Evaluation of inflammatory activity in Crohn's disease and ulcerative colitis

Crohn's disease and ulcerative colitis evolve with a relapsing and remitting course.Determination of inflammatory state is crucial for the assessment of disease activity and for tailoring therapy.However,no simple diagnostic test for monitoring intestinal inflammation is available.Noninvasive markers give only indirect assessments of disease activity.Histopathological or endoscopical examinations accurately assess inflammatory activity,but they are invasive,time consuming and expensive and therefore are unsuitable for routine use.Imaging procedures are not applicable for ulcerative colitis.The usefulness of ultrasound and Doppler imag-ing in assessing disease activity is still a matter of discussion for Crohn's disease,and an increased interest in computed tomography enterograph (CTE) has been seen,mainly because it can delineate the extent and severity of bowel wall inflammation,besides detecting extraluminal findings.Until now,the available data concerning the accuracy of magnetic resonance enterography in detecting disease activity is less than CTE.Due to this,clinical activity indices are still commonly used for both diseases.

Murine model to study brain,behavior and immunity during hepatic encephalopathy

AIM:To propose an alternative model of hepatic encephalopathy(HE) in mice,resembling the human features of the disease.METHODS:Mice received two consecutive intraperitoneal injections of thioacetamide(TAA) at low dosage(300 mg/kg).Liver injury was assessed by serum transaminase levels(ALT) and liver histology(hematoxylin and eosin).Neutrophil infiltration was estimated by confocal liver intravital microscopy.Coagulopathy was evaluated using prolonged prothrombin and partial thromboplastin time.Hemodynamic parameters were measured through tail cuff.Ammonia levels were quantified in serum and brain samples.Electroencephalography(EEG) and psychomotor activity score were performed to show brain function.Brain edema was evaluated using magnetic resonance imaging.RESULTS:Mice submitted to the TAA regime developed massive liver injury,as shown by elevation of serum ALT levels and a high degree of liver necrosis.An intense hepatic neutrophil accumulation occurred in response to TAA-induced liver injury.This led to mice mortality and weight loss,which was associated with severe coagulopathy.Furthermore,TAA-treated mice presented with increased serum and cerebral levels of ammonia,in parallel with alterations in EEG spectrum and discrete brain edema,as shown by magnetic resonance imaging.In agreement with this,neuropsychomotor abnormalities ensued 36 h after TAA,fulfilling several HE features observed in humans.In this context of liver injury and neurological dysfunction,we observed lung inflammation and alterations in blood pressure and heart rate that were indicative of multiple organ dysfunction syndrome.CONCLUSION:In summary,we describe a new murine model of hepatic encephalopathy comprising multiple features of the disease in humans,which may provide new insights for treatment.