Reduced mip-1β as a trait marker and reduced il-7 and il-12 as state markers of anorexia nervosa

Johanna Louise Keeler; Olivia Patsalos; Raymond Chung; Ulrike Schmidt; Gerome Breen; Janet Treasure; Hubertus Himmerich; Bethan Dalton

doi:10.3390/jpm11080814

Reduced mip-1β as a trait marker and reduced il-7 and il-12 as state markers of anorexia nervosa

Johanna Louise Keeler^*, Olivia Patsalos, Raymond Chung, Ulrike Schmidt, Gerome Breen, Janet Treasure, Hubertus Himmerich, Bethan Dalton

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

9 Citations (Scopus)

Abstract

Alterations in certain inflammatory markers have been found in individuals with anorexia nervosa (AN). However, their relation to clinical characteristics has not been extensively explored, nor is it clear whether they are trait or state features of the disorder. This cross-sectional study measured serum concentrations of 36 inflammatory markers in people with acute AN (n = 56), recovered AN (rec-AN; n = 24) and healthy controls (HC; n = 51). The relationship between body mass index (BMI), eating disorder psychopathology, depression symptoms and inflammatory markers was assessed. Statistical models controlled for variables known to influence cytokine concentrations (i.e., age, ethnicity, smoking status and medication usage). Overall, most inflammatory markers including pro-inflammatory cytokines were unchanged in AN and rec-AN. However, in AN and rec-AN, concentrations of macrophage inflammatory protein (MIP)-1β were lower than HCs. Interleukin (IL)-7 and IL-12/IL-23p40 were reduced in AN, and concentrations of macrophage-derived chemokine, MIP-1α and tumor necrosis factor-α were reduced in rec-AN compared to HC. In conclusion, a reduc-tion in MIP-1β may be a trait marker of the illness, whereas reductions in IL-7 and IL-12/IL-23p40 may be state markers. The absence of increased pro-inflammatory cytokines in AN is contradictory to the wider literature, although the inclusion of covariates may explain our differing findings.

Original language	English
Article number	814
Journal	Journal of Personalized Medicine
Volume	11
Issue number	8
DOIs	https://doi.org/10.3390/jpm11080814
Publication status	Published - Aug 2021

Keywords

Anorexia nervosa
Brain-derived neurotrophic factor
Chemokines
Crossectional
Cytokines
Inflammatory markers

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@article{bee3cbbe2b9847918e47fb6a618c8c13,

title = "Reduced mip-1β as a trait marker and reduced il-7 and il-12 as state markers of anorexia nervosa",

abstract = "Alterations in certain inflammatory markers have been found in individuals with anorexia nervosa (AN). However, their relation to clinical characteristics has not been extensively explored, nor is it clear whether they are trait or state features of the disorder. This cross-sectional study measured serum concentrations of 36 inflammatory markers in people with acute AN (n = 56), recovered AN (rec-AN; n = 24) and healthy controls (HC; n = 51). The relationship between body mass index (BMI), eating disorder psychopathology, depression symptoms and inflammatory markers was assessed. Statistical models controlled for variables known to influence cytokine concentrations (i.e., age, ethnicity, smoking status and medication usage). Overall, most inflammatory markers including pro-inflammatory cytokines were unchanged in AN and rec-AN. However, in AN and rec-AN, concentrations of macrophage inflammatory protein (MIP)-1β were lower than HCs. Interleukin (IL)-7 and IL-12/IL-23p40 were reduced in AN, and concentrations of macrophage-derived chemokine, MIP-1α and tumor necrosis factor-α were reduced in rec-AN compared to HC. In conclusion, a reduc-tion in MIP-1β may be a trait marker of the illness, whereas reductions in IL-7 and IL-12/IL-23p40 may be state markers. The absence of increased pro-inflammatory cytokines in AN is contradictory to the wider literature, although the inclusion of covariates may explain our differing findings.",

keywords = "Anorexia nervosa, Brain-derived neurotrophic factor, Chemokines, Crossectional, Cytokines, Inflammatory markers",

author = "Keeler, {Johanna Louise} and Olivia Patsalos and Raymond Chung and Ulrike Schmidt and Gerome Breen and Janet Treasure and Hubertus Himmerich and Bethan Dalton",

note = "Funding Information: Acknowledgments: Johanna Keeler received a PhD stipend from the Medical Research Council (reference number: MR/N013700/1). Bethan Dalton was supported by a studentship awarded by the Department of Psychological Medicine, King{\textquoteright}s College London (KCL) and the Institute of Psychiatry, Psychology and Neuroscience (IoPPN), KCL. Gerome Breen, Hubertus Himmerich, Olivia Patsalos and Janet Treasure received salary support from the National Institute for Health Research (NIHR) Biomedical Research Centre (BRC) at the South London and Maudsley NHS Foundation Trust (SLaM) and KCL. Ulrike Schmidt is supported by an NIHR Senior Investigator Award. We thank NIHR BioResource volunteers for their participation, and gratefully acknowledge NIHR BioResource centres, NHS Trusts and staff for their contribution. We thank the National Institute for Health Research, NHS Blood and Transplant, and Health Data Research UK as part of the Digital Innovation Hub Programme. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health and Social Care. Publisher Copyright: {\textcopyright} 2021 by the authors. Licensee MDPI, Basel, Switzerland. Copyright: Copyright 2021 Elsevier B.V., All rights reserved.",

year = "2021",

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doi = "10.3390/jpm11080814",

language = "English",

volume = "11",

journal = "Journal of Personalized Medicine",

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AU - Keeler, Johanna Louise

AU - Patsalos, Olivia

AU - Chung, Raymond

AU - Schmidt, Ulrike

AU - Breen, Gerome

AU - Treasure, Janet

AU - Himmerich, Hubertus

AU - Dalton, Bethan

N1 - Funding Information: Acknowledgments: Johanna Keeler received a PhD stipend from the Medical Research Council (reference number: MR/N013700/1). Bethan Dalton was supported by a studentship awarded by the Department of Psychological Medicine, King’s College London (KCL) and the Institute of Psychiatry, Psychology and Neuroscience (IoPPN), KCL. Gerome Breen, Hubertus Himmerich, Olivia Patsalos and Janet Treasure received salary support from the National Institute for Health Research (NIHR) Biomedical Research Centre (BRC) at the South London and Maudsley NHS Foundation Trust (SLaM) and KCL. Ulrike Schmidt is supported by an NIHR Senior Investigator Award. We thank NIHR BioResource volunteers for their participation, and gratefully acknowledge NIHR BioResource centres, NHS Trusts and staff for their contribution. We thank the National Institute for Health Research, NHS Blood and Transplant, and Health Data Research UK as part of the Digital Innovation Hub Programme. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health and Social Care. Publisher Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland. Copyright: Copyright 2021 Elsevier B.V., All rights reserved.

PY - 2021/8

Y1 - 2021/8

N2 - Alterations in certain inflammatory markers have been found in individuals with anorexia nervosa (AN). However, their relation to clinical characteristics has not been extensively explored, nor is it clear whether they are trait or state features of the disorder. This cross-sectional study measured serum concentrations of 36 inflammatory markers in people with acute AN (n = 56), recovered AN (rec-AN; n = 24) and healthy controls (HC; n = 51). The relationship between body mass index (BMI), eating disorder psychopathology, depression symptoms and inflammatory markers was assessed. Statistical models controlled for variables known to influence cytokine concentrations (i.e., age, ethnicity, smoking status and medication usage). Overall, most inflammatory markers including pro-inflammatory cytokines were unchanged in AN and rec-AN. However, in AN and rec-AN, concentrations of macrophage inflammatory protein (MIP)-1β were lower than HCs. Interleukin (IL)-7 and IL-12/IL-23p40 were reduced in AN, and concentrations of macrophage-derived chemokine, MIP-1α and tumor necrosis factor-α were reduced in rec-AN compared to HC. In conclusion, a reduc-tion in MIP-1β may be a trait marker of the illness, whereas reductions in IL-7 and IL-12/IL-23p40 may be state markers. The absence of increased pro-inflammatory cytokines in AN is contradictory to the wider literature, although the inclusion of covariates may explain our differing findings.

AB - Alterations in certain inflammatory markers have been found in individuals with anorexia nervosa (AN). However, their relation to clinical characteristics has not been extensively explored, nor is it clear whether they are trait or state features of the disorder. This cross-sectional study measured serum concentrations of 36 inflammatory markers in people with acute AN (n = 56), recovered AN (rec-AN; n = 24) and healthy controls (HC; n = 51). The relationship between body mass index (BMI), eating disorder psychopathology, depression symptoms and inflammatory markers was assessed. Statistical models controlled for variables known to influence cytokine concentrations (i.e., age, ethnicity, smoking status and medication usage). Overall, most inflammatory markers including pro-inflammatory cytokines were unchanged in AN and rec-AN. However, in AN and rec-AN, concentrations of macrophage inflammatory protein (MIP)-1β were lower than HCs. Interleukin (IL)-7 and IL-12/IL-23p40 were reduced in AN, and concentrations of macrophage-derived chemokine, MIP-1α and tumor necrosis factor-α were reduced in rec-AN compared to HC. In conclusion, a reduc-tion in MIP-1β may be a trait marker of the illness, whereas reductions in IL-7 and IL-12/IL-23p40 may be state markers. The absence of increased pro-inflammatory cytokines in AN is contradictory to the wider literature, although the inclusion of covariates may explain our differing findings.

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KW - Inflammatory markers

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Reduced mip-1β as a trait marker and reduced il-7 and il-12 as state markers of anorexia nervosa

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Keywords

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