a Expression of PBLD, tight junction (TJ) proteins, and the nuclear factor (NF)-κB signaling pathway was evaluated by immunoblotting in paired colon tissues from patients with UC (n = 6). β-actin served as an internal control. N normal colon tissue, I inflamed colon tissue. b Expression of PBLD mRNA was analyzed by quantitative reverse-transcriptase (qRT)-PCR in paired inflamed and non-inflamed colon tissue samples from UC patients (n = 9). Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) was used as an internal control. **p < 0.01. c Expression of PBLD mRNA was assessed using a published dataset (GSE75214; N = 108; normal controls, n = 11; inactive UC, n = 23; active UC, n = 74) ****p < 0.0001. d, e Levels of TNF-α and IL-6 mRNA were analyzed using qRT-PCR in paired inflamed and non-inflamed colon tissue samples from patiens with UC (n = 9). f Spearman’s correlation analysis between PBLD and TNF-α mRNA levels (r = −0.5501, p = 0.0180). g Spearman’s correlation analysis between PBLD and IL-6 mRNA levels (r = −0.6099, p = 0.0072). h, i Occludin and ZO-1 mRNA levels were analyzed using qRT-PCR in paired inflamed and non-inflamed colon tissue samples from patients with UC (n = 9). j Spearman’s correlation between PBLD and occludin mRNA levels (r = 0.4716, p = 0.0482). k Spearman’s correlation between PBLD and ZO-1 mRNA levels (r = 0.7172, p = 0.0008). l PBLD mRNA levels were analyzed using a published dataset from patients with UC who received infliximab treatment. (GSE16879; N = 24; those who responded to treatment, n = 8; nonresponders, n = 16). UCR-beforeT responder before infliximab treatment, UCR-afterT responder after infliximab treatment, UCNR-beforeT nonresponder before infliximab treatment, UCNR-afterT nonresponder after infliximab treatment.