Editorial - Journal of Pulmonology and Clinical Research (2017) Journal of Pulmonology and Clinical Research (Special Issue 1-2017)

Eosinophilic pancreatitis need an attention.

School of Medicine, Tulane University, New Orleans, USA

*Corresponding Author:

Murli Manohar, Ph.D.
School of Medicine
Tulane University
New Orleans
USA
E-mail: mmanohar@tulane.edu

Accepted Date: October 04th, 2017

Citation: Manohar M. Editorial on eosinophilic pancreatitis. J Pulmonol Clin Res. 2017;1(1):1-2.

Abstract

Inflammatory diseases include a vast array of disorders and conditions that are characterized by inflammation, such as allergy, asthma, eosinophilic gastrointestinal disorders including pancreatitis [1-6]. The data indicates, 13 to 45/100,000 people in United States are having acute pancreatitis (AP) annually, whereas, chronic pancreatitis (CP) varies from 4.4 to 11.9/100,000 [1-3]. Pancreatitis is the inflammation of pancreas and arises due to several reasons such as alcohol abuse, mutation in trypsinogen gene, gallstones, and several drugs and food induced. Pancreatitis is of two types; the initial shock of pancreatitis is called acute pancreatitis and when these episodes frequency occurs several time it leads chronic pancreatitis. Pancreatic inflammation is characterized by destruction of acinar cells, which lead activation of several inflammatory cells like mast cells, neutrophils, macrophages and granulocytes such as basophils and eosinophils that secrete several pro-inflammatory cytokines [2,3].

Inflammatory diseases include a vast array of disorders and conditions that are characterized by inflammation, such as allergy, asthma, eosinophilic gastrointestinal disorders including pancreatitis [1-6]. The data indicates, 13 to 45/100,000 people in United States are having acute pancreatitis (AP) annually, whereas, chronic pancreatitis (CP) varies from 4.4 to 11.9/100,000 [1-3]. Pancreatitis is the inflammation of pancreas and arises due to several reasons such as alcohol abuse, mutation in trypsinogen gene, gallstones, and several drugs and food induced. Pancreatitis is of two types; the initial shock of pancreatitis is called acute pancreatitis and when these episodes frequency occurs several time it leads chronic pancreatitis. Pancreatic inflammation is characterized by destruction of acinar cells, which lead activation of several inflammatory cells like mast cells, neutrophils, macrophages and granulocytes such as basophils and eosinophils that secrete several pro-inflammatory cytokines [2,3]. Eosinophils develop during hematopoiesis in the bone marrow before going into bloodstream and about 1-6% of white blood cells. They have about half-life of 8 to 18 hours in the bloodstream, and mostly reside in the tissues where they can live for several weeks [7]. Eosinophils play key role in the mucosal immune system of the gastrointestinal tract during normal and inflammatory conditions. In normal conditions, the mucosa of the digestive tract is the only organ harboring a substantial number of eosinophils, which, if need be, get activated and exert several effector and immunoregulatory functions [8]. Eosinophils promote tissue fibrosis by secreting pro-fibrotic TGF-b1 and other cytokines [9]. Several cases reports have been cited in the literature indicating the accumulation of eosinophils in pancreatitis patients and termed this condition as “Eosinophilic Pancreatitis (EP)” [10-14] but detailed mechanistic analysis of eosinophilic pancreatitis is ignored and not well explored.

We recently reported an important role of eosinophils in cerulein-induced chronic pancreatitis. Even we first time located eosinophils accumulation and degranulation followed by induced mast cells and its degranulation and acinar cells atrophy in the pancreas of cerulein-induced murine model of pancreatitis. Our data also indicates that the eosinophils deficient GATA 1 mice show reduced pancreatic remodeling compared to wild type or IL-5 gene deficient mice following cerulein-induced chronic pancreatitis [15]. These experimental data indicate that eosinophils accumulation and degranulation may be critical in promoting pancreatitis pathogenesis including fibrosis that is the major concern for the treatment options. Further, we extended our study to see the role of eosinophils in human pancreatic malignant, non-malignant and healthy biopsies and confirmed the accumulation and degranulation of eosinophils, mast cells, induced IgE level and induced collagen deposition in malignant pancreatic biopsies as compared to healthy control [16]. Taken together, our experimental and translational approaches indicate that indeed eosinophilic pancreatitis may be an independent disease entity that needs appropriate attention to understand the mechanism of eosinophils accumulation in the pancreas and in promoting pancreatic fibrosis including malignancy.

References

1. Manohar M. Pathogenic mechanisms of pancreatitis. World J Gastrointest Pharmacol Ther. 2017;8(1):10-25.
2. Manohar MVA, Venkateshaiah SU, Sanders NL, et al. A Chronic Pancreatitis Associated Acute Respiratory Failure. MOJ Immunology. 2017;5(2):1-7.
3. Manohar MVA, Venkateshaiah SU, Mishra A. Immunological Responses Involved In Promoting Acute and Chronic Pancreatitis. J Clin Immunol Res. 2017;1:1-8.
4. Venkateshaiah SU. Possible Noninvasive Biomarker of Eosinophilic Esophagitis Clinical and Experimental Evidence. Case Rep Gastroenterol. 2016;10(3):685-692.
5. Venkateshaiah SU. Regulatory effects of IL-15 on allergen-induced airway obstruction. J Allergy Clin Immunol. 2017.
6. Verma AK, Blecker UMH, Collins Mishra A. Role of vasoactive intestinal peptide in promoting the pathogenesis of eosinophilic esophagitis (EoE). Cell Mol Gastroenterol Hepatol. 2017.
7. Kovalszki APF, Weller. Eosinophilia. Prim Care. 2016;43(4):607-617.
8. Straumann A, Safroneeva E. Eosinophils in the gastrointestinal tract friends or foes. Acta Gastroenterol Belg. 2012;75(3):310-315.
9. Aceves SS. Remodeling and fibrosis in chronic eosinophil inflammation. Dig Dis. 2014;32(2):15-21.
10. Bastid C. Eosinophilic pancreatitis report of a case. Pancreas. 1990;5(1):104-107.
11. Lyngbaek S. Recurrent acute pancreatitis due to eosinophilic gastroenteritis. Case Report and Literature Review. 2006;7(2):211-7.
12. Kakodkar S. Eosinophilic Pancreatitis Diagnosed With Endoscopic Ultrasound. ACG Case Rep J. 2015;2(4):239-41.
13. Flejou JF, Potet F, Bernades P. Eosinophilic pancreatitis a rare manifestation of digestive allergy. Gastroenterol Clin Biol. 1989;13(9):731-3.
14. Reppucci J. Eosinophilic Pancreatitis A Rare Cause of Recurrent Acute Pancreatitis. Case Rep Gastroenterol. 2017;11(1):120-126.
15. Manohar M. Role of eosinophils in the initiation and progression of pancreatitis pathogenesis. Am J Physiol Gastrointest Liver Physiol. 2017.
16. Manohar M, Alok KV, Sathisha Venkateshaiah U, et al. Significance of eosinophils in pathogenesis of pancreatitis associated malignancy. J Gastroenterol Pancreatol Liver Disorders. 2017.