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Detailed analysis of serum glycans in sepsis and acute pancreatitis

Sepsis and acute pancreatitis are both conditions involving acute phase (AP) response triggered by different stimulus. Although the expression of genes for AP proteins is regulated mainly at transcriptional level post-transcriptional mechanisms were also shown to participate. In this work we present changes in pattern of N-linked glycans released from serum of a patient with sepsis and a patient with acute pancreatitis through the disease and compare them with glycans released from normal serum. Sera from patients were taken at time of reporting to hospital and then three more times through first eight days of hospitalisation. Blood from a healthy individual was drawn on one occasion only. The glycans were released using N-glycosydase F, an enzyme that specifically removes N-linked glycans, and subjected to NP-HPLC combined with exoglycosidase digestions and to mass spectrometry. The glycan structures present have been identified and their levels through the course of disease have been followed and compared to control. Our results show that changes of serum glycans occur very early in acute inflammation. The proportions of different glycans are changing daily. These changes are complex and can be observed in tri- and tetrasialylated structures, mannose structures, level of fucosylation and degree of branching. The complex changes in glycans during acute inflammation are not surprising knowing how complex and diverse acute phase response is and in how many different processes glycans play important roles. These changes may occure via changes in the biosynthesis and glycosylation processing of the AP glycoproteins and can be part of regulatory processes during inflammation since it had been shawn that some of these sugars participate in immunomodulation presumably having beneficial effects. The differences found between conditions are probably due to the fact that, although AP response is a unique homeostatic mechanism, differences in patterns of mediator production and response itself are depending on the nature and site of inflammation which was the case here.

glycans; sepsis; pancreatitis

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