Figure 5
Figure 5. TLR-specific activation of BEAS 2B cells by Gram-negative bacteria. (A) Induction of IL-6 production in BEAS 2B with either E coli LPS (100 ng/mL) or PAM3CSK4 (200 ng/mL). (B) Dose-dependent induction of IL-6 secretion by heat-inactivated bacteria (E coli WT, E coli K12, K pneumoniae, and P aeruginosa) in BEAS 2B cells. Error bars show ± SEM. (C) Inhibitory effects of anti-TLR4, anti–MD-2, anti-TLR2, and anti-CD14 mAbs in the activation of cells by 107/mL Gram-negative bacteria (E coli WT, E coli K12, K pneumoniae, and P aeruginosa; 3 different experiments). Because the magnitude of IL-6 production was variable between different experiments, results are given as the percentage of inhibition of IL-6 release compared with the condition with the isotype control antibody (corresponding to 100% activation). Duplicates were performed for all conditions tested. Horizontal lines represent the mean.

TLR-specific activation of BEAS 2B cells by Gram-negative bacteria. (A) Induction of IL-6 production in BEAS 2B with either E coli LPS (100 ng/mL) or PAM3CSK4 (200 ng/mL). (B) Dose-dependent induction of IL-6 secretion by heat-inactivated bacteria (E coli WT, E coli K12, K pneumoniae, and P aeruginosa) in BEAS 2B cells. Error bars show ± SEM. (C) Inhibitory effects of anti-TLR4, anti–MD-2, anti-TLR2, and anti-CD14 mAbs in the activation of cells by 107/mL Gram-negative bacteria (E coli WT, E coli K12, K pneumoniae, and P aeruginosa; 3 different experiments). Because the magnitude of IL-6 production was variable between different experiments, results are given as the percentage of inhibition of IL-6 release compared with the condition with the isotype control antibody (corresponding to 100% activation). Duplicates were performed for all conditions tested. Horizontal lines represent the mean.

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