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Table 1 Table summarizing CP changes in inflammatory diseases

From: Choroid plexus and the blood–cerebrospinal fluid barrier in disease

CategoryDisorderChoroidal epithelial cellsJunctionsImmune cellsTransportersOthers
Inflammation and infectionSystemic inflammation↑ COX-2 and IκBα expression
[113, 115]
↓ Occludin mRNA expression
[116]
  ↑ CCL2 expression
[122]
↑ TLR1, TLR3, TLR4, CD14 expression
↓ Occludin expression
[110,111,112, 114, 116]
   ↑ Expression of ICAM-1, GlyCAM-1, MAdCAM-1, Jam2, Selpl, chemokines CXCL1, CCL7, CCL2, IL-16
[123]
↑ TNFα expression
[119, 120]
   Collagen I cleavage
[118]
↑ Il-1β, TNFα, LPTGDS expression
[102]
   ↑ mRNA expression of TNFRI, TNFRII, IL1β, IL1 receptor type I, type II, Il6 and its signal transducing component – Il6 signal transducer
[121]
↑ LCN2 expression
[103, 104]
    
↑ Expression of Hamp, Cp, Fth1, Stat3, Smad4, Tfr2, Il6 genes
[107]
    
↑ MMP-8 expression
[118]
    
↑ EVs secretion
[125]
    
Bacterial infections(Streptococcus suis)
fibrinous exudate, disruption of epithelial “brush border”
[134]
(Streptococcus suis)
Disruption of normal pattern of the TJ—Occludin, ZO-1, claudin-1
[128]
↓ (Streptococcus suis)
Number of epiplexus cells
[134]
(Haemophilus influenzae)
Paracellular invasion into CSF
[145]
↑ (Streptococcus pneumoniae)
NF-κB, PAF, laminin receptor expression in CP endothelial cells
[136]
↓ (Streptococcus pneumoniae)
TNFα -mRNA expression
[138]
↓ (Streptococcus suis)
Claudin-2 expression
[131]
 (Listeria monocytogenes)
Using the “Trojan horse” mechanism by occupying mononuclear cells in the CP
[139]
 
(Streptococcus suis)
Apoptosis and necrosis of CP epithelial cells
[132]
  (Streptococcus suis)
Transcellular migration in endocytic vacuoles
[133]
 
(Listeria monocytogenes)
Interaction of internalin A and B with E-cadherin on CP epithelial cells
[140]
  (Streptococcus suis)
Transepithelial migration of polymorphonuclear leukocytes
[135]
 
↑ (Streptococcus suis)
ICAM-1, VCAM-1, MMP-3, NFκB, MAPK, TNFα, Il-1β, IL-6, IL-8, LIF, ARG1, ARG2, NOS2, indoleamine 2,3-dioxygenase expression
[129,130,131]
  (Neisseria meningitidis)
Migration through CP epithelial cells
[148]
 
(Streptococcus pneumoniae)
Antibacterial effect of TLR2
[136]
  (Escherichia coli)
Invasion through CP epithelial cells
[144]
 
↑ (Neisseria meningitidis)
IL6, CCL20, CXCL1-3, Nfkbiz, GM-CSF expression
[150]
  (Haemophilus influenzae)
Transcellular migration from the basolateral side of CP epithelial cells
[146]
 
(Listeria monocytogenes)
Activation of MAPKs, Erk1/2 and p38
[142]
    
Viral infections(Echovirus 30)
Invasion and replication in CP epithelial cells
[161]
 (HIV)
MHC II + dendritic cells in the CP as reservoir of HIV
[160]
(Zika virus)
Entry to the brain through CP epithelial cells
[152]
(HIV)
Endothelial cells in the CP as a reservoir of HIV
[159]
↑ (Echovirus 30)
CXCL3, CXCL10, CXCL11, CCL20, IL8, IL7, M-CSF expression
[162]
 (HIV)
Monocytes-like cells in the CP as a reservoir of HIV
[156]
  
(Polyomavirus JC)
CP cells as a reservoir
[153]
 (Coxsackievirus B3)
Diapedesis of infected myeloid cells expressing high level of Ki67 and pERK1/2 through the TJ of the CP
[163]
  
Fungal infections    (Cryptococcuis neoformans)
CP plexitis in HIV patients
[170, 172]
Parasitic infections(Trypanosoma brucei)
Present in perivascular region of CP and in CP epithelial cells
[174]
 (Leishmania chagasi)
Infiltration of inflammatory cells with lymphoplasmatic morphology around the blood vessels and diffusely in CP stroma
[176]
 (Leishmania chagasi)
Deposits of perivascular hyaline substances
[176]
(Trypanosoma evansi)
Edema and rupture of the CP epithelial cell layer
[175]
 (Trypanosoma evansi)
Infiltration of CP by inflammatory cells
[175]
 ↑ (Leishmania infantum)
TLR2 and TLR9 expression,
no changes in TLR4 expression
[177]
  (Leishmania infantum)
Inflammatory infiltration via CD3+ T lymphocytes
[176]
 (Leishmania infantum)
Accumulation of perivascular hyaline substances consistent with IgG and parasite DNA
[176]