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Fig. 1 | Molecular Medicine

Fig. 1

From: Proinflammatory Cytokine Expression Contributes to Brain Injury Provoked By Chronic Monocyte Activation

Fig. 1

Monocyte activation in BCG-primed and saline-treated control rats. (A) Total monocyte counts before 2 weeks and after priming. In saline-treated group, n = 4–6; in BCG-treated group, n = 6–8. (B) Number of monocytes exhibiting spontaneous superoxide production before and 2 weeks after priming. In saline-treated group, n = 4–6; in BCG-treated group, n = 6–8. (C) Flow cytometry analysis of expression of β2-integrins in freshly isolated monocytes 2 weeks after BCG or saline priming. Data represent means ± SEM of triplicate samples from two separate experiments. (D) Adhesion of monocytes from BCG or saline-treated rats to cerebromicrovascular endothelial cells. Two weeks after BCG or saline priming, monocytes were isolated and added to untreated, TNF + IL-1 stimulated or to TNF + IL-1 stimulated and anti-ICAM1-treated endothelial cell cultures. Data represent mean ± SEM of triplicate samples from two separate experiments. Numbers of adherent cells were determined as described in Material and Methods. Asterisks denote statistical significance between saline- and BCG-treated groups; *p < 0.05, **p < 0.01. In panel D, the cross denotes statistical significance between adhesion of BCG-primed monocytes to TNF + IL-1-treated endothelium and adhesion to untreated or ICAM-1 blocked endothelium; + p < 0.05, p < 0.05 adhesion of saline monocytes to TNF + IL1-treated endothelium vs adhesion to ICAM-1 blocked endothelium. ANOVA followed by Student’s t-test with Bonferoni correction was used to calculate statistical significance of the changes between the various groups.

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