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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
  ↑ CCL2 expression
↑ 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
↑ TNFα expression
[119, 120]
   Collagen I cleavage
↑ Il-1β, TNFα, LPTGDS expression
   ↑ mRNA expression of TNFRI, TNFRII, IL1β, IL1 receptor type I, type II, Il6 and its signal transducing component – Il6 signal transducer
↑ LCN2 expression
[103, 104]
↑ Expression of Hamp, Cp, Fth1, Stat3, Smad4, Tfr2, Il6 genes
↑ MMP-8 expression
↑ EVs secretion
Bacterial infections(Streptococcus suis)
fibrinous exudate, disruption of epithelial “brush border”
(Streptococcus suis)
Disruption of normal pattern of the TJ—Occludin, ZO-1, claudin-1
↓ (Streptococcus suis)
Number of epiplexus cells
(Haemophilus influenzae)
Paracellular invasion into CSF
↑ (Streptococcus pneumoniae)
NF-κB, PAF, laminin receptor expression in CP endothelial cells
↓ (Streptococcus pneumoniae)
TNFα -mRNA expression
↓ (Streptococcus suis)
Claudin-2 expression
 (Listeria monocytogenes)
Using the “Trojan horse” mechanism by occupying mononuclear cells in the CP
(Streptococcus suis)
Apoptosis and necrosis of CP epithelial cells
  (Streptococcus suis)
Transcellular migration in endocytic vacuoles
(Listeria monocytogenes)
Interaction of internalin A and B with E-cadherin on CP epithelial cells
  (Streptococcus suis)
Transepithelial migration of polymorphonuclear leukocytes
↑ (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
  (Neisseria meningitidis)
Migration through CP epithelial cells
(Streptococcus pneumoniae)
Antibacterial effect of TLR2
  (Escherichia coli)
Invasion through CP epithelial cells
↑ (Neisseria meningitidis)
IL6, CCL20, CXCL1-3, Nfkbiz, GM-CSF expression
  (Haemophilus influenzae)
Transcellular migration from the basolateral side of CP epithelial cells
(Listeria monocytogenes)
Activation of MAPKs, Erk1/2 and p38
Viral infections(Echovirus 30)
Invasion and replication in CP epithelial cells
MHC II + dendritic cells in the CP as reservoir of HIV
(Zika virus)
Entry to the brain through CP epithelial cells
Endothelial cells in the CP as a reservoir of HIV
↑ (Echovirus 30)
CXCL3, CXCL10, CXCL11, CCL20, IL8, IL7, M-CSF expression
Monocytes-like cells in the CP as a reservoir of HIV
(Polyomavirus JC)
CP cells as a reservoir
 (Coxsackievirus B3)
Diapedesis of infected myeloid cells expressing high level of Ki67 and pERK1/2 through the TJ of the CP
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
 (Leishmania chagasi)
Infiltration of inflammatory cells with lymphoplasmatic morphology around the blood vessels and diffusely in CP stroma
 (Leishmania chagasi)
Deposits of perivascular hyaline substances
(Trypanosoma evansi)
Edema and rupture of the CP epithelial cell layer
 (Trypanosoma evansi)
Infiltration of CP by inflammatory cells
 ↑ (Leishmania infantum)
TLR2 and TLR9 expression,
no changes in TLR4 expression
  (Leishmania infantum)
Inflammatory infiltration via CD3+ T lymphocytes
 (Leishmania infantum)
Accumulation of perivascular hyaline substances consistent with IgG and parasite DNA