P Selectins and immunological profiles in HCV and Schistosoma mansoniinduced chronic liver disease

Abstract

BackgroundHepatitis C virus (HCV) and Schistosoma mansoni are major causes of chronic liver disease (CLD) in which immune alteration is common. Recent studies suggested that certain platelets and lymphocytes activation markers may have an impact on progression of CLD. This study aimed to evaluate the potential of platelets and lymphocytes activation molecules expression on the pathogenesis of CLD in distinct or concomitant chronic HCV and schistosomiasis mansoni infections.MethodsThe study populations were divided into group-I: patients with chronic schistosomiasis mansoni, group-II: HCV patients without cirrhosis, group-III: patients with combined liver diseases without cirrhosis, group-IV: patients with chronic HCV and liver cirrhosis and group-V: Age and sex matched healthy individuals as normal controls. All groups were subjected to full clinical evaluation, ELISA anti-HCV antibodies screening, parasitological examination for diagnosing S. mansoni and flow cytometry for lymphocyte (CD3, CD4, CD8, CD19, CD22, & CD56) and platelets activation (CD41, CD42 & CD62P (P- selectins)) markers.ResultsThe platelet count was significantly decreased in HCV and/or S. mansoni patients. The total T-lymphocytes and T-helper cells were significantly reduced, while T-cytotoxics were increased. The patients possessed a significantly higher platelets activation marker; CD62P (P-selectins) and higher mean fluorescent intensity (MFI) positivity. There were considerable correlations between platelets count and both of CD62P and MFI.ConclusionOur Findings suggest an increased expression of certain platelets and lymphocytes activation markers in chronic HCV and S. mansoni induced CLD that may have a role in disease progression.

Cytoprotective Effects of Hydrogen Sulfide in Novel Rat Models of Non-Erosive Esophagitis

“…GERD is among the most common diseases in the world, and largely because of this high incidence, is one of the most expensive to treat. The non-erosive form of GERD has been increasing in frequency in recent years, mainly in parallel with the rise in incidence of various metabolic disorders (e.g., type-2 diabetes, metabolic syndrome, obesity) [3] . Non-erosive reflux disease accounts for over 75% of all global cases of GERD [3] .…”

“…The non-erosive form of GERD has been increasing in frequency in recent years, mainly in parallel with the rise in incidence of various metabolic disorders (e.g., type-2 diabetes, metabolic syndrome, obesity) [3] . Non-erosive reflux disease accounts for over 75% of all global cases of GERD [3] . Recent studies have revealed a significant failure of proton pump inhibitor therapy in patients with metabolic disease-associated GERD [9] , .…”

“…Gastroesophageal reflux disease (GERD) is a chronic, acid-related condition with extensive global, social and economic impacts [1] – [3] . Considerable progress has been made in understanding the pathogenesis of this disorder.…”

“…Moreover many metabolic disorders and diet-related chronic diseases appear to play key roles in the pathogenesis of GERD and non-erosive reflux disease [17] , [20] , [21] . Indeed, experimental long-term postprandial hyperglycemia contributes to impairment of the esophageal barrier function [3] , . This impairment includes esophageal ischemia and hypoxia secondary to microvascular changes and peroxynitrite-mediated endothelial and enteric neuron damage [24] , [25] .…”

CD62P and P10 as predictive markers for assessing the efficacy of hemodialysis in treating end‐stage renal disease

“…Correspondingly, increased CD62P level indicates greater inflammatory responses and thrombosis and is strongly associated with a blood hypercoagulable state which commonly occurs in patients with ESRD . On the basis of the information provided above, it is concluded that CD62P acts as a key factor in the process of platelet aggregation and has become a marker for platelet activation to evaluate the progression of disease related with inflammation and thrombosis . On the other hand, thrombospondin (TSP), another alpha‐granule content in platelets, found on the surface of stimulated platelets, is subsequently recognized by its monoclonal antibody P10 to trigger the platelet aggregation process .…”