Pancreatitis

Acute pancreatitis (AP) is a disease in which pancreatic enzymes self-digest pancreatic tissue for various reasons, resulting in tissue edema and necrosis. Inflammation occurs due to damage to alveolar cells and the release of multiple chemokines, cytokines, and adhesion molecules. The severity of AP exacerbates when excess TNF-α enters circulation and induces the creation of other cytokines, including IL-1, IL-6, and IL-8. Ultimately, this triggers a chain of amplified responses that lead to a cytokine storm.

Figure 1. Role of lymphocyte subsets in secondary infections in acute pancreatitis (AP). (Ding L, et al., 2020)

Pancreatitis & Cytokines

• IL-1

Neutrophils and macrophages infiltrated in the pancreas are the main source of IL-1β. IL-1β induces the production of other inflammatory cytokines (TNF-α, IL-1, IL-6) and causes macrophages to accumulate in the inflamed pancreatic tissue. It also activates neutrophils making them involved in the development of multiple organ failure in severe AP. In addition, IL-1 directly stimulates the production, storage, and/or release of pancreatic enzymes and exacerbates the vacuolar degeneration of the adenohypophysis.

• IL-6

Serum IL-6 concentrations are persistently elevated during the development of AP, and lowering IL-6 significantly ameliorates the extent of pancreatic damage. IL-6 is also involved in multiorgan damage in AP, and IL-6 secretion peaks are significantly higher in patients with AP with systemic complications than in those without.

• IL-8

Studies have shown that IL-8 promotes the progression of AP from localized damage to systemic complications.IL-8 exacerbates endothelial cell damage by chemisorption and by enhancing the action of intracellular adhesion molecules on endothelial cells. In addition, IL-8 induces neutrophil deformation and L-selectin detachment from the surface of neutrophils, facilitating neutrophil travel to areas of inflammation.

• TNF-α

Macrophages infiltrated into pancreatic tissues are the main source of TNF-α. TNF-α promotes leukocyte aggregation and activation at inflammatory sites, releasing various inflammatory mediators such as PAF, NO, and oxygen radicals. Moreover, it contributes to leukocyte adhesion and extravasation, capillary leakage, and tissue damage by up-regulating the action of adhesion molecules on the vascular endothelium. In conclusion, TNF-α overstimulation results in a cascade reaction that causes severe damage to one pancreatic tissue.

• Platelet-activating Factor (PAF)

Recently, it has been found that injection of PAF into the superior pancreaticoduodenal artery can lead to pancreatic edema, vesicular cell degeneration, and necrosis. PAF is an important mediator in the initiation and amplification of endogenous inflammation, mainly causing an increase in capillary permeability and blood viscosity, ultimately leading to pancreatic microcirculation ischemia. Meanwhile, PAF promotes the secretion and activation of pancreatic enzymes, which further participate in the digestive process of pancreatic enzymes themselves during AP.

We Provide Multiple Products but not Limited to

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• Recombinant Human IL-1β protein, GMP Grade
• Recombinant Human IL-6 Protein, GMP Grade
• Recombinant Human TNF protein, GMP Grade
• Recombinant Rat Tnf protein, His-tag, GMP Grade
• Recombinant Human PDGFB Protein, GMP Grade

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