Table 1.

Table summarizing CP changes in inflammatory diseases

Category	Disorder	Choroidal epithelial cells	Junctions	Immune cells	Transporters	Others
Inflammation and infection	Systemic inflammation	↑ COX-2 and IκBα expression [113, 115]	↓ Occludin mRNA expression [116]			↑ CCL2 expression [122]
		↑ TLR1, TLR3, TLR4, CD14 expression ↓ Occludin expression [110–112, 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 [129–131]			(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]