Lauren Breithaupt , Laura M. Holsen , Chunni Ji , Jie Hu , Felicia Petterway , Megan Rosa-Caldwell , Ida A.K. Nilsson , Jennifer J. Thomas , Kyle A. Williams , Regine Boutin , Meghan Slattery , Cynthia M. Bulik , Steven E. Arnold , Elizabeth A. Lawson , Madhusmita Misra , Kamryn T. Eddy
{"title":"识别神经性厌食症的状态标记物:利用多重分析法复制和扩展炎症相关生物标志物","authors":"Lauren Breithaupt , Laura M. Holsen , Chunni Ji , Jie Hu , Felicia Petterway , Megan Rosa-Caldwell , Ida A.K. Nilsson , Jennifer J. Thomas , Kyle A. Williams , Regine Boutin , Meghan Slattery , Cynthia M. Bulik , Steven E. Arnold , Elizabeth A. Lawson , Madhusmita Misra , Kamryn T. Eddy","doi":"10.1016/j.bpsgos.2024.100332","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><p>Proteomics offers potential for detecting and monitoring anorexia nervosa (AN) and its variant, atypical AN (atyp-AN). However, research has been limited by small protein panels, a focus on adult AN, and lack of replication.</p></div><div><h3>Methods</h3><p>In this study, we performed Olink multiplex profiling of 92 inflammation-related proteins in females with AN/atyp-AN (<em>n</em> = 64), all of whom were ≤90% of expected body weight, and age-matched healthy control individuals (<em>n</em> = 44).</p></div><div><h3>Results</h3><p>Five proteins differed significantly between the primary AN/atyp-AN group and the healthy control group (lower levels: HGF, IL-18R1, TRANCE; higher levels: CCL23, LIF-R). The expression levels of 3 proteins (lower IL-18R1, TRANCE; higher LIF-R) were uniquely disrupted in participants with AN in our primary model. No unique expression levels emerged for atyp-AN. In the total sample, 12 proteins (ADA, CD5, CD6, CXCL1, FGF-21, HGF, IL-12B, IL18, IL-18R1, SIRT2, TNFSF14, TRANCE) were positively correlated with body mass index and 5 proteins (CCL11, FGF-19, IL8, LIF-R, OPG) were negatively correlated with body mass index in our primary models.</p></div><div><h3>Conclusions</h3><p>Our results replicate the results of a previous study that demonstrated a dysregulated inflammatory status in AN and extend those results to atyp-AN. Of the 17 proteins correlated with body mass index, 11 were replicated from a previous study that used similar methods, highlighting the promise of inflammatory protein expression levels as biomarkers of AN disease monitoring. Our findings underscore the complexity of AN and atyp-AN by highlighting the inability of the identified proteins to differentiate between these 2 subtypes, thereby emphasizing the heterogeneous nature of these disorders.</p></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 5","pages":"Article 100332"},"PeriodicalIF":4.0000,"publicationDate":"2024-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000454/pdfft?md5=7a886594028244d17c0b0de18cd0c355&pid=1-s2.0-S2667174324000454-main.pdf","citationCount":"0","resultStr":"{\"title\":\"Identification of State Markers in Anorexia Nervosa: Replication and Extension of Inflammation-Associated Biomarkers Using Multiplex Profiling\",\"authors\":\"Lauren Breithaupt , Laura M. Holsen , Chunni Ji , Jie Hu , Felicia Petterway , Megan Rosa-Caldwell , Ida A.K. Nilsson , Jennifer J. Thomas , Kyle A. Williams , Regine Boutin , Meghan Slattery , Cynthia M. Bulik , Steven E. Arnold , Elizabeth A. Lawson , Madhusmita Misra , Kamryn T. Eddy\",\"doi\":\"10.1016/j.bpsgos.2024.100332\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><p>Proteomics offers potential for detecting and monitoring anorexia nervosa (AN) and its variant, atypical AN (atyp-AN). However, research has been limited by small protein panels, a focus on adult AN, and lack of replication.</p></div><div><h3>Methods</h3><p>In this study, we performed Olink multiplex profiling of 92 inflammation-related proteins in females with AN/atyp-AN (<em>n</em> = 64), all of whom were ≤90% of expected body weight, and age-matched healthy control individuals (<em>n</em> = 44).</p></div><div><h3>Results</h3><p>Five proteins differed significantly between the primary AN/atyp-AN group and the healthy control group (lower levels: HGF, IL-18R1, TRANCE; higher levels: CCL23, LIF-R). The expression levels of 3 proteins (lower IL-18R1, TRANCE; higher LIF-R) were uniquely disrupted in participants with AN in our primary model. No unique expression levels emerged for atyp-AN. In the total sample, 12 proteins (ADA, CD5, CD6, CXCL1, FGF-21, HGF, IL-12B, IL18, IL-18R1, SIRT2, TNFSF14, TRANCE) were positively correlated with body mass index and 5 proteins (CCL11, FGF-19, IL8, LIF-R, OPG) were negatively correlated with body mass index in our primary models.</p></div><div><h3>Conclusions</h3><p>Our results replicate the results of a previous study that demonstrated a dysregulated inflammatory status in AN and extend those results to atyp-AN. Of the 17 proteins correlated with body mass index, 11 were replicated from a previous study that used similar methods, highlighting the promise of inflammatory protein expression levels as biomarkers of AN disease monitoring. Our findings underscore the complexity of AN and atyp-AN by highlighting the inability of the identified proteins to differentiate between these 2 subtypes, thereby emphasizing the heterogeneous nature of these disorders.</p></div>\",\"PeriodicalId\":72373,\"journal\":{\"name\":\"Biological psychiatry global open science\",\"volume\":\"4 5\",\"pages\":\"Article 100332\"},\"PeriodicalIF\":4.0000,\"publicationDate\":\"2024-05-08\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.sciencedirect.com/science/article/pii/S2667174324000454/pdfft?md5=7a886594028244d17c0b0de18cd0c355&pid=1-s2.0-S2667174324000454-main.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biological psychiatry global open science\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2667174324000454\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biological psychiatry global open science","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2667174324000454","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
Identification of State Markers in Anorexia Nervosa: Replication and Extension of Inflammation-Associated Biomarkers Using Multiplex Profiling
Background
Proteomics offers potential for detecting and monitoring anorexia nervosa (AN) and its variant, atypical AN (atyp-AN). However, research has been limited by small protein panels, a focus on adult AN, and lack of replication.
Methods
In this study, we performed Olink multiplex profiling of 92 inflammation-related proteins in females with AN/atyp-AN (n = 64), all of whom were ≤90% of expected body weight, and age-matched healthy control individuals (n = 44).
Results
Five proteins differed significantly between the primary AN/atyp-AN group and the healthy control group (lower levels: HGF, IL-18R1, TRANCE; higher levels: CCL23, LIF-R). The expression levels of 3 proteins (lower IL-18R1, TRANCE; higher LIF-R) were uniquely disrupted in participants with AN in our primary model. No unique expression levels emerged for atyp-AN. In the total sample, 12 proteins (ADA, CD5, CD6, CXCL1, FGF-21, HGF, IL-12B, IL18, IL-18R1, SIRT2, TNFSF14, TRANCE) were positively correlated with body mass index and 5 proteins (CCL11, FGF-19, IL8, LIF-R, OPG) were negatively correlated with body mass index in our primary models.
Conclusions
Our results replicate the results of a previous study that demonstrated a dysregulated inflammatory status in AN and extend those results to atyp-AN. Of the 17 proteins correlated with body mass index, 11 were replicated from a previous study that used similar methods, highlighting the promise of inflammatory protein expression levels as biomarkers of AN disease monitoring. Our findings underscore the complexity of AN and atyp-AN by highlighting the inability of the identified proteins to differentiate between these 2 subtypes, thereby emphasizing the heterogeneous nature of these disorders.