Clinics related to acute pancreatitis wonder whether IFN-γ can attenuate pancreatic injury or not.

Acute pancreatitis (AP) is an inflammatory disease of the pancreatic tissue associated with little or no fi brosis of the gland. Continued clinical and experimental studies/trials are important for understanding AP pathogenesis and its current treatment approaches. Meng et al. [] contribute to our knowledge on NF-ĸB and cytokines IL- and IL- in experimental AP at  h,  h,  h and  h after IFN-γ treatment. However, the messages are implicit both in presentation of results and in the paper itself are complicated by the fact that is likely to be data interferences in relation to AP treated with IFN-γ. For instance, the conclusion that “the increase in NF-ĸB and IL- may exert infl uence on pro-infl ammatory cytokines to deteriorate infl ammation in the pancreas. Th us, to control the IFN-γ might has promise to attenuate pancreatitis... IFN-γ treatment might be associated with JAK-STAT mediated transcription activation” is based on a speculative opinion. Th ere are just similar sentences taken from diff erent articles excepting for cited references in introduction section, the amount of the application dose for IFN-γ is unknown and the authors are no interpretation their own fi ndings on discussion section in this study. According to this study, serum amylase level, the edema, the NF-ĸB and TNF-α expression in the pancreas were signifi cantly increased in the treatment of IFN-γ after AP. As a result of these fi ndings, the application of IFN-γ can cause a deleterious eff ect within the pancreas in the course of AP. On the other hand, Hayashi et al. [] reported that recombinant murine IFN-γ therapy markedly alleviated acute pancreatitis when administered  hours in mice, with reduced NF-ĸB activation and COX- expression. Th us, IFN-γ may possess anti-infl ammatory eff ects on AP by repression of the proinfl ammatory consequences of NF-ĸB activation. In addition, Rau et al. [] have indicated that immunostimulative treatment with recombinant rat IFN-γ attenuated the progression of intrapancreatic necrosis within the fi rst  hours after AP induction along with a substantial reduction of subsequent neutrophil tissue infi ltration and decreased TNF-α at the late stage of AP. Moreover, plasma IFN-γ concentration is known to increase at the early stage of disease in mild and severe AP patients compared with healthy controls. Th erefore, immunostimulative regime could be more eff ective during the late stage of this disease when infectious complications and immunoparalysis might be a dominant cause of mortality in the course of AP. Actually, pharmacological therapies are limited in the treatment of AP, and none of the therapeutic agents used for therapy are eff ectively curative. Regardless of AP severity, hospitalization of the patients with suspected acute pancreatitis for observation and diagnostic study is generally mandatory. After the diagnosis, patients with moderate to severe disease should be transferred to the ICU for observation, and supportive treatments and interventions. Treatment may change depending on the etiology and severity of the disease. Antibiotic therapy, peritoneal lavage, sphincterotomy with ERCP and even surgical operations can be applied [, ]. Novel eff ective therapeutic strategies in the treatment of AP may be evolved.