Alcohol and Smoking Mediated Modulations in Adaptive Immunity in Pancreatitis

• Published in: Cells (Basel, Switzerland) Switzerland), 2020-08, Vol.9 (8), p.1880
• Main Authors: Bhatia, Rakesh, Thompson, Christopher, Ganguly, Koelina, Singh, Shailender, Batra, Surinder K, Kumar, Sushil
• Format: Article
• Language: English
• Subjects: Acute Disease; acute pancreatitis; Adaptive immunity; Adaptive Immunity - immunology; Adaptive Immunity - physiology; Alcohol; Alcoholic beverages; Animals; Antigens; Apoptosis; Beta cells; CD4 antigen; CD4 Antigens - metabolism; CD8 antigen; CD8 Antigens - metabolism; chronic pancreatitis; Cytokines; Cytotoxicity; Enzymes; Health aspects; Humans; Immune response; Inflammation; Ligands; Lymphocytes; Lymphocytes T; Mortality; Natural killer cells; Neutrophils; Pancreas; Pancreas - immunology; Pancreas - metabolism; Pancreatitis; Pancreatitis - immunology; Pancreatitis - metabolism; Parenchyma; Pathology; Perforin; Physiological aspects; Recruitment; Review; Risk factors; Smoking; Systemic inflammatory response syndrome; Therapeutic applications
• ISSN: 2073-4409; 2073-4409
• DOI: 10.3390/cells9081880

Pancreatitis is a condition of pancreatic inflammation driven by injury to the pancreatic parenchyma. The extent of acinar insult, intensity, and type of immune response determines the severity of the disease. Smoking, alcohol and autoimmune pancreatitis are some of the predominant risk factors that increase the risk of pancreatitis by differentially influencing the adaptive immune system. The overall decrease in peripheral lymphocyte (T-, B- and (natural killer T-) NKT-cell) count and increased infiltration into the damaged pancreatic tissue highlight the contribution of adaptive immunity in the disease pathology. Smoking and alcohol modulate the responsiveness and apoptosis of T- and B-cells during pancreatic insult. Acute pancreatitis worsens with smoking and alcohol, leading to the development of systemic inflammatory response syndrome and compensatory anti-inflammatory response syndrome, suggesting the critical role of adaptive immunity in fatal outcomes such as multiple organ dysfunction. The presence of CD4 and CD8 T-lymphocytes and perforin-expressing cells in the fibrotic tissue in chronic pancreatitis modulate the severity of the disease. Due to their important role in altering the severity of the disease, attempts to target adaptive immune mediators will be critical for the development of novel therapeutic interventions.