Whole-blood expression of inflammasome- and glucocorticoid-related mRNAs correctly separates treatment-resistant depressed patients from drug-free and responsive patients in the BIODEP study

The mRNA expression signatures associated with the ‘pro-inflammatory’ phenotype of depression, and the differential signatures associated with depression subtypes and the effects of antidepressants, are still unknown. We examined 130 depressed patients (58 treatment-resistant, 36 antidepressant-resp...

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Published inTranslational psychiatry Vol. 10; no. 1; p. 232
Main Authors Cattaneo, Annamaria, Ferrari, Clarissa, Turner, Lorinda, Mariani, Nicole, Enache, Daniela, Hastings, Caitlin, Kose, Melisa, Lombardo, Giulia, McLaughlin, Anna P., Nettis, Maria A., Nikkheslat, Naghmeh, Sforzini, Luca, Worrell, Courtney, Zajkowska, Zuzanna, Cattane, Nadia, Lopizzo, Nicola, Mazzelli, Monica, Pointon, Linda, Cowen, Philip J., Cavanagh, Jonathan, Harrison, Neil A., de Boer, Peter, Jones, Declan, Drevets, Wayne C., Mondelli, Valeria, Bullmore, Edward T., Pariante, Carmine M.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 23.07.2020
Nature Publishing Group
Subjects
692/53/2422
692/699/476/1414
Antidepressive Agents
Behavioral Sciences
Biological Psychology
Cytokines
Glucocorticoids
Humans
Inflammasomes
Medicine
Medicine & Public Health
Neurosciences
Pharmacotherapy
Psychiatry
Receptors, Glucocorticoid - genetics
RNA, Messenger
Treatment resistance
Online AccessGet full text

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Abstract The mRNA expression signatures associated with the ‘pro-inflammatory’ phenotype of depression, and the differential signatures associated with depression subtypes and the effects of antidepressants, are still unknown. We examined 130 depressed patients (58 treatment-resistant, 36 antidepressant-responsive and 36 currently untreated) and 40 healthy controls from the BIODEP study, and used whole-blood mRNA qPCR to measure the expression of 16 candidate mRNAs, some never measured before: interleukin ( IL)-1-beta , IL-6 , TNF-alpha , macrophage inhibiting factor ( MIF ), glucocorticoid receptor ( GR ), SGK1 , FKBP5 , the purinergic receptor P2RX7 , CCL2 , CXCL12 , c-reactive protein ( CRP ), alpha-2-macroglobulin ( A2M ), acquaporin-4 ( AQP4 ), ISG15 , STAT1 and USP-18 . All genes but AQP4 , ISG15 and USP-18 were differentially regulated. Treatment-resistant and drug-free depressed patients had both increased inflammasome activation (higher P2RX7 and proinflammatory cytokines/chemokines mRNAs expression) and glucocorticoid resistance (lower GR and higher FKBP5 mRNAs expression), while responsive patients had an intermediate phenotype with, additionally, lower CXCL12 . Most interestingly, using binomial logistics models we found that a signature of six mRNAs ( P2RX7 , IL-1-beta, IL-6 , TNF-alpha, CXCL12 and GR ) distinguished treatment-resistant from responsive patients, even after adjusting for other variables that were different between groups, such as a trait- and state-anxiety, history of childhood maltreatment and serum CRP. Future studies should replicate these findings in larger, longitudinal cohorts, and test whether this mRNA signature can identify patients that are more likely to respond to adjuvant strategies for treatment-resistant depression, including combinations with anti-inflammatory medications.
AbstractList The mRNA expression signatures associated with the ‘pro-inflammatory’ phenotype of depression, and the differential signatures associated with depression subtypes and the effects of antidepressants, are still unknown. We examined 130 depressed patients (58 treatment-resistant, 36 antidepressant-responsive and 36 currently untreated) and 40 healthy controls from the BIODEP study, and used whole-blood mRNA qPCR to measure the expression of 16 candidate mRNAs, some never measured before: interleukin (IL)-1-beta, IL-6, TNF-alpha, macrophage inhibiting factor (MIF), glucocorticoid receptor (GR), SGK1, FKBP5, the purinergic receptor P2RX7, CCL2, CXCL12, c-reactive protein (CRP), alpha-2-macroglobulin (A2M), acquaporin-4 (AQP4), ISG15, STAT1 and USP-18. All genes but AQP4, ISG15 and USP-18 were differentially regulated. Treatment-resistant and drug-free depressed patients had both increased inflammasome activation (higher P2RX7 and proinflammatory cytokines/chemokines mRNAs expression) and glucocorticoid resistance (lower GR and higher FKBP5 mRNAs expression), while responsive patients had an intermediate phenotype with, additionally, lower CXCL12. Most interestingly, using binomial logistics models we found that a signature of six mRNAs (P2RX7, IL-1-beta, IL-6, TNF-alpha, CXCL12 and GR) distinguished treatment-resistant from responsive patients, even after adjusting for other variables that were different between groups, such as a trait- and state-anxiety, history of childhood maltreatment and serum CRP. Future studies should replicate these findings in larger, longitudinal cohorts, and test whether this mRNA signature can identify patients that are more likely to respond to adjuvant strategies for treatment-resistant depression, including combinations with anti-inflammatory medications.
The mRNA expression signatures associated with the ‘pro-inflammatory’ phenotype of depression, and the differential signatures associated with depression subtypes and the effects of antidepressants, are still unknown. We examined 130 depressed patients (58 treatment-resistant, 36 antidepressant-responsive and 36 currently untreated) and 40 healthy controls from the BIODEP study, and used whole-blood mRNA qPCR to measure the expression of 16 candidate mRNAs, some never measured before: interleukin ( IL)-1-beta , IL-6 , TNF-alpha , macrophage inhibiting factor ( MIF ), glucocorticoid receptor ( GR ), SGK1 , FKBP5 , the purinergic receptor P2RX7 , CCL2 , CXCL12 , c-reactive protein ( CRP ), alpha-2-macroglobulin ( A2M ), acquaporin-4 ( AQP4 ), ISG15 , STAT1 and USP-18 . All genes but AQP4 , ISG15 and USP-18 were differentially regulated. Treatment-resistant and drug-free depressed patients had both increased inflammasome activation (higher P2RX7 and proinflammatory cytokines/chemokines mRNAs expression) and glucocorticoid resistance (lower GR and higher FKBP5 mRNAs expression), while responsive patients had an intermediate phenotype with, additionally, lower CXCL12 . Most interestingly, using binomial logistics models we found that a signature of six mRNAs ( P2RX7 , IL-1-beta, IL-6 , TNF-alpha, CXCL12 and GR ) distinguished treatment-resistant from responsive patients, even after adjusting for other variables that were different between groups, such as a trait- and state-anxiety, history of childhood maltreatment and serum CRP. Future studies should replicate these findings in larger, longitudinal cohorts, and test whether this mRNA signature can identify patients that are more likely to respond to adjuvant strategies for treatment-resistant depression, including combinations with anti-inflammatory medications.
The mRNA expression signatures associated with the 'pro-inflammatory' phenotype of depression, and the differential signatures associated with depression subtypes and the effects of antidepressants, are still unknown. We examined 130 depressed patients (58 treatment-resistant, 36 antidepressant-responsive and 36 currently untreated) and 40 healthy controls from the BIODEP study, and used whole-blood mRNA qPCR to measure the expression of 16 candidate mRNAs, some never measured before: interleukin (IL)-1-beta, IL-6, TNF-alpha, macrophage inhibiting factor (MIF), glucocorticoid receptor (GR), SGK1, FKBP5, the purinergic receptor P2RX7, CCL2, CXCL12, c-reactive protein (CRP), alpha-2-macroglobulin (A2M), acquaporin-4 (AQP4), ISG15, STAT1 and USP-18. All genes but AQP4, ISG15 and USP-18 were differentially regulated. Treatment-resistant and drug-free depressed patients had both increased inflammasome activation (higher P2RX7 and proinflammatory cytokines/chemokines mRNAs expression) and glucocorticoid resistance (lower GR and higher FKBP5 mRNAs expression), while responsive patients had an intermediate phenotype with, additionally, lower CXCL12. Most interestingly, using binomial logistics models we found that a signature of six mRNAs (P2RX7, IL-1-beta, IL-6, TNF-alpha, CXCL12 and GR) distinguished treatment-resistant from responsive patients, even after adjusting for other variables that were different between groups, such as a trait- and state-anxiety, history of childhood maltreatment and serum CRP. Future studies should replicate these findings in larger, longitudinal cohorts, and test whether this mRNA signature can identify patients that are more likely to respond to adjuvant strategies for treatment-resistant depression, including combinations with anti-inflammatory medications.The mRNA expression signatures associated with the 'pro-inflammatory' phenotype of depression, and the differential signatures associated with depression subtypes and the effects of antidepressants, are still unknown. We examined 130 depressed patients (58 treatment-resistant, 36 antidepressant-responsive and 36 currently untreated) and 40 healthy controls from the BIODEP study, and used whole-blood mRNA qPCR to measure the expression of 16 candidate mRNAs, some never measured before: interleukin (IL)-1-beta, IL-6, TNF-alpha, macrophage inhibiting factor (MIF), glucocorticoid receptor (GR), SGK1, FKBP5, the purinergic receptor P2RX7, CCL2, CXCL12, c-reactive protein (CRP), alpha-2-macroglobulin (A2M), acquaporin-4 (AQP4), ISG15, STAT1 and USP-18. All genes but AQP4, ISG15 and USP-18 were differentially regulated. Treatment-resistant and drug-free depressed patients had both increased inflammasome activation (higher P2RX7 and proinflammatory cytokines/chemokines mRNAs expression) and glucocorticoid resistance (lower GR and higher FKBP5 mRNAs expression), while responsive patients had an intermediate phenotype with, additionally, lower CXCL12. Most interestingly, using binomial logistics models we found that a signature of six mRNAs (P2RX7, IL-1-beta, IL-6, TNF-alpha, CXCL12 and GR) distinguished treatment-resistant from responsive patients, even after adjusting for other variables that were different between groups, such as a trait- and state-anxiety, history of childhood maltreatment and serum CRP. Future studies should replicate these findings in larger, longitudinal cohorts, and test whether this mRNA signature can identify patients that are more likely to respond to adjuvant strategies for treatment-resistant depression, including combinations with anti-inflammatory medications.
ArticleNumber 232
Author Sforzini, Luca
Zajkowska, Zuzanna
Pointon, Linda
Drevets, Wayne C.
Turner, Lorinda
Mondelli, Valeria
Mazzelli, Monica
Mariani, Nicole
Bullmore, Edward T.
Nettis, Maria A.
Kose, Melisa
Cattaneo, Annamaria
Worrell, Courtney
de Boer, Peter
Cowen, Philip J.
Enache, Daniela
Jones, Declan
Pariante, Carmine M.
Nikkheslat, Naghmeh
Lopizzo, Nicola
McLaughlin, Anna P.
Cattane, Nadia
Cavanagh, Jonathan
Lombardo, Giulia
Harrison, Neil A.
Hastings, Caitlin
Ferrari, Clarissa
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CorporateAuthor the Neuroimmunology of Mood Disorders and Alzheimer’s Disease (NIMA) Consortium
Neuroimmunology of Mood Disorders and Alzheimer’s Disease (NIMA) Consortium
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Snippet The mRNA expression signatures associated with the ‘pro-inflammatory’ phenotype of depression, and the differential signatures associated with depression...
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Antidepressive Agents
Behavioral Sciences
Biological Psychology
Cytokines
Glucocorticoids
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Inflammasomes
Medicine
Medicine & Public Health
Neurosciences
Pharmacotherapy
Psychiatry
Receptors, Glucocorticoid - genetics
RNA, Messenger
Treatment resistance
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