Figures & data
Figure 1. (A) Diff-Quik staining of mononuclear cells (MNCs) and polymorphonuclear leukocytes (PMNs). (B) Cancer killing activity (CKA) of MNCs and PMNs on healthy donors (n = 8; mean ± SEM; two-tailed Student’s t-test; ***, p < .001).
![Figure 1. (A) Diff-Quik staining of mononuclear cells (MNCs) and polymorphonuclear leukocytes (PMNs). (B) Cancer killing activity (CKA) of MNCs and PMNs on healthy donors (n = 8; mean ± SEM; two-tailed Student’s t-test; ***, p < .001).](/cms/asset/9fb61e2b-d158-4511-983f-d63b252de052/ists_a_1645112_f0001_c.jpg)
Figure 2. (A) Variation in the PMN CKA of 10 students (subjects 1–10) under final examination stress stimulation. (B–D) Changes in the levels of three stress hormones in undergraduate students around exam week. Blood was collected from the subjects at 8:00 AM around exam week and the concentration of endogenous cortisol, epinephrine, and norepinephrine in the plasma was measured by ELISA (examination week was from Day 3 to Day 5 and is marked in gray; n = 10; mean ± SEM; one-way ANOVA with Dunnett’s post hoc test; *, p < .05; **, p < .01; ***, p < .001).
![Figure 2. (A) Variation in the PMN CKA of 10 students (subjects 1–10) under final examination stress stimulation. (B–D) Changes in the levels of three stress hormones in undergraduate students around exam week. Blood was collected from the subjects at 8:00 AM around exam week and the concentration of endogenous cortisol, epinephrine, and norepinephrine in the plasma was measured by ELISA (examination week was from Day 3 to Day 5 and is marked in gray; n = 10; mean ± SEM; one-way ANOVA with Dunnett’s post hoc test; *, p < .05; **, p < .01; ***, p < .001).](/cms/asset/f6c41bc5-77ab-4723-93bb-6223c5a4c40f/ists_a_1645112_f0002_b.jpg)
Figure 3. Cytotoxicity of stress hormone co-culture with PMNs for 24 h. Cells were treated with hydrocortisone (A), epinephrine (B), norepinephrine (C), or a mixture of the three (D) for 24 h after which the relative viable cell number was measured using a CCK-8 assay (n = 4; mean ± SD; one-way ANOVA with Dunnett’s post hoc test).
![Figure 3. Cytotoxicity of stress hormone co-culture with PMNs for 24 h. Cells were treated with hydrocortisone (A), epinephrine (B), norepinephrine (C), or a mixture of the three (D) for 24 h after which the relative viable cell number was measured using a CCK-8 assay (n = 4; mean ± SD; one-way ANOVA with Dunnett’s post hoc test).](/cms/asset/9fd05725-4fe8-480b-90a1-e23d7bd20699/ists_a_1645112_f0003_c.jpg)
Figure 4. Cytotoxicity of stress hormone co-culture with A549 cells for 24 h. Cells were treated with hydrocortisone (A), epinephrine (B), norepinephrine (C), or a mixture of the three (D) for 24 h after which relative viable cell number was measured using a CCK-8 assay (n = 4; mean ± SD; one-way ANOVA with Dunnett’s post-hoc test; *, p < .05; **, p < .01; ***, p < .001).
![Figure 4. Cytotoxicity of stress hormone co-culture with A549 cells for 24 h. Cells were treated with hydrocortisone (A), epinephrine (B), norepinephrine (C), or a mixture of the three (D) for 24 h after which relative viable cell number was measured using a CCK-8 assay (n = 4; mean ± SD; one-way ANOVA with Dunnett’s post-hoc test; *, p < .05; **, p < .01; ***, p < .001).](/cms/asset/ca059333-0a2d-48c6-beb7-02468dd94d96/ists_a_1645112_f0004_c.jpg)
Figure 5. Effects of stress hormones on PMN and MNC CKA were investigated under stress hormones and whole blood co-culture conditions. Blood donated from healthy volunteers was co-incubated with 100× physiological concentrations of hydrocortisone (20 µg/mL), epinephrine (10 ng/mL), norepinephrine (50 ng/mL), or a mixture of the three at 37 °C for 24 h. PMNs (A) and MNCs (B) were isolated and incubated with A549 cells at 37 °C for a further 24 h, after which CKA was measured using a CCK-8 assay (n = 4; mean ± SEM; one-way ANOVA with Dunnett’s post hoc test; *, p < .05).
![Figure 5. Effects of stress hormones on PMN and MNC CKA were investigated under stress hormones and whole blood co-culture conditions. Blood donated from healthy volunteers was co-incubated with 100× physiological concentrations of hydrocortisone (20 µg/mL), epinephrine (10 ng/mL), norepinephrine (50 ng/mL), or a mixture of the three at 37 °C for 24 h. PMNs (A) and MNCs (B) were isolated and incubated with A549 cells at 37 °C for a further 24 h, after which CKA was measured using a CCK-8 assay (n = 4; mean ± SEM; one-way ANOVA with Dunnett’s post hoc test; *, p < .05).](/cms/asset/ddf24064-e3c1-4ca5-a4ed-d2eb87324e38/ists_a_1645112_f0005_c.jpg)
Figure 6. Effects of stress hormones on PMN and MNC CKA were investigated under the in vitro CKA reaction system co-culture conditions. PMNs (A) and MNCs (B) were isolated from whole blood donated from healthy volunteers and co-incubated with 100× the physiological concentration of hydrocortisone (20 µg/mL), epinephrine (10 ng/mL), norepinephrine (50 ng/mL), or a mixture of the three in the CKA reaction system consisting of PMN and A549 cells at 37 °C for 24 h, after which CKA was measured using a CCK-8 assay (n = 4; mean ± SEM; one-way ANOVA with Dunnett’s post hoc test; *, p < .05; **, p < .01).
![Figure 6. Effects of stress hormones on PMN and MNC CKA were investigated under the in vitro CKA reaction system co-culture conditions. PMNs (A) and MNCs (B) were isolated from whole blood donated from healthy volunteers and co-incubated with 100× the physiological concentration of hydrocortisone (20 µg/mL), epinephrine (10 ng/mL), norepinephrine (50 ng/mL), or a mixture of the three in the CKA reaction system consisting of PMN and A549 cells at 37 °C for 24 h, after which CKA was measured using a CCK-8 assay (n = 4; mean ± SEM; one-way ANOVA with Dunnett’s post hoc test; *, p < .05; **, p < .01).](/cms/asset/f9069ee4-8b30-4715-8aee-54770a02fec0/ists_a_1645112_f0006_c.jpg)