PMID- 35994946
OWN - NLM
STAT- MEDLINE
DCOM- 20220914
LR  - 20221108
IS  - 1872-8421 (Electronic)
IS  - 0165-5728 (Linking)
VI  - 371
DP  - 2022 Oct 15
TI  - The role of damage associated molecular pattern molecules (DAMPs) and 
      permeability of the blood-brain barrier in depression and neuroinflammation.
PG  - 577951
LID - S0165-5728(22)00146-1 [pii]
LID - 10.1016/j.jneuroim.2022.577951 [doi]
AB  - Depression is a heterogeneous mental disorder characterized by feelings of 
      sadness and loss of interest that render the subject unable to handle basic daily 
      activities such as sleeping, eating, or working. Neurobiological traits leading 
      to depression include genetic background, early life abuse, life stressors, and 
      systemic and central inflammatory profiles. Several clinical and preclinical 
      reports documented that depression shows an increase in pro-inflammatory markers 
      such as interleukin (IL-)1beta, IL-6, IL-12, tumor necrosis factor (TNF), and 
      interferon (IFN)-gamma; and a decrease in anti-inflammatory IL-4, IL-10, and 
      transforming growth factor (TGF)-beta species. Inflammatory activation may trigger 
      and maintain depression. Dynamic crosstalk between the peripheral immune system 
      and the central nervous system (CNS) such as activated endothelial cells, 
      monocytes, monocyte-derived dendritic cells, macrophages, T cells, and microglia 
      has been proposed as a leading cause of neuroinflammation. Notably, 
      pro-inflammatory cytokines disrupt the hypothalamic-pituitary-adrenal (HPA) axis 
      and serotonergic, noradrenergic, dopaminergic, and glutamatergic 
      neurotransmission. While still under investigation, peripheral cytokines can 
      engage brain pathways and affect the central synthesis of HPA hormones and 
      neurotransmitters through several mechanisms such as activation of the vagus 
      nerve, increasing the permeability of the blood-brain barrier (BBB), altered 
      cytokines transport systems, and engaging toll-like receptors (TLRs) by 
      pathogen-associated molecular patterns (PAMPs) or damage-associated molecular 
      patterns (DAMPs). However, physiological mechanisms that favor time-dependent 
      central inflammation before or during illness are not totally understood. This 
      review will provide preclinical and clinical evidence of DAMPs and the BBB 
      permeability as contributors to depression and neuroinflammation. We will also 
      discuss pharmacologic approaches that could potentially modulate DAMPs and BBB 
      permeability for future interventions against major depression.
CI  - Copyright (c) 2022 Elsevier B.V. All rights reserved.
FAU - Serna-Rodriguez, Maria Fernanda
AU  - Serna-Rodriguez MF
AD  - Universidad Autonoma de Nuevo Leon, Facultad de Medicina, Departamento de 
      Bioquimica y Medicina Molecular. Monterrey CP. 64460, Nuevo Leon, Mexico.
FAU - Bernal-Vega, Sofia
AU  - Bernal-Vega S
AD  - Universidad Autonoma de Nuevo Leon, Facultad de Medicina, Departamento de 
      Bioquimica y Medicina Molecular. Monterrey CP. 64460, Nuevo Leon, Mexico.
FAU - de la Barquera, Jose Alfonso Ontiveros-Sanchez
AU  - de la Barquera JAO
AD  - Universidad Autonoma de Nuevo Leon, Facultad de Medicina Monterrey, Departamento 
      de Psiquiatria, Monterrey CP. 64460, Nuevo Leon, Mexico.
FAU - Camacho-Morales, Alberto
AU  - Camacho-Morales A
AD  - Universidad Autonoma de Nuevo Leon, Facultad de Medicina, Departamento de 
      Bioquimica y Medicina Molecular. Monterrey CP. 64460, Nuevo Leon, Mexico. 
      Electronic address: alberto.camachomr@uanl.edu.mx.
FAU - Perez-Maya, Antonio Ali
AU  - Perez-Maya AA
AD  - Universidad Autonoma de Nuevo Leon, Facultad de Medicina, Departamento de 
      Bioquimica y Medicina Molecular. Monterrey CP. 64460, Nuevo Leon, Mexico. 
      Electronic address: antonio.perezmy@uanl.edu.mx.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20220817
PL  - Netherlands
TA  - J Neuroimmunol
JT  - Journal of neuroimmunology
JID - 8109498
RN  - 0 (Alarmins)
RN  - 0 (Cytokines)
SB  - IM
MH  - *Alarmins
MH  - *Blood-Brain Barrier/pathology
MH  - Cytokines/metabolism
MH  - Depression
MH  - Endothelial Cells/metabolism
MH  - Humans
MH  - Neuroinflammatory Diseases
MH  - Permeability
OTO - NOTNLM
OT  - Blood-brain barrier
OT  - Cytokines
OT  - DAMPs
OT  - Depression
OT  - Neuroinflammation
COIS- Declaration of Competing Interest The authors of this manuscript declare that 
      they have no conflict of interest.
EDAT- 2022/08/23 06:00
MHDA- 2022/09/15 06:00
CRDT- 2022/08/22 18:24
PHST- 2022/02/17 00:00 [received]
PHST- 2022/08/03 00:00 [revised]
PHST- 2022/08/13 00:00 [accepted]
PHST- 2022/08/23 06:00 [pubmed]
PHST- 2022/09/15 06:00 [medline]
PHST- 2022/08/22 18:24 [entrez]
AID - S0165-5728(22)00146-1 [pii]
AID - 10.1016/j.jneuroim.2022.577951 [doi]
PST - ppublish
SO  - J Neuroimmunol. 2022 Oct 15;371:577951. doi: 10.1016/j.jneuroim.2022.577951. Epub 
      2022 Aug 17.