Journal of the Pancreas Open Access

Immune Dysfunction in Patients and Immune Response to Pancreas Failure

Sara Amin Abdellah^* Department of Gastroenterology, Faculty of Medicine, University of Gezira, Wad Madani, Sudan
^*Correspondence: Sara Amin Abdellah, Department of Gastroenterology, Faculty of Medicine, University of Gezira, Sudan, Email:

Received: 02-Sep-2022, Manuscript No. IPP-22-14819; Editor assigned: 05-Sep-2022, Pre QC No. IPP-22-14819(PQ); Reviewed: 13-Sep-2022, QC No. IPP-22-14819; Revised: 27-Sep-2022, Manuscript No. IPP-22-14819(R); Published: 30-Sep-2022, DOI: 10.35841/1590-8577- 23.9.767

Introduction

Human ageing is characterized by physical and physiological weakness, which has a significant impact on the immune system. In this setting, ageing is linked to losses in adaptive and innate immunity, a condition known as immunosenescence. Immunosenescence is a new concept that describes the age-related remodeling of innate and adaptive immunological systems. As a result, aged people typically have persistent low-level inflammation, greater infection rates, and chronic illnesses. A study of immune system changes throughout ageing could give a potentially helpful biomarker for evaluating immunological senescence treatment [1].

Acute pancreatitis is one of the most common gastrointestinal reasons for hospitalization. Although chronic pancreatitis is less common, it has a significant impact on patients' quality of life. Pancreatic cancer has a high mortality rate and is one of the top five cancer-related causes of death. The prevalence of pancreatic disorders is expected to rise in the coming years. Pancreatitis risk and aetiology vary with age and gender, and all pancreatic disorders affect the black population more than any other race. Gallstones are the most common cause of acute pancreatitis, and cholecystectomy prevents future attacks. The single most important health risk for chronic pancreatitis remains alcohol. Smoking is a risk factor for both acute and chronic pancreatitis, and its effects may interact with those of alcohol. Smoking and non-O blood groups are significant risk factors for pancreatic cancer. Smoking cessation and alcohol abstinence can slow the progression of pancreatitis and reduce recurrence; smoking cessation is the most effective strategy for lowering the risk of pancreatic cancer [2].

Pancreatitis is a frequent condition with high morbidity and mortality, but little is understood about its pathophysiology, and no specific or efficient treatment exists. Studies in genetic and experimental mice models have shown that it develops through dysregulated autophagy and unresolved inflammation. The severity of the disease is determined by whether the inflammatory response resolves or amplifies, resulting in multi-organ failure. Autophagy dysregulation may enhance the inflammatory response in the pancreas. We explore the roles of autophagy and inflammation in pancreatitis, as well as regulatory mechanisms and links between disturbed pathways. We identify gaps in our knowledge and outline research perspectives. The identification of pathogenic pathways may lead to the identification of new targets for treating or lowering the severity of pancreatitis [3].

Diabetes is a condition marked by a relative or absolute shortage of insulin, resulting in hyperglycemia. Diabetes is classified into two types: type 1 diabetes and type 2 diabetes. Type 1 diabetes is characterized by an autoimmune attack on the insulin-producing pancreatic beta cells, whereas type 2 diabetes is caused by insulin resistance combined with a failure of the beta cells to adjust. Animal models for type 1 diabetes range from mice that acquire autoimmune diabetes spontaneously to chemical ablation of pancreatic beta cells. Obese and non-obese animal models with variable degrees of insulin resistance and beta cell failure are used to study type 2 diabetes. This overview discusses some of the current models used in diabetes research. The use of transgenic and knock-out mouse models is also mentioned. More than one animal model should ideally be utilised to mimic the variability exhibited in diabetic individuals [4].

Cellular defence mechanisms include inflammation and autophagy. When these pathways are disrupted, pathologic outcomes such as oxidative stress, metabolic deficiencies, and cell death result. Pancreatitis and pancreatic cancer are both characterized by unresolved inflammation and impaired autophagy control. Furthermore, obesity, a risk factor for pancreatitis and pancreatic cancer, stimulates inflammation and inhibits or deregulates autophagy, facilitating the onset and progression of pancreatic illnesses [5].

Conclusion

However, very little known about the interactions between inflammation, autophagy, and obesity in the promotion of exocrine pancreatic diseases. We discuss the roles of inflammation and autophagy in pancreatic disorders, as well as their dysregulation by obesity. We talk about the links between disrupted pathways and crucial areas for future research.

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