{'fraction_non_alphanumeric': 0.02410755679184052, 'fraction_numerical': 0.00927213722763097, 'mean_word_length': 5.219020172910663, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Histological and immunohistochemical study of the role of glutamine on lipopolysaccharide-induced pancreatitis and associated lung injury

Background Lipopolysaccharide (LPS) is an important factor in the incidence of sepsis. Sepsis is associated with acute pancreatitis, which might be complicated by multiorgan dysfunction, among which is the lung. Glutamine (GLN) is an essential amino acid that plays a significant role in cell homeostasis and organ metabolism. The aim of this study was to investigate the possible protective role of GLN against LPS-induced pancreatitis and the associated lung injury. Materials and methods Twenty-four male albino rats were divided into three groups (n=8 each). The first group served as the control group; the second received an intravenous injection of 5 mg/kg LPS; and the third group was given an intraperitoneal dose of 0.75 g/kg of l-GLN with LPS. After 6 h, the pancreas and lungs were dissected, processed, sectioned, and stained with H&E and with an immunohistochemical stain for heat shock protein 70 (HSP70). Area percentage of HSP70-positive immunoreactivity was measured, followed by statistical analysis. Results The LPS group demonstrated mononuclear cellular infiltration of mostly neutrophils within the connective tissue septa of the pancreas. This was not detected in the group treated with GLN. HSP70-positive immunoreactivity was detected in the apical part of pancreatic acinar cells in the LPS group, which was significantly increased in the GLN-treated group. The lungs of the LPS group showed thickened interalveolar septa with massive inflammatory cellular infiltration. This was diminished in the GLN-treated group. Positive HSP70 immunoreactivity was detected in type II pneumocytes and in the inflammatory cells within the interalveolar septa. This finding was more abundant in the GLN-treated group. Conclusion LPS induced an inflammatory process associated with an increase in HSP70 immunoexpression in both the pancreas and the lung, a finding that was markedly increased in GLN-treated animals. This denotes that GLN might play an anti-inflammatory role by elevating HSP70 expression.