Fig 2: PMN-released cytokines may induce frameshift mutations, internal ROS production and DNA oxidation. (A) 2 × 106 PMNs were activated with 0.5 nM PMA for 16 h and supernatants were subjected to a bead-based cytokine assay (Biorad) measured on a Bio-plex 200 instrument (Biorad). Treatment with 25 ng/ml IL-6, IL-8 or TNF-a decreased cell count and increased MR in HCT116 + chr3-A10 (B) or HCEC-1CT-[CA]26 (C). (D) Culture of HCEC-1CT with 25 ng/ml IL-6, IL-8 or TNF-a induced internal ROS production (as measured by DCFDA and expressed as relative fluorescent units, RFU) in a time-dependent manner, with the highest upregulation at 3 h. (E) HCT116 + chr3 cells were exposed to IL-6, PMA or H2O2 for 24 h. The formation of oxidized purines (8-oxo-dG) was analyzed with and without FPG. DNA migration was evaluated using single cell gel electrophoresis and computer-aided analysis. Bars indicate means ± SD of results obtained from 150 cells from three slides each experimental condition (t-test).

Fig 3: Quantification of serum-soluble mediators differentially expressed in HDs and EBOV_S.Measurement of serum-soluble mediators (pg/ml) from n = 39 HDs and n = 35 EBOV_S with the Bio-Plex 200 SystemTM (Bio-Rad). Pro-inflammatory and anti-inflammatory cytokines (a). Markers of T cell function (b). Markers of gastric tissue integrity (c). The differences between HDs and EBOV_S were evaluated in nonparametric Mann–Whitney U tests. Median values ± IQR are shown. Source data are provided as a Source Data file.

Fig 4: TILRR overexpression in VK2/E6E7 cells increased the production of Pro-inflammatory cytokine/chemokine(s) in the presence or absence of added IL-1ß. VK2/E6E7 (5 × 105cells/well) cells were co-transfected with either pEZ-TILRR-M68 (1.0 µg/5 × 105 cells) or pEZ-NEG-M68 (1.0 µg/5 × 105 cells) with PmaxGFP (0.2 µg/5 × 105 cells) vector as explained in materials and methods section. In parallel, cells were incubated with or without the addition of IL-1ß (1 nM) in serum free Keratinocyte SFM (1X) (VK2/E6E7) media and then the cultured media were collected (see methods). Thirteen different inflammatory cytokines were measured using an in-house developed multiplex cytokine/chemokine(s) bead assay with BioPlex 200 (BIORAD). The data represent the relative level of vector+TILRR, in the presence or absence of IL-1ß, compared to the empty vector control. The sample measurements below the detection limit were assigned as zero. The data represent mean of three independent experiments (mean ± SEM). Statistical comparisons conducted using student t-test with 95% CI, all p < 0.05 were reported and indicated using an asterisks' *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.

Fig 5: TILRR overexpression in HeLa cells increased the production of Pro-inflammatory cytokine/chemokine(s) in the presence or absence of added IL-1ß. HeLa (5 × 105cells/well) cells were co-transfected with either pEZ-TILRR-M68 (1.0 µg/5 × 105 cells) or pEZ-NEG-M68 (1.0 µg/5 × 105 cells) with PmaxGFP (0.2 µg/5 × 105 cells) vector as explained in materials and methods section. In parallel, cells were incubated with or without the addition of IL-1ß (1 nM) in serum free DMEM (HeLa) media and then the cultured media were collected (see methods). Thirteen different inflammatory cytokines were measured using an in-house developed multiplex cytokine/chemokine(s) bead assay with BioPlex 200 (BIORAD). The data represent the relative level of vector + TILRR, in the presence or absence of IL-1ß, compared to the empty vector control. The sample measurements below the detection limit were assigned as zero. The data represent mean of three independent experiments (mean ± SEM). Statistical comparisons conducted using student t-test with 95% CI, all p < 0.05 were reported and indicated using an asterisks' *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.