Table 2.
Markers | Original characterization | CHME3 cells | HMC3 cells | References | |||
---|---|---|---|---|---|---|---|
Resting | Stimulated | Resting | Stimulated | Resting | Stimulated | ||
Pro-inflammatory molecules | |||||||
IL-6 | 1553 ± 142 | IL-1α: > 2500 LPS: 2110 ± 111 |
20–950/sizable amount | LPS: 2–4 fold ↑ IL-1β: 50 fold ↑ IFNγ: modest ↑ IL-1β + IFNγ: additional ↑ Aβ1–40: 2–12 fold ↑ Aβ1–40 + IFNγ: no- additional ↑ Aβ1–42: no effect α-MSH: ↑ EPA: ↑ HCV NS3: ↑ |
Sizable amount /(mRNA level) | HIV-vector: ↑ HIV-U937: ↑ |
[17, 20, 21, 30, 36, 37, 40, 43, 47, 48] |
TNFα | ND | ND | 4–8/ND | Aβ1–40: no effect Aβ1–42: modest ↑ HCV NS3: ↑ |
(mRNA level) | [17, 21, 37, 40, 43, 44, 47] | |
IL-1α | ND | Aβ1–40: no effect | [47] | ||||
IL-1β | ND | Aβ1–40: no effect HCV NS3: ↑ |
ND /(mRNA level) | [21, 30, 40, 47] | |||
Caspase-1 | ND | Aβ1–40: no effect | [47] | ||||
IL-12 | LPS:↑ | [52] | |||||
IFNγ | LPS:↑ | ND | [30, 52] | ||||
iNOS | 16% of cells (positive immunoreactivity) | (mRNA level) | [20, 36] | ||||
ROS | Sizable amount | HIV TAT-C protein: modest ↑ | [20, 21] | ||||
Antinflammatory molecules | |||||||
IL-4 | ND | [30] | |||||
IL-10 | 5,4 | Aβ1–42: no effect | ND | [30, 43] | |||
TGFβ1 | ~ 8 | (mRNA level) | [20, 37] | ||||
TGFβ2 | ~ 100 | [37] | |||||
Chemokines | |||||||
CCL2 | HIV-U937: ↑ | [30] | |||||
CCL5 | Sizable amount | HIV-vector: ↑ HIV-U937: ↑ |
[30] | ||||
IL-8 | HCV NS3: ↑ | [40] | |||||
CXCL10 | HIV-vector: ↑ HIV-U937: ↑ |
[30] |
Levels of cytokines and chemokines assessed in the incubation media are reported. Data are expressed as pg/ml ± SD secreted in 24-h incubation experiments. ND, not-detectable. ↑, increased production. Several inflammatory genes (i.e., iNOS, IL-1β, TNFα, IL-6, MHCII antigens, ARG1, and IL-10) were found to be expressed at the mRNA levels, in the CHME3 cells when co-cultured with differentiated neuronal SH-SY5Y wild type cells for 24, 48, 72 h. These markers were significantly upregulated in presence of the SHswe differentiated neuronal cells, with major modifications observed for IL-1β and IL-6 gene expression at 72 h [50]. In addition, the mRNA levels of both pro-inflammatory (IL-1β, IL-6, and TNFα) and anti-inflammatory (IFNβ, IL-4, and IL-10) cytokines increased in response to CHME3 cell infection with the Japanese Encephalitis Virus (JEV) [53, 54]