Abstract
Objective This study is aimed at investigating the enriched functions of polymeric immunoglobulin receptor (PIGR) and its correlations with liver fibrosis stage. Methods PIGR mRNA expression in normal liver, liver fibrosis, hepatic stellate cells (HSCs), and hepatitis virus infection samples was calculated in Gene Expression Omnibus (GEO) and Oncomine databases. Enrichment analysis of PIGR-related genes was conducted in Metascape and Gene Set Enrichment Analysis (GSEA). Logistic model and ROC curve were performed to evaluate the correlations between pIgR and liver fibrosis. Results PIGR mRNA was upregulated in advanced liver fibrosis, cirrhosis compared to normal liver (all p < 0.05). PIGR mRNA was also overexpressed in activated HSCs compared to senescent HSCs, liver stem/progenitor cells, and reverted HSCs (all p < 0.05). Enrichment analysis revealed that PIGR-related genes involved in the defense response to virus and interferon (IFN) signaling. In GEO series, PIGR mRNA was also upregulated by hepatitis virus B, C, D, and E infection (all p < 0.05). After adjusting age and gender, multivariate logistic regression models revealed that high PIGR in the liver was a risk factor for liver fibrosis (OR = 82.2, p < 0.001). The area under curve (AUC), positive predictive value (PPV), negative predictive value (NPV), sensitivity, and specificity of PIGR for liver fibrosis stage >2 were 0.84, 0.86, 0.7, 0.61, and 0.90. Conclusion PIGR was correlated with liver fibrosis and might involve in hepatitis virus infection and HSC transdifferentiation.
Highlights
The polymeric immunoglobulin receptor (PIGR) is exclusively originated from intestinal epithelial cells
Microarray experiments of 13 cirrhosis samples and 10 normal liver samples in Wurmbach Liver dataset were addressed in Human Genome U133 Plus 2.0 Array platform [33], and Transcriptome levels of PIGR in 19 normal liver samples and 58 cirrhosis samples in Mas Liver dataset were examined in Human Genome U133A 2.0 Array platform [34]
PIGR mRNA was downregulated in cirrhosis samples than that in normal liver in Mas Liver dataset (p < 0:0001, Figure 1(b))
Summary
The polymeric immunoglobulin receptor (PIGR) is exclusively originated from intestinal epithelial cells. It captured and transcytosed dimeric IgA (dIgA) from lamina propria to intestinal lumen across epithelial cells and participated in mucosal immune system [1, 2]. Previous evidences revealed that proinflammatory cytokines released by innate and adaptive immune cells including interferon, tumor necrosis factor (TNF), interleukins, and lymphotoxin could stimulate the expression of PIGR [1,2,3,4,5,6,7,8,9]. PIGR had a cross talk of transforming growth factor-β with inflammatory mediators like tumor necrosis factor-α, interferon-γ, and interleukin-4, resulting in the induction of epithelial-mesenchymal transition (EMT) [13].
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