Hepatitis C virus (HCV) currently affects approximately 71 million people worldwide and causes extensive liver damage that can transition into hepatocellular carcinoma (HCC), a deadly malignant liver cancer. Unfortunately, patients tend to seek diagnostic testing late, when more severe symptoms exist, indicating advanced disease with severe fibrosis. There is a gap in knowledge about the immunologic process of HCV-induced fibrosis and cirrhosis development. Interleukin-33 (IL-33) is a cytokine implicated in various inflammatory and fibrotic diseases. We hypothesize that IL-33 plays a role in the pathogenesis of HCV, particularly in fibrosis and cirrhosis development leading to malignant transformation and thus may serve as an inflammatory biomarker. We studied livers from normal subjects - no liver-related diagnoses (n=6), subjects with HCV-cirrhosis (n=7), and subjects with HCV/HCC (n=7). We performed immunohistochemistry on paraffin-embedded liver tissue sections using a human IL-33 antibody and DAB staining system. To quantify our results, we performed image analyses quantifying IL-33 chromogen stain using an algorithm to calculate the signal strength of an image to determine the amount of antibody-specific chromogen per pixel, expressed in energy units per pixel (eu/px). We found that IL-33 is normally expressed in human hepatocytes; it is expressed at higher levels in HCV-cirrhosis patients and at lower levels in HCV-HCC patients. We plan to expand this study by including more patients in the future.
|Original language||American English|
|State||Published - 22 Aug 2020|
|Event||Oklahoma State University Center for Health Sciences Research Day 2019 - Oklahoma State University Center for Health Sciences, TULSA, United States|
Duration: 21 Feb 2019 → 22 Feb 2019
|Conference||Oklahoma State University Center for Health Sciences Research Day 2019|
|Abbreviated title||Research Day 2019|
|Period||21/02/19 → 22/02/19|