A Genome-Wide Functional Genomics Approach Identifies Susceptibility Pathways to Fungal Bloodstream Infection in Humans
Candidemia, one of the most common causes of fungal bloodstream infection, leads to mortality rates up to 40% in affected patients. Understanding genetic mechanisms for differential susceptibility to candidemia may aid in designing host-directed therapies. We performed the first genome-wide associat...
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| Veröffentlicht in: | The Journal of infectious diseases 2019-07, Vol.220 (5), p.862-872 |
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| creator | Jaeger, Martin Matzaraki, Vasiliki Aguirre-Gamboa, Raúl Gresnigt, Mark S. Chu, Xiaojing Johnson, Melissa D. Oosting, Marije Smeekens, Sanne P. Withoff, Sebo Jonkers, Iris Perfect, John R. van de Veerdonk, Frank L. Kullberg, Bart-Jan Joosten, Leo A. B. Li, Yang Wijmenga, Cisca Netea, Mihai G. Kumar, Vinod |
| description | Candidemia, one of the most common causes of fungal bloodstream infection, leads to mortality rates up to 40% in affected patients. Understanding genetic mechanisms for differential susceptibility to candidemia may aid in designing host-directed therapies.
We performed the first genome-wide association study on candidemia, and we integrated these data with variants that affect cytokines in different cellular systems stimulated with Candida albicans.
We observed strong association between candidemia and a variant, rs8028958, that significantly affects the expression levels of PLA2G4B in blood. We found that up to 35% of the susceptibility loci affect in vitro cytokine production in response to Candida. Furthermore, potential causal genes located within these loci are enriched for lipid and arachidonic acid metabolism. Using an independent cohort, we also showed that the numbers of risk alleles at these loci are negatively correlated with reactive oxygen species and interleukin-6 levels in response to Candida. Finally, there was a significant correlation between susceptibility and allelic scores based on 16 independent candidemia-associated single-nucleotide polymorphisms that affect monocyte-derived cytokines, but not with T cell-derived cytokines.
Our results prioritize the disturbed lipid homeostasis and oxidative stress as potential mechanisms that affect monocyte-derived cytokines to influence susceptibility to candidemia. |
| doi_str_mv | 10.1093/infdis/jiz206 |
| format | Article |
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We performed the first genome-wide association study on candidemia, and we integrated these data with variants that affect cytokines in different cellular systems stimulated with Candida albicans.
We observed strong association between candidemia and a variant, rs8028958, that significantly affects the expression levels of PLA2G4B in blood. We found that up to 35% of the susceptibility loci affect in vitro cytokine production in response to Candida. Furthermore, potential causal genes located within these loci are enriched for lipid and arachidonic acid metabolism. Using an independent cohort, we also showed that the numbers of risk alleles at these loci are negatively correlated with reactive oxygen species and interleukin-6 levels in response to Candida. Finally, there was a significant correlation between susceptibility and allelic scores based on 16 independent candidemia-associated single-nucleotide polymorphisms that affect monocyte-derived cytokines, but not with T cell-derived cytokines.
Our results prioritize the disturbed lipid homeostasis and oxidative stress as potential mechanisms that affect monocyte-derived cytokines to influence susceptibility to candidemia.</description><identifier>ISSN: 0022-1899</identifier><identifier>ISSN: 1537-6613</identifier><identifier>EISSN: 1537-6613</identifier><identifier>DOI: 10.1093/infdis/jiz206</identifier><identifier>PMID: 31241743</identifier><language>eng</language><publisher>United States: Oxford University Press</publisher><subject>Alleles ; Arachidonic acid ; Candida ; Candida albicans - immunology ; Candida albicans - pathogenicity ; Candidemia ; Candidemia - genetics ; Candidemia - microbiology ; Chromosomes, Human, Pair 15 ; Cohort Studies ; Cytokines ; Cytokines - blood ; Cytokines - genetics ; Cytokines - metabolism ; Disease Susceptibility ; FUNGI ; Genetic Loci ; Genome-wide association studies ; Genome-Wide Association Study ; Genomes ; Genomics ; Group IV Phospholipases A2 - blood ; Group IV Phospholipases A2 - genetics ; Group IV Phospholipases A2 - metabolism ; Homeostasis ; Host-Pathogen Interactions - genetics ; Host-Pathogen Interactions - immunology ; Humans ; Interleukin 6 ; Interleukin-6 - genetics ; Lipid metabolism ; Lymphocytes T ; Major and Brief Reports ; Monocytes ; Oxidative Stress ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Single-nucleotide polymorphism ; Susceptibility</subject><ispartof>The Journal of infectious diseases, 2019-07, Vol.220 (5), p.862-872</ispartof><rights>The Author(s) 2019</rights><rights>The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.</rights><rights>info:eu-repo/semantics/openAccess</rights><rights>The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c461t-a1eb8051fed1ae231784880d7707c727f7164908f0799f4785be92c4042364803</citedby><cites>FETCH-LOGICAL-c461t-a1eb8051fed1ae231784880d7707c727f7164908f0799f4785be92c4042364803</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,26544,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31241743$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jaeger, Martin</creatorcontrib><creatorcontrib>Matzaraki, Vasiliki</creatorcontrib><creatorcontrib>Aguirre-Gamboa, Raúl</creatorcontrib><creatorcontrib>Gresnigt, Mark S.</creatorcontrib><creatorcontrib>Chu, Xiaojing</creatorcontrib><creatorcontrib>Johnson, Melissa D.</creatorcontrib><creatorcontrib>Oosting, Marije</creatorcontrib><creatorcontrib>Smeekens, Sanne P.</creatorcontrib><creatorcontrib>Withoff, Sebo</creatorcontrib><creatorcontrib>Jonkers, Iris</creatorcontrib><creatorcontrib>Perfect, John R.</creatorcontrib><creatorcontrib>van de Veerdonk, Frank L.</creatorcontrib><creatorcontrib>Kullberg, Bart-Jan</creatorcontrib><creatorcontrib>Joosten, Leo A. B.</creatorcontrib><creatorcontrib>Li, Yang</creatorcontrib><creatorcontrib>Wijmenga, Cisca</creatorcontrib><creatorcontrib>Netea, Mihai G.</creatorcontrib><creatorcontrib>Kumar, Vinod</creatorcontrib><title>A Genome-Wide Functional Genomics Approach Identifies Susceptibility Pathways to Fungal Bloodstream Infection in Humans</title><title>The Journal of infectious diseases</title><addtitle>J Infect Dis</addtitle><description>Candidemia, one of the most common causes of fungal bloodstream infection, leads to mortality rates up to 40% in affected patients. Understanding genetic mechanisms for differential susceptibility to candidemia may aid in designing host-directed therapies.
We performed the first genome-wide association study on candidemia, and we integrated these data with variants that affect cytokines in different cellular systems stimulated with Candida albicans.
We observed strong association between candidemia and a variant, rs8028958, that significantly affects the expression levels of PLA2G4B in blood. We found that up to 35% of the susceptibility loci affect in vitro cytokine production in response to Candida. Furthermore, potential causal genes located within these loci are enriched for lipid and arachidonic acid metabolism. Using an independent cohort, we also showed that the numbers of risk alleles at these loci are negatively correlated with reactive oxygen species and interleukin-6 levels in response to Candida. Finally, there was a significant correlation between susceptibility and allelic scores based on 16 independent candidemia-associated single-nucleotide polymorphisms that affect monocyte-derived cytokines, but not with T cell-derived cytokines.
Our results prioritize the disturbed lipid homeostasis and oxidative stress as potential mechanisms that affect monocyte-derived cytokines to influence susceptibility to candidemia.</description><subject>Alleles</subject><subject>Arachidonic acid</subject><subject>Candida</subject><subject>Candida albicans - immunology</subject><subject>Candida albicans - pathogenicity</subject><subject>Candidemia</subject><subject>Candidemia - genetics</subject><subject>Candidemia - microbiology</subject><subject>Chromosomes, Human, Pair 15</subject><subject>Cohort Studies</subject><subject>Cytokines</subject><subject>Cytokines - blood</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Disease Susceptibility</subject><subject>FUNGI</subject><subject>Genetic Loci</subject><subject>Genome-wide association studies</subject><subject>Genome-Wide Association Study</subject><subject>Genomes</subject><subject>Genomics</subject><subject>Group IV Phospholipases A2 - blood</subject><subject>Group IV Phospholipases A2 - genetics</subject><subject>Group IV Phospholipases A2 - metabolism</subject><subject>Homeostasis</subject><subject>Host-Pathogen Interactions - genetics</subject><subject>Host-Pathogen Interactions - immunology</subject><subject>Humans</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - genetics</subject><subject>Lipid metabolism</subject><subject>Lymphocytes T</subject><subject>Major and Brief Reports</subject><subject>Monocytes</subject><subject>Oxidative Stress</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Single-nucleotide polymorphism</subject><subject>Susceptibility</subject><issn>0022-1899</issn><issn>1537-6613</issn><issn>1537-6613</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>3HK</sourceid><recordid>eNpdkc1v1DAQxS0EokvhyBGwxIVL6PgjtnNBWirarlQJJEAcLW_idL1K7K3tUC1_PV7SroCTJc9v3ryZh9BLAu8JNOzM-b5z6WzrflEQj9CC1ExWQhD2GC0AKK2IapoT9CylLQBwJuRTdMII5URytkB3S3xpfRht9cN1Fl9Mvs0ueDPM365NeLnbxWDaDV511mfXO5vw1ym1dpfd2g0u7_EXkzd3Zp9wDgeJm9L-cQihSzlaM-KV7-0fWew8vppG49Nz9KQ3Q7Iv7t9T9P3i07fzq-r68-XqfHldtVyQXBli1wpq0tuOGEsZkYorBZ2UIFtJZS-J4A2oHmTT9Fyqem0b2nLglAmugJ2iD7PublqPtmvLBtEMehfdaOJeB-P0vxXvNvom_NRCCCkbXgTezAJtdCk7r32IRhNQNdUFkKIQ7-5HxHA72ZT16Mp1hsF4G6akKRWSg6z5wc3b_9BtmGK5dqE4V5wLEKxQ1cPIkFK0_dEuAX0IXc-h6zn0wr_-e8cj_ZByAV7NwDblEI_14qtWZQf2G81wsyE</recordid><startdate>20190731</startdate><enddate>20190731</enddate><creator>Jaeger, Martin</creator><creator>Matzaraki, Vasiliki</creator><creator>Aguirre-Gamboa, Raúl</creator><creator>Gresnigt, Mark S.</creator><creator>Chu, Xiaojing</creator><creator>Johnson, Melissa D.</creator><creator>Oosting, Marije</creator><creator>Smeekens, Sanne P.</creator><creator>Withoff, Sebo</creator><creator>Jonkers, Iris</creator><creator>Perfect, John R.</creator><creator>van de Veerdonk, Frank L.</creator><creator>Kullberg, Bart-Jan</creator><creator>Joosten, Leo A. B.</creator><creator>Li, Yang</creator><creator>Wijmenga, Cisca</creator><creator>Netea, Mihai G.</creator><creator>Kumar, Vinod</creator><general>Oxford University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>3HK</scope><scope>5PM</scope></search><sort><creationdate>20190731</creationdate><title>A Genome-Wide Functional Genomics Approach Identifies Susceptibility Pathways to Fungal Bloodstream Infection in Humans</title><author>Jaeger, Martin ; Matzaraki, Vasiliki ; Aguirre-Gamboa, Raúl ; Gresnigt, Mark S. ; Chu, Xiaojing ; Johnson, Melissa D. ; Oosting, Marije ; Smeekens, Sanne P. ; Withoff, Sebo ; Jonkers, Iris ; Perfect, John R. ; van de Veerdonk, Frank L. ; Kullberg, Bart-Jan ; Joosten, Leo A. B. ; Li, Yang ; Wijmenga, Cisca ; Netea, Mihai G. ; Kumar, Vinod</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c461t-a1eb8051fed1ae231784880d7707c727f7164908f0799f4785be92c4042364803</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Alleles</topic><topic>Arachidonic acid</topic><topic>Candida</topic><topic>Candida albicans - immunology</topic><topic>Candida albicans - pathogenicity</topic><topic>Candidemia</topic><topic>Candidemia - genetics</topic><topic>Candidemia - microbiology</topic><topic>Chromosomes, Human, Pair 15</topic><topic>Cohort Studies</topic><topic>Cytokines</topic><topic>Cytokines - blood</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Disease Susceptibility</topic><topic>FUNGI</topic><topic>Genetic Loci</topic><topic>Genome-wide association studies</topic><topic>Genome-Wide Association Study</topic><topic>Genomes</topic><topic>Genomics</topic><topic>Group IV Phospholipases A2 - blood</topic><topic>Group IV Phospholipases A2 - genetics</topic><topic>Group IV Phospholipases A2 - metabolism</topic><topic>Homeostasis</topic><topic>Host-Pathogen Interactions - genetics</topic><topic>Host-Pathogen Interactions - immunology</topic><topic>Humans</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - genetics</topic><topic>Lipid metabolism</topic><topic>Lymphocytes T</topic><topic>Major and Brief Reports</topic><topic>Monocytes</topic><topic>Oxidative Stress</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Single-nucleotide polymorphism</topic><topic>Susceptibility</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jaeger, Martin</creatorcontrib><creatorcontrib>Matzaraki, Vasiliki</creatorcontrib><creatorcontrib>Aguirre-Gamboa, Raúl</creatorcontrib><creatorcontrib>Gresnigt, Mark S.</creatorcontrib><creatorcontrib>Chu, Xiaojing</creatorcontrib><creatorcontrib>Johnson, Melissa D.</creatorcontrib><creatorcontrib>Oosting, Marije</creatorcontrib><creatorcontrib>Smeekens, Sanne P.</creatorcontrib><creatorcontrib>Withoff, Sebo</creatorcontrib><creatorcontrib>Jonkers, Iris</creatorcontrib><creatorcontrib>Perfect, John R.</creatorcontrib><creatorcontrib>van de Veerdonk, Frank L.</creatorcontrib><creatorcontrib>Kullberg, Bart-Jan</creatorcontrib><creatorcontrib>Joosten, Leo A. B.</creatorcontrib><creatorcontrib>Li, Yang</creatorcontrib><creatorcontrib>Wijmenga, Cisca</creatorcontrib><creatorcontrib>Netea, Mihai G.</creatorcontrib><creatorcontrib>Kumar, Vinod</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><collection>NORA - Norwegian Open Research Archives</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of infectious diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jaeger, Martin</au><au>Matzaraki, Vasiliki</au><au>Aguirre-Gamboa, Raúl</au><au>Gresnigt, Mark S.</au><au>Chu, Xiaojing</au><au>Johnson, Melissa D.</au><au>Oosting, Marije</au><au>Smeekens, Sanne P.</au><au>Withoff, Sebo</au><au>Jonkers, Iris</au><au>Perfect, John R.</au><au>van de Veerdonk, Frank L.</au><au>Kullberg, Bart-Jan</au><au>Joosten, Leo A. B.</au><au>Li, Yang</au><au>Wijmenga, Cisca</au><au>Netea, Mihai G.</au><au>Kumar, Vinod</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Genome-Wide Functional Genomics Approach Identifies Susceptibility Pathways to Fungal Bloodstream Infection in Humans</atitle><jtitle>The Journal of infectious diseases</jtitle><addtitle>J Infect Dis</addtitle><date>2019-07-31</date><risdate>2019</risdate><volume>220</volume><issue>5</issue><spage>862</spage><epage>872</epage><pages>862-872</pages><issn>0022-1899</issn><issn>1537-6613</issn><eissn>1537-6613</eissn><abstract>Candidemia, one of the most common causes of fungal bloodstream infection, leads to mortality rates up to 40% in affected patients. Understanding genetic mechanisms for differential susceptibility to candidemia may aid in designing host-directed therapies.
We performed the first genome-wide association study on candidemia, and we integrated these data with variants that affect cytokines in different cellular systems stimulated with Candida albicans.
We observed strong association between candidemia and a variant, rs8028958, that significantly affects the expression levels of PLA2G4B in blood. We found that up to 35% of the susceptibility loci affect in vitro cytokine production in response to Candida. Furthermore, potential causal genes located within these loci are enriched for lipid and arachidonic acid metabolism. Using an independent cohort, we also showed that the numbers of risk alleles at these loci are negatively correlated with reactive oxygen species and interleukin-6 levels in response to Candida. Finally, there was a significant correlation between susceptibility and allelic scores based on 16 independent candidemia-associated single-nucleotide polymorphisms that affect monocyte-derived cytokines, but not with T cell-derived cytokines.
Our results prioritize the disturbed lipid homeostasis and oxidative stress as potential mechanisms that affect monocyte-derived cytokines to influence susceptibility to candidemia.</abstract><cop>United States</cop><pub>Oxford University Press</pub><pmid>31241743</pmid><doi>10.1093/infdis/jiz206</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; NORA - Norwegian Open Research Archives; Alma/SFX Local Collection |
| subjects | Alleles Arachidonic acid Candida Candida albicans - immunology Candida albicans - pathogenicity Candidemia Candidemia - genetics Candidemia - microbiology Chromosomes, Human, Pair 15 Cohort Studies Cytokines Cytokines - blood Cytokines - genetics Cytokines - metabolism Disease Susceptibility FUNGI Genetic Loci Genome-wide association studies Genome-Wide Association Study Genomes Genomics Group IV Phospholipases A2 - blood Group IV Phospholipases A2 - genetics Group IV Phospholipases A2 - metabolism Homeostasis Host-Pathogen Interactions - genetics Host-Pathogen Interactions - immunology Humans Interleukin 6 Interleukin-6 - genetics Lipid metabolism Lymphocytes T Major and Brief Reports Monocytes Oxidative Stress Reactive oxygen species Reactive Oxygen Species - metabolism Single-nucleotide polymorphism Susceptibility |
| title | A Genome-Wide Functional Genomics Approach Identifies Susceptibility Pathways to Fungal Bloodstream Infection in Humans |
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