Effect of Endotoxemia in Suckling Rats on Pancreatic Integrity and Exocrine Function in Adults: A Review Report

Abstract

Background. Endotoxin (LPS), the component of Gram-negative bacteria, is responsible for sepsis and neonatal mortality, but low concentrations of LPS produced tissue protection in experimental studies. The effects of LPS applied to the suckling rats on the pancreas of adult animals have not been previously explored. We present the impact of neonatal endotoxemia on the pancreatic exocrine function and on the acute pancreatitis which has been investigated in the adult animals. Endotoxemia was induced in suckling rats by intraperitoneal application of LPS from Escherichia coli or Salmonella typhi. In the adult rats, pretreated in the early period of life with LPS, histological manifestations of acute pancreatitis have been reduced. Pancreatic weight and plasma lipase activity were decreased, and SOD concentration was reversed and accompanied by a significant reduction of lipid peroxidation products (MDA + 4 HNE) in the pancreatic tissue. In the pancreatic acini, the significant increases in protein signals for toll-like receptor 4 and for heat shock protein 60 were found. Signal for the CCK1 receptor was reduced and pancreatic secretory responses to caerulein were diminished, whereas basal enzyme secretion was unaffected. These pioneer studies have shown that exposition of suckling rats to endotoxin has an impact on the pancreas in the adult organism.

Dietary Polysaccharide from Enteromorpha Clathrata Modulates Gut Microbiota and Promotes the Growth of Akkermansia muciniphila, Bifidobacterium spp. and Lactobacillus spp.

“…Lipopolysaccharide (LPS)-binding protein (LBP) is a well-established biomarker for studying the antigen load from the gut [ 57 , 58 ]. As an acute phase protein, it specifically binds to LPSs from the Gram-negative bacteria and antigens from the Gram-positive bacteria [ 57 , 58 ]. Therefore, to give an overall evaluation of the effect of ECP on gut microbiota, we further determined the serum LBP levels of male and female mice in different groups.…”

Microbiome-Gut-Brain Axis and Toll-Like Receptors in Parkinson’s Disease

“…The dysregulation of immune response to environmental and/or microbial agents is associated with the onset of inflammatory bowel disease in genetically susceptible individuals [ 39 ]. On the other hand, exposition to low amounts of LPS in early life can affect the ability of the immune cells to produce the cytokines, increasing the resistance of the organism to systemic diseases such as pancreatic inflammation [ 40 ].…”

Probiotics Alleviate the Progressive Deterioration of Motor Functions in a Mouse Model of Parkinson’s Disease

“…Earlier studies have reported the relationship between the brain and the GI system, the so-called gut-brain axis or brain-gut axis. It has been hypothesized that GI dysfunctions could reflect the disruptions of the microbiome-gut-brain axis, leading to serious GI inflammatory diseases (e.g., acute pancreatitis or inflammatory bowel disease), endothelial dysfunction, altered immune functioning and regulation of appetite control, neural inflammation, subsequent neurodegeneration, cognitive or psychoneurological disorders (e.g., depression, anxiety, autism, dementia), and disease progression of PD [8][9][10][11][12][13][14][15][16][17][18][19]. In addition to the use of peptides for the improvement of gastrointestinal or digestive dysfunctions [13,[20][21][22], and in order to improve GI function and the balance of microbiota, probiotics could be one of the powerful tools to be used for altering the PD-associated microbiota composition and mitigating the related inflammatory process [12,23].…”