Activation of the cholinergic anti-inflammatory system in peripheral blood mononuclear cells from patients with Borderline Personality Disorder

dc.contributor.authorDíaz Marsa, Marina Francisca
dc.contributor.authorMac-Dowell Mata, Karina Soledad
dc.contributor.authorGuemes, Itziar
dc.contributor.authorRubio, Víctor
dc.contributor.authorCarrasco Perera, José Luis
dc.contributor.authorLeza Cerro, Juan Carlos
dc.date.accessioned2025-01-29T14:41:11Z
dc.date.available2025-01-29T14:41:11Z
dc.date.issued2012
dc.description.abstractA case-control study including patients (n = 20) with Borderline Personality Disorder (BPD) and healthy controls (n = 33) was carried out. To avoid interferences of other clinical conditions on biological findings, patients were free of current major depressive episodes or substance dependence disorders, and had no life history of schizophrenia, bipolar or neuropsychiatric disorders. Patients were free of medication for at least two weeks at the time of the study. Studies carried out in peripheral mononuclear blood cells and plasma evidence a systemic inflammatory condition in unstable-impulsive BPD patients. Specifically, a significant increase in some intracellular components of two main pro-inflammatory pathways such as iNOS and COX-2, as well as an increase in the plasma levels of the inflammatory cytokine IL1β. Interestingly, patients have an increase in the protein expression of the anti-inflammatory subtype of nicotinic receptor α7nAChR. This finding may reflect a possible mechanism trying to maintain intracellular inflammation pathways under control. All together, these results describe an imbalanced, pro-inflammatory and oxidant phenotype in BPD patients independent of plasma cotinine levels. Although more scientific evidence is needed, the determination of multiple components of pro- and anti-inflammatory cellular pathways have interesting potential as biological markers for BPD and other generalized impulsive syndromes, specially data obtained with α7nAChR and its lack of correlation with plasma levels of nicotine metabolites. Their pharmacological modulation with receptor modulators can be a promising therapeutic target to take into account in mental health conditions associated with inflammatory or oxido/nitrosative consequences. Also, identifying at-risk individuals would be of importance for early detection and intervention in adolescent subjects before they present severe behavioural problems.
dc.description.departmentDepto. de Medicina Legal, Psiquiatría y Patología
dc.description.facultyFac. de Medicina
dc.description.refereedTRUE
dc.description.statuspub
dc.identifier.citationDíaz-Marsá M, Macdowell KS, Guemes I, Rubio V, Carrasco JL, Leza JC. Activation of the cholinergic anti-inflammatory system in peripheral blood mononuclear cells from patients with borderline personality disorder. J Psychiatr Res. 2012 Dec;46(12):1610-7. doi: 10.1016/j.jpsychires.2012.09.009. Epub 2012 Oct 17. PMID: 23083519.
dc.identifier.doi10.1016/j.jpsychires.2012.09.009
dc.identifier.issn0022-3956
dc.identifier.officialurlhttps://doi.org/10.1016/j.jpsychires.2012.09.009
dc.identifier.pmid23083519
dc.identifier.relatedurlhttps://www.sciencedirect.com/journal/journal-of-psychiatric-research
dc.identifier.urihttps://hdl.handle.net/20.500.14352/116941
dc.issue.number12
dc.journal.titleJournal of Psychiatric Research
dc.language.isoeng
dc.page.final1617
dc.page.initial1610
dc.publisherElsevier
dc.rights.accessRightsrestricted access
dc.subject.cdu616.89
dc.subject.keywordBorderline Personality Disorder
dc.subject.keywordBiomarker
dc.subject.keywordInflammatory/antiinflamamtory balance
dc.subject.keywordCholinergic receptor
dc.subject.ucmCiencias Biomédicas
dc.subject.unesco32 Ciencias Médicas
dc.titleActivation of the cholinergic anti-inflammatory system in peripheral blood mononuclear cells from patients with Borderline Personality Disorder
dc.typejournal article
dc.type.hasVersionVoR
dc.volume.number46
dspace.entity.typePublication
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relation.isAuthorOfPublicationd7de3e71-d141-4e63-ab4c-a71249846532
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relation.isAuthorOfPublication.latestForDiscovery7223c575-c4d9-48e4-84cf-2d692e698630

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