1 Liver + 4 Diseases = n Drugs

• Published in: The Journal of immunology (1950) 2023-05, Vol.210 (1_Supplement), p.176-176.11
• Main Authors: Dell, Garrison Jeffrey, Steele, Hope, Cheng, Jason Liang, Breckenridge, Joey Emery, Willicut, Ashley, Ghastine, Andrew, Culberson, Erica, Herro, Rana
• Format: Article
• Language: English
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.210.Supp.176.11

The burden placed on the global population by the instance of liver diseases is significant and there exists a great need for accurate diagnostic method alternatives to invasive biopsy. Here we conduct a comparative histopathological and transcriptomic analyses of 4 models of liver diseases to identify distinct biological pathways which aide in understanding the mechanisms of each disease and provide insight into biomarkers for diagnosing disease, monitoring disease progression, and for evaluating future therapeutic efficacy. The NASH model is metabolically induced by high fat/high fructose diet, whereas the three other models are hepatotoxicants, and involve Allyl Alcohol (AA), 4,4′-Methylenedianiline (MDA), or Bromobenzene (BB). Analysis of liver sections stained with Hematoxylin and Eosin and Masson’s trichrome revealed distinct pathological differences between each of the models. These differences were further confirmed by gene set enrichments and pathway analyses. This transcriptomic comparative study outlines distinct pathways important for inflammation, steatosis and fibrosis of the liver that are unique to each model in addition to common pathways contributing to disease pathogenesis. It further validates the histopathological features characteristic of each disorder.