Innate immune responses following Kawasaki disease and toxic shock syndrome
The pathogenesis of Kawasaki disease (KD) remains unknown and there is accumulating evidence for the importance of the innate immune system in initiating and mediating the host inflammatory response. We compared innate immune responses in KD and toxic shock syndrome (TSS) participants more than two...
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| description | The pathogenesis of Kawasaki disease (KD) remains unknown and there is accumulating evidence for the importance of the innate immune system in initiating and mediating the host inflammatory response. We compared innate immune responses in KD and toxic shock syndrome (TSS) participants more than two years after their acute illness with control participants to investigate differences in their immune phenotype. Toxic shock syndrome shares many clinical features with KD; by including both disease groups we endeavoured to explore changes in innate immune responses following acute inflammatory illnesses more broadly. We measured the in vitro production of interferon (IFN)-γ, tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-1 receptor antagonist (IL-1ra), and IL-10 following whole blood stimulation with toll-like receptor and inflammasome ligands in 52 KD, 20 TSS, and 53 control participants in a case-control study. Analyses were adjusted for age, sex, and unstimulated cytokine concentrations. Compared to controls, KD participants have reduced IL-1ra production in response to stimulation with double stranded RNA (geometric mean ratio (GMR) 0.37, 95% CI 0.15, 0.89, p = 0.03) and increased IL-6 production in response to incubation with Lyovec™ (GMR 5.48, 95% CI 1.77, 16.98, p = 0.004). Compared to controls, TSS participants have increased IFN-γ production in response to peptidoglycan (GMR 4.07, 95% CI 1.82, 9.11, p = 0.001), increased IL-1β production to lipopolysaccharide (GMR 1.64, 95% CI 1.13, 2.38, p = 0.01) and peptidoglycan (GMR 1.61, 95% CI 1.11, 2.33, p = 0.01), and increased IL-6 production to peptidoglycan (GMR 1.45, 95% CI 1.10, 1.92, p = 0.01). Years following the acute illness, individuals with previous KD or TSS exhibit a pro-inflammatory innate immune phenotype suggesting a possible underlying immunological susceptibility or innate immune memory. |
| doi_str_mv | 10.1371/journal.pone.0191830 |
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We compared innate immune responses in KD and toxic shock syndrome (TSS) participants more than two years after their acute illness with control participants to investigate differences in their immune phenotype. Toxic shock syndrome shares many clinical features with KD; by including both disease groups we endeavoured to explore changes in innate immune responses following acute inflammatory illnesses more broadly. We measured the in vitro production of interferon (IFN)-γ, tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-1 receptor antagonist (IL-1ra), and IL-10 following whole blood stimulation with toll-like receptor and inflammasome ligands in 52 KD, 20 TSS, and 53 control participants in a case-control study. Analyses were adjusted for age, sex, and unstimulated cytokine concentrations. Compared to controls, KD participants have reduced IL-1ra production in response to stimulation with double stranded RNA (geometric mean ratio (GMR) 0.37, 95% CI 0.15, 0.89, p = 0.03) and increased IL-6 production in response to incubation with Lyovec™ (GMR 5.48, 95% CI 1.77, 16.98, p = 0.004). Compared to controls, TSS participants have increased IFN-γ production in response to peptidoglycan (GMR 4.07, 95% CI 1.82, 9.11, p = 0.001), increased IL-1β production to lipopolysaccharide (GMR 1.64, 95% CI 1.13, 2.38, p = 0.01) and peptidoglycan (GMR 1.61, 95% CI 1.11, 2.33, p = 0.01), and increased IL-6 production to peptidoglycan (GMR 1.45, 95% CI 1.10, 1.92, p = 0.01). Years following the acute illness, individuals with previous KD or TSS exhibit a pro-inflammatory innate immune phenotype suggesting a possible underlying immunological susceptibility or innate immune memory.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0191830</identifier><identifier>PMID: 29447181</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adolescent ; Adult ; Aneurysms ; Biology and Life Sciences ; Cardiology ; Case-Control Studies ; Child ; Comparative analysis ; Coronary vessels ; Cytokines ; Development and progression ; Double-stranded RNA ; Female ; Genetic aspects ; Heart ; Hospitals ; Humans ; Illnesses ; Immune response ; Immune system ; Immunity, Innate ; Immunological memory ; Immunology ; Incubation ; Infectious diseases ; Inflammasomes ; Inflammasomes - metabolism ; Inflammation ; Inflammatory response ; Innate immunity ; Interferon ; Interleukin 1 ; Interleukin 1 receptor antagonist ; Interleukin 10 ; Interleukin 6 ; Kawasaki disease ; Kawasaki syndrome ; Lipopolysaccharides ; Male ; Medicine ; Medicine and Health Sciences ; Mucocutaneous lymph node syndrome ; Mucocutaneous Lymph Node Syndrome - immunology ; Pathogenesis ; Peptidoglycans ; Phenotypes ; Physiological aspects ; Prognosis ; Proteins ; Ribonucleic acid ; RNA ; Sepsis ; Septic shock ; Shock, Septic - immunology ; Stimulation ; Toll-like receptors ; Toll-Like Receptors - metabolism ; Toxic diseases ; Toxic shock syndrome ; Tumor necrosis factor-α ; Tumors ; Veins & arteries ; Young Adult ; γ-Interferon</subject><ispartof>PloS one, 2018-02, Vol.13 (2), p.e0191830</ispartof><rights>COPYRIGHT 2018 Public Library of Science</rights><rights>2018 Chen 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>2018 Chen et al 2018 Chen et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-9988d2a22cd55e2334dd9d8bacbffc00e98e8a9dc88df96919022b099d568eb83</citedby><cites>FETCH-LOGICAL-c692t-9988d2a22cd55e2334dd9d8bacbffc00e98e8a9dc88df96919022b099d568eb83</cites><orcidid>0000-0003-3301-8031</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/PMC5813928/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5813928/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29447181$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Katherine Y H</creatorcontrib><creatorcontrib>Messina, Nicole</creatorcontrib><creatorcontrib>Germano, Susie</creatorcontrib><creatorcontrib>Bonnici, Rhian</creatorcontrib><creatorcontrib>Freyne, Bridget</creatorcontrib><creatorcontrib>Cheung, Michael</creatorcontrib><creatorcontrib>Goldsmith, Greta</creatorcontrib><creatorcontrib>Kollmann, Tobias R</creatorcontrib><creatorcontrib>Levin, Michael</creatorcontrib><creatorcontrib>Burgner, David</creatorcontrib><creatorcontrib>Curtis, Nigel</creatorcontrib><title>Innate immune responses following Kawasaki disease and toxic shock syndrome</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The pathogenesis of Kawasaki disease (KD) remains unknown and there is accumulating evidence for the importance of the innate immune system in initiating and mediating the host inflammatory response. We compared innate immune responses in KD and toxic shock syndrome (TSS) participants more than two years after their acute illness with control participants to investigate differences in their immune phenotype. Toxic shock syndrome shares many clinical features with KD; by including both disease groups we endeavoured to explore changes in innate immune responses following acute inflammatory illnesses more broadly. We measured the in vitro production of interferon (IFN)-γ, tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-1 receptor antagonist (IL-1ra), and IL-10 following whole blood stimulation with toll-like receptor and inflammasome ligands in 52 KD, 20 TSS, and 53 control participants in a case-control study. Analyses were adjusted for age, sex, and unstimulated cytokine concentrations. Compared to controls, KD participants have reduced IL-1ra production in response to stimulation with double stranded RNA (geometric mean ratio (GMR) 0.37, 95% CI 0.15, 0.89, p = 0.03) and increased IL-6 production in response to incubation with Lyovec™ (GMR 5.48, 95% CI 1.77, 16.98, p = 0.004). Compared to controls, TSS participants have increased IFN-γ production in response to peptidoglycan (GMR 4.07, 95% CI 1.82, 9.11, p = 0.001), increased IL-1β production to lipopolysaccharide (GMR 1.64, 95% CI 1.13, 2.38, p = 0.01) and peptidoglycan (GMR 1.61, 95% CI 1.11, 2.33, p = 0.01), and increased IL-6 production to peptidoglycan (GMR 1.45, 95% CI 1.10, 1.92, p = 0.01). Years following the acute illness, individuals with previous KD or TSS exhibit a pro-inflammatory innate immune phenotype suggesting a possible underlying immunological susceptibility or innate immune memory.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aneurysms</subject><subject>Biology and Life Sciences</subject><subject>Cardiology</subject><subject>Case-Control Studies</subject><subject>Child</subject><subject>Comparative analysis</subject><subject>Coronary vessels</subject><subject>Cytokines</subject><subject>Development and progression</subject><subject>Double-stranded RNA</subject><subject>Female</subject><subject>Genetic aspects</subject><subject>Heart</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Illnesses</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunity, Innate</subject><subject>Immunological memory</subject><subject>Immunology</subject><subject>Incubation</subject><subject>Infectious diseases</subject><subject>Inflammasomes</subject><subject>Inflammasomes - metabolism</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Innate immunity</subject><subject>Interferon</subject><subject>Interleukin 1</subject><subject>Interleukin 1 receptor antagonist</subject><subject>Interleukin 10</subject><subject>Interleukin 6</subject><subject>Kawasaki disease</subject><subject>Kawasaki syndrome</subject><subject>Lipopolysaccharides</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Mucocutaneous lymph node syndrome</subject><subject>Mucocutaneous Lymph Node Syndrome - immunology</subject><subject>Pathogenesis</subject><subject>Peptidoglycans</subject><subject>Phenotypes</subject><subject>Physiological aspects</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Sepsis</subject><subject>Septic shock</subject><subject>Shock, Septic - immunology</subject><subject>Stimulation</subject><subject>Toll-like receptors</subject><subject>Toll-Like Receptors - metabolism</subject><subject>Toxic diseases</subject><subject>Toxic shock syndrome</subject><subject>Tumor necrosis factor-α</subject><subject>Tumors</subject><subject>Veins & arteries</subject><subject>Young Adult</subject><subject>γ-Interferon</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkltr3DAQhU1padK0_6C0hkKhD7vVxfZKL4UQelkSCPT2KmRp5NXGljaS3ST_vnLXCWtooehBYvTNmeFwsuwlRktMV_j91g_ByXa58w6WCHPMKHqUHWNOyaIiiD4-eB9lz2LcIlRSVlVPsyPCi2KFGT7OztfOyR5y23WDgzxATHoRYm582_ob65r8XN7IKK9srm0EGSGXTue9v7UqjxuvrvJ453TwHTzPnhjZRngx3SfZj08fv599WVxcfl6fnV4sVMVJv-CcMU0kIUqXJRBKC625ZrVUtTEKIeAMmORaJczwimOOCKkR57qsGNSMnmSv97q71kcx-RAFQYgUDJOySsR6T2gvt2IXbCfDnfDSij8FHxohQ29VC4IXlKwKhGqoTMGY4clbjCiqlUQGqnHah2naUHegFbg-yHYmOv9xdiMa_0uUDFNORoE3k0Dw1wPE_h8rT1Qj01bWGZ_EVGejEqclWa0o5cVILf9CpaOhsyolwdhUnzW8mzUkpofbvpFDjGL97ev_s5c_5-zbA3YDsu030bdDb1N85mCxB1XwMQYwD85hJMYg37shxiCLKcip7dWh6w9N98mlvwG-q-3j</recordid><startdate>20180215</startdate><enddate>20180215</enddate><creator>Chen, Katherine Y H</creator><creator>Messina, Nicole</creator><creator>Germano, Susie</creator><creator>Bonnici, Rhian</creator><creator>Freyne, Bridget</creator><creator>Cheung, Michael</creator><creator>Goldsmith, Greta</creator><creator>Kollmann, Tobias R</creator><creator>Levin, Michael</creator><creator>Burgner, David</creator><creator>Curtis, Nigel</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-3301-8031</orcidid></search><sort><creationdate>20180215</creationdate><title>Innate immune responses following Kawasaki disease and toxic shock syndrome</title><author>Chen, Katherine Y H ; Messina, Nicole ; Germano, Susie ; Bonnici, Rhian ; Freyne, Bridget ; Cheung, Michael ; Goldsmith, Greta ; Kollmann, Tobias R ; Levin, Michael ; Burgner, David ; Curtis, Nigel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-9988d2a22cd55e2334dd9d8bacbffc00e98e8a9dc88df96919022b099d568eb83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aneurysms</topic><topic>Biology and Life Sciences</topic><topic>Cardiology</topic><topic>Case-Control Studies</topic><topic>Child</topic><topic>Comparative analysis</topic><topic>Coronary vessels</topic><topic>Cytokines</topic><topic>Development and progression</topic><topic>Double-stranded RNA</topic><topic>Female</topic><topic>Genetic aspects</topic><topic>Heart</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Illnesses</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunity, Innate</topic><topic>Immunological memory</topic><topic>Immunology</topic><topic>Incubation</topic><topic>Infectious diseases</topic><topic>Inflammasomes</topic><topic>Inflammasomes - 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Katherine Y H</au><au>Messina, Nicole</au><au>Germano, Susie</au><au>Bonnici, Rhian</au><au>Freyne, Bridget</au><au>Cheung, Michael</au><au>Goldsmith, Greta</au><au>Kollmann, Tobias R</au><au>Levin, Michael</au><au>Burgner, David</au><au>Curtis, Nigel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Innate immune responses following Kawasaki disease and toxic shock syndrome</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2018-02-15</date><risdate>2018</risdate><volume>13</volume><issue>2</issue><spage>e0191830</spage><pages>e0191830-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The pathogenesis of Kawasaki disease (KD) remains unknown and there is accumulating evidence for the importance of the innate immune system in initiating and mediating the host inflammatory response. We compared innate immune responses in KD and toxic shock syndrome (TSS) participants more than two years after their acute illness with control participants to investigate differences in their immune phenotype. Toxic shock syndrome shares many clinical features with KD; by including both disease groups we endeavoured to explore changes in innate immune responses following acute inflammatory illnesses more broadly. We measured the in vitro production of interferon (IFN)-γ, tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-1 receptor antagonist (IL-1ra), and IL-10 following whole blood stimulation with toll-like receptor and inflammasome ligands in 52 KD, 20 TSS, and 53 control participants in a case-control study. Analyses were adjusted for age, sex, and unstimulated cytokine concentrations. Compared to controls, KD participants have reduced IL-1ra production in response to stimulation with double stranded RNA (geometric mean ratio (GMR) 0.37, 95% CI 0.15, 0.89, p = 0.03) and increased IL-6 production in response to incubation with Lyovec™ (GMR 5.48, 95% CI 1.77, 16.98, p = 0.004). Compared to controls, TSS participants have increased IFN-γ production in response to peptidoglycan (GMR 4.07, 95% CI 1.82, 9.11, p = 0.001), increased IL-1β production to lipopolysaccharide (GMR 1.64, 95% CI 1.13, 2.38, p = 0.01) and peptidoglycan (GMR 1.61, 95% CI 1.11, 2.33, p = 0.01), and increased IL-6 production to peptidoglycan (GMR 1.45, 95% CI 1.10, 1.92, p = 0.01). Years following the acute illness, individuals with previous KD or TSS exhibit a pro-inflammatory innate immune phenotype suggesting a possible underlying immunological susceptibility or innate immune memory.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>29447181</pmid><doi>10.1371/journal.pone.0191830</doi><tpages>e0191830</tpages><orcidid>https://orcid.org/0000-0003-3301-8031</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2018-02, Vol.13 (2), p.e0191830 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_2002481256 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Adolescent Adult Aneurysms Biology and Life Sciences Cardiology Case-Control Studies Child Comparative analysis Coronary vessels Cytokines Development and progression Double-stranded RNA Female Genetic aspects Heart Hospitals Humans Illnesses Immune response Immune system Immunity, Innate Immunological memory Immunology Incubation Infectious diseases Inflammasomes Inflammasomes - metabolism Inflammation Inflammatory response Innate immunity Interferon Interleukin 1 Interleukin 1 receptor antagonist Interleukin 10 Interleukin 6 Kawasaki disease Kawasaki syndrome Lipopolysaccharides Male Medicine Medicine and Health Sciences Mucocutaneous lymph node syndrome Mucocutaneous Lymph Node Syndrome - immunology Pathogenesis Peptidoglycans Phenotypes Physiological aspects Prognosis Proteins Ribonucleic acid RNA Sepsis Septic shock Shock, Septic - immunology Stimulation Toll-like receptors Toll-Like Receptors - metabolism Toxic diseases Toxic shock syndrome Tumor necrosis factor-α Tumors Veins & arteries Young Adult γ-Interferon |
| title | Innate immune responses following Kawasaki disease and toxic shock syndrome |
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