Multiple factors are involved in pathogenesis of liver inflammation—hepatitis. Hepatitis has multiple origins as facets of the noxae that produces this inflammation. Selective recruitment and retention of certain immune populations occur during diverse liver diseases, and the immune cells play a critical role in development and resolution of liver inflammation, extracellular matrix deposition, and cell death.Nonalcoholic steatohepatitis (NASH) presents similar histopathologic picture and affects about 3 percent of the lean and 19 percent of the obese nondrinking population. Nonalcoholic, nonviral inflammation of the liver encompasses diseases with different degrees of severity, from simple steatohepatitis to cirrhosis, liver failure, or hepatocellular carcinoma. Currently the “golden standard” to diagnose the severity of hepatitis is liver biopsy. Several noninvasive procedures have been proposed. There is a lack of an adequate knowledge on the mechanism and proper noninvasive monitoring in NASH and drug-induced liver injury (DILI). This basic knowledge similarly afflicts drug development programs since it is difficult to predict which new therapeutic compounds may be effective and safe. A better understanding of predisposing genetic factors and pathophysiology, with attendant progress in diagnostic and predictive biomarkers, could be expected to reap substantial benefits for afflicted patients in the provision of optimal medical care, as well as substantial savings in healthcare costs. Knowledge of the genetic, metabolic, and immune basis of individual patients is conducive to safe and effective drug use in hepatitis. We invite investigators to contribute original research articles as well as review articles that cover these aspects of non-alcohol-induced hepatitis. Potential topics include, but are not limited to:

• Parenchymal and nonparenchymal cells in development and progression of non-alcohol-induced liver injury
• Role of immune system in developing hypersensitive syndrome leading to DILI
• Genes and immune system involved in DILI and NASH
• Mediators of inflammation pathogenesis role of immune system
• Cytokines and chemokines in NASH and DILI
• Nonparenchymal cells signalling for fibrosis in non-alcohol-induced liver damage
• Laboratory assessment in NASH and DILI
• Hepatocellular carcinoma and nonalcoholic steatohepatitis
• Therapeutic interventions

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