of Mtb. In addition, MSCs secreted nitric oxide after Mtb infection, and inhibition of NO by N(G)-monomethyl-L-arginine enhanced intracellular survival of Mtb. MSCs can be grown in large numbers in vitro, and autologous MSCs transfused into tuberculosis patients have been found to be safe and improve lung immunity. Thus, MSCs are novel phagocytic cells with a potential for immunotherapy in treating multidrug-resistant tuberculosis.
DOI: 10.1038/s41598-017-15290-z
PubMed: 29118429
PubMed Central: PMC5678154
Affiliations:
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Hunter</name><affiliation wicri:level="1"><nlm:affiliation>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030</wicri:regionArea><wicri:noRegion>77030</wicri:noRegion></affiliation></author><author><name sortKey="Jagannath, Chinnaswamy" sort="Jagannath, Chinnaswamy" uniqKey="Jagannath C" first="Chinnaswamy" last="Jagannath">Chinnaswamy Jagannath</name><affiliation wicri:level="1"><nlm:affiliation>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030, USA. Chinnaswamy.Jagannath@uth.tmc.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030</wicri:regionArea><wicri:noRegion>77030</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:29118429</idno><idno type="pmid">29118429</idno><idno type="doi">10.1038/s41598-017-15290-z</idno><idno type="pmc">PMC5678154</idno><idno type="wicri:Area/Main/Corpus">000686</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000686</idno><idno type="wicri:Area/Main/Curation">000686</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000686</idno><idno type="wicri:Area/Main/Exploration">000686</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Mesenchymal stem cells internalize Mycobacterium tuberculosis through scavenger receptors and restrict bacterial growth through autophagy.</title><author><name sortKey="Khan, Arshad" sort="Khan, Arshad" uniqKey="Khan A" first="Arshad" last="Khan">Arshad Khan</name><affiliation wicri:level="1"><nlm:affiliation>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030</wicri:regionArea><wicri:noRegion>77030</wicri:noRegion></affiliation></author><author><name sortKey="Mann, Lovepreet" sort="Mann, Lovepreet" uniqKey="Mann L" first="Lovepreet" last="Mann">Lovepreet Mann</name><affiliation wicri:level="3"><nlm:affiliation>Dept. of Obstetrics, Gynecology and Reproductive Sciences, UTHSC-, Houston, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Dept. of Obstetrics, Gynecology and Reproductive Sciences, UTHSC-, Houston</wicri:regionArea><placeName><settlement type="city">Houston</settlement><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Papanna, Ramesha" sort="Papanna, Ramesha" uniqKey="Papanna R" first="Ramesha" last="Papanna">Ramesha Papanna</name><affiliation wicri:level="3"><nlm:affiliation>Dept. of Obstetrics, Gynecology and Reproductive Sciences, UTHSC-, Houston, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Dept. of Obstetrics, Gynecology and Reproductive Sciences, UTHSC-, Houston</wicri:regionArea><placeName><settlement type="city">Houston</settlement><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Lyu, Mi Ae" sort="Lyu, Mi Ae" uniqKey="Lyu M" first="Mi-Ae" last="Lyu">Mi-Ae Lyu</name><affiliation wicri:level="3"><nlm:affiliation>Dept. of Obstetrics, Gynecology and Reproductive Sciences, UTHSC-, Houston, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Dept. of Obstetrics, Gynecology and Reproductive Sciences, UTHSC-, Houston</wicri:regionArea><placeName><settlement type="city">Houston</settlement><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Singh, Christopher R" sort="Singh, Christopher R" uniqKey="Singh C" first="Christopher R" last="Singh">Christopher R. Singh</name><affiliation wicri:level="1"><nlm:affiliation>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030</wicri:regionArea><wicri:noRegion>77030</wicri:noRegion></affiliation></author><author><name sortKey="Olson, Scott" sort="Olson, Scott" uniqKey="Olson S" first="Scott" last="Olson">Scott Olson</name><affiliation wicri:level="3"><nlm:affiliation>Dept. of Pediatric Surgery, UTHSC-, Houston, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Dept. of Pediatric Surgery, UTHSC-, Houston</wicri:regionArea><placeName><settlement type="city">Houston</settlement><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Eissa, N Tony" sort="Eissa, N Tony" uniqKey="Eissa N" first="N Tony" last="Eissa">N Tony Eissa</name><affiliation wicri:level="2"><nlm:affiliation>Dept. of Pulmonary Medicine, Baylor college of Medicine, Houston, TX, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Dept. of Pulmonary Medicine, Baylor college of Medicine, Houston, TX</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Cirillo, Jeffrey" sort="Cirillo, Jeffrey" uniqKey="Cirillo J" first="Jeffrey" last="Cirillo">Jeffrey Cirillo</name><affiliation wicri:level="1"><nlm:affiliation>Dept. of Microbial Pathogenesis and Immunology, Center for Airborne Pathogens Research and Imaging, Texas A&M Health Science Center, College of Medicine, Bryan, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Dept. of Microbial Pathogenesis and Immunology, Center for Airborne Pathogens Research and Imaging, Texas A&M Health Science Center, College of Medicine, Bryan</wicri:regionArea><wicri:noRegion>Bryan</wicri:noRegion></affiliation></author><author><name sortKey="Das, Gobardhan" sort="Das, Gobardhan" uniqKey="Das G" first="Gobardhan" last="Das">Gobardhan Das</name><affiliation wicri:level="1"><nlm:affiliation>Center for Molecular Medicine, Jawaharlal Nehru University, New Delhi, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Center for Molecular Medicine, Jawaharlal Nehru University, New Delhi</wicri:regionArea><wicri:noRegion>New Delhi</wicri:noRegion></affiliation></author><author><name sortKey="Hunter, Robert L" sort="Hunter, Robert L" uniqKey="Hunter R" first="Robert L" last="Hunter">Robert L. Hunter</name><affiliation wicri:level="1"><nlm:affiliation>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030</wicri:regionArea><wicri:noRegion>77030</wicri:noRegion></affiliation></author><author><name sortKey="Jagannath, Chinnaswamy" sort="Jagannath, Chinnaswamy" uniqKey="Jagannath C" first="Chinnaswamy" last="Jagannath">Chinnaswamy Jagannath</name><affiliation wicri:level="1"><nlm:affiliation>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030, USA. Chinnaswamy.Jagannath@uth.tmc.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030</wicri:regionArea><wicri:noRegion>77030</wicri:noRegion></affiliation></author></analytic><series><title level="j">Scientific reports</title><idno type="eISSN">2045-2322</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Autophagy (physiology)</term><term>Beclin-1 (genetics)</term><term>Beclin-1 (metabolism)</term><term>Cells, Cultured (MeSH)</term><term>Humans (MeSH)</term><term>Lipoproteins, LDL (metabolism)</term><term>Macrophages (metabolism)</term><term>Mesenchymal Stem Cells (metabolism)</term><term>Mesenchymal Stem Cells (microbiology)</term><term>Microbial Viability (MeSH)</term><term>Mycobacterium tuberculosis (growth & development)</term><term>Mycobacterium tuberculosis (physiology)</term><term>Phagocytosis (physiology)</term><term>Phagosomes (metabolism)</term><term>RNA Interference (MeSH)</term><term>Receptors, Scavenger (genetics)</term><term>Receptors, Scavenger (metabolism)</term><term>THP-1 Cells (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Autophagie (physiologie)</term><term>Bécline-1 (génétique)</term><term>Bécline-1 (métabolisme)</term><term>Cellules THP-1 (MeSH)</term><term>Cellules cultivées (MeSH)</term><term>Cellules souches mésenchymateuses (microbiologie)</term><term>Cellules souches mésenchymateuses (métabolisme)</term><term>Humains (MeSH)</term><term>Interférence par ARN (MeSH)</term><term>Lipoprotéines LDL (métabolisme)</term><term>Macrophages (métabolisme)</term><term>Mycobacterium tuberculosis (croissance et développement)</term><term>Mycobacterium tuberculosis (physiologie)</term><term>Phagocytose (physiologie)</term><term>Phagosomes (métabolisme)</term><term>Récepteurs éboueurs (génétique)</term><term>Récepteurs éboueurs (métabolisme)</term><term>Viabilité microbienne (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Beclin-1</term><term>Receptors, Scavenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Beclin-1</term><term>Lipoproteins, LDL</term><term>Receptors, Scavenger</term></keywords><keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Mycobacterium tuberculosis</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Mycobacterium tuberculosis</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Bécline-1</term><term>Récepteurs éboueurs</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Macrophages</term><term>Mesenchymal Stem Cells</term><term>Phagosomes</term></keywords><keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Cellules souches mésenchymateuses</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Mesenchymal Stem Cells</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Bécline-1</term><term>Cellules souches mésenchymateuses</term><term>Lipoprotéines LDL</term><term>Macrophages</term><term>Phagosomes</term><term>Récepteurs éboueurs</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Autophagie</term><term>Mycobacterium tuberculosis</term><term>Phagocytose</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Autophagy</term><term>Mycobacterium tuberculosis</term><term>Phagocytosis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cells, Cultured</term><term>Humans</term><term>Microbial Viability</term><term>RNA Interference</term><term>THP-1 Cells</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules THP-1</term><term>Cellules cultivées</term><term>Humains</term><term>Interférence par ARN</term><term>Viabilité microbienne</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Human mesenchymal stem cells (MSCs) express scavenger receptors that internalize lipids, including oxidized low-density lipoprotein (oxLDL). We report that MSCs phagocytose Mycobacterium tuberculosis (Mtb) through two types of scavenger receptors (SRs; MARCO and SR-B1), as blockade of the receptors with antibodies or siRNA knockdown decreased the uptake of Mtb. MSCs also expressed mannose receptor (MR) that was found to endocytose rhodamine-labeled mannosylated BSA (rMBSA), though the receptor was not involved in the uptake of Mtb. Dil-oxLDL and rMBSA taken up into MSC endosomes colocalized with Mtb phagosomes, thus suggesting that the latter were fusion competent. Phagocytosed Mtb did not replicate within MSCs, thus suggesting an intrinsic control of bacterial growth. Indeed, MSCs exhibited intrinsic autophagy, which was up-regulated after activation with rapamycin. SiRNA knockdown of autophagy initiator beclin-1 enhanced Mtb survival, whereas rapamycin-induced autophagy increased intracellular killing of Mtb. In addition, MSCs secreted nitric oxide after Mtb infection, and inhibition of NO by N(G)-monomethyl-L-arginine enhanced intracellular survival of Mtb. MSCs can be grown in large numbers in vitro, and autologous MSCs transfused into tuberculosis patients have been found to be safe and improve lung immunity. Thus, MSCs are novel phagocytic cells with a potential for immunotherapy in treating multidrug-resistant tuberculosis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29118429</PMID><DateCompleted><Year>2019</Year><Month>07</Month><Day>08</Day></DateCompleted><DateRevised><Year>2019</Year><Month>07</Month><Day>08</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><Issue>1</Issue><PubDate><Year>2017</Year><Month>11</Month><Day>08</Day></PubDate></JournalIssue><Title>Scientific reports</Title><ISOAbbreviation>Sci Rep</ISOAbbreviation></Journal><ArticleTitle>Mesenchymal stem cells internalize Mycobacterium tuberculosis through scavenger receptors and restrict bacterial growth through autophagy.</ArticleTitle><Pagination><MedlinePgn>15010</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41598-017-15290-z</ELocationID><Abstract><AbstractText>Human mesenchymal stem cells (MSCs) express scavenger receptors that internalize lipids, including oxidized low-density lipoprotein (oxLDL). We report that MSCs phagocytose Mycobacterium tuberculosis (Mtb) through two types of scavenger receptors (SRs; MARCO and SR-B1), as blockade of the receptors with antibodies or siRNA knockdown decreased the uptake of Mtb. MSCs also expressed mannose receptor (MR) that was found to endocytose rhodamine-labeled mannosylated BSA (rMBSA), though the receptor was not involved in the uptake of Mtb. Dil-oxLDL and rMBSA taken up into MSC endosomes colocalized with Mtb phagosomes, thus suggesting that the latter were fusion competent. Phagocytosed Mtb did not replicate within MSCs, thus suggesting an intrinsic control of bacterial growth. Indeed, MSCs exhibited intrinsic autophagy, which was up-regulated after activation with rapamycin. SiRNA knockdown of autophagy initiator beclin-1 enhanced Mtb survival, whereas rapamycin-induced autophagy increased intracellular killing of Mtb. In addition, MSCs secreted nitric oxide after Mtb infection, and inhibition of NO by N(G)-monomethyl-L-arginine enhanced intracellular survival of Mtb. MSCs can be grown in large numbers in vitro, and autologous MSCs transfused into tuberculosis patients have been found to be safe and improve lung immunity. Thus, MSCs are novel phagocytic cells with a potential for immunotherapy in treating multidrug-resistant tuberculosis.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Khan</LastName><ForeName>Arshad</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0003-3655-2854</Identifier><AffiliationInfo><Affiliation>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mann</LastName><ForeName>Lovepreet</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Dept. of Obstetrics, Gynecology and Reproductive Sciences, UTHSC-, Houston, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Papanna</LastName><ForeName>Ramesha</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Dept. of Obstetrics, Gynecology and Reproductive Sciences, UTHSC-, Houston, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lyu</LastName><ForeName>Mi-Ae</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>Dept. of Obstetrics, Gynecology and Reproductive Sciences, UTHSC-, Houston, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Singh</LastName><ForeName>Christopher R</ForeName><Initials>CR</Initials><AffiliationInfo><Affiliation>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Olson</LastName><ForeName>Scott</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Dept. of Pediatric Surgery, UTHSC-, Houston, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Eissa</LastName><ForeName>N Tony</ForeName><Initials>NT</Initials><AffiliationInfo><Affiliation>Dept. of Pulmonary Medicine, Baylor college of Medicine, Houston, TX, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cirillo</LastName><ForeName>Jeffrey</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Dept. of Microbial Pathogenesis and Immunology, Center for Airborne Pathogens Research and Imaging, Texas A&M Health Science Center, College of Medicine, Bryan, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Das</LastName><ForeName>Gobardhan</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Center for Molecular Medicine, Jawaharlal Nehru University, New Delhi, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hunter</LastName><ForeName>Robert L</ForeName><Initials>RL</Initials><AffiliationInfo><Affiliation>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jagannath</LastName><ForeName>Chinnaswamy</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Dept. of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, TX, 77030, USA. Chinnaswamy.Jagannath@uth.tmc.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>11</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Sci Rep</MedlineTA><NlmUniqueID>101563288</NlmUniqueID><ISSNLinking>2045-2322</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000071186">Beclin-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008077">Lipoproteins, LDL</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051116">Receptors, Scavenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C099252">oxidized low density 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