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Published on: May 10, 2024
Hippocampal Microglia Activation Induced by Acute Pancreatic Injury in Rats
Tamires Cabral-França1,2,3, Fernanda Ferreira Cruz4, Paulo Cesar Silva2
1Postgraduate Program in Surgical Science, Department of Surgery, School of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Background:
Acute pancreatitis is an inflammation of the pancreatic glandular parenchyma that causes injury with or without the destruction of pancreatic acini. Clinical and experimental evidence suggest that certain systemic proinflammatory mediators may be responsible for initiating the fundamental mechanisms involved in microglial reactivity. Here, we investigated the possible repercussions of acute pancreatitis (AP) on the production of inflammatory mediators in the brain parenchyma focusing on microglial activation in the hippocampus.
Methods:
The acute pancreatic injury in rats was induced by a pancreas ligation surgical procedure (PLSP) on the splenic lobe, which corresponds to approximately 10% of total mass of the pancreas. Blood samples were collected via intracardiac puncture for the measurement of serum amylase. After euthanasia, frozen or paraffin-embedded brains and pancreas were analyzed using qRT-PCR or immunohistochemistry, respectively.
Results:
Immunohistochemistry assays showed a large number of Iba1 and PU.1-positive cells in the CA1, CA3, and dentate gyrus (DG) regions of the hippocampus of the PLSP group. TNF-α mRNA expression was significantly higher in the brain from PLSP group. NLRP3 inflammasome expression was found to be significantly increased in the pancreas and brain of rats of the PLSP group. High levels of BNDF mRNA were found in the rat brain of PLSP group. In contrast, NGF mRNA levels were significantly higher in the control group versus PLSP group.
Conclusion:
Our findings suggest that AP has the potential to induce morphological changes in microglia consistent with an activated phenotype.
Insights
Acute pancreatitis (AP) can activate microglia in the hippocampus, a key brain region. This study shows AP induces inflammatory changes in the brain, suggesting a link between pancreatic inflammation and neuroinflammation.
Area of Science:
- Neuroscience
- Gastroenterology
- Immunology
Background:
- Acute pancreatitis (AP) is pancreatic inflammation potentially linked to systemic inflammatory mediators.
- Evidence suggests a connection between systemic inflammation and microglial reactivity in the brain.
- This study investigates AP's impact on brain inflammatory mediators and hippocampal microglial activation.
Purpose of the Study:
- To determine if acute pancreatitis induces microglial activation in the rat hippocampus.
- To analyze the expression of inflammatory mediators in the brain following acute pancreatitis.
Main Methods:
- Acute pancreatitis induced in rats via pancreas ligation surgical procedure (PLSP).
- Serum amylase measured from blood samples.
- Brain and pancreas tissues analyzed using qRT-PCR and immunohistochemistry for inflammatory markers and microglial activation (Iba1, PU.1).
Main Results:
- Increased Iba1 and PU.1 positive cells observed in hippocampal regions (CA1, CA3, DG) of the PLSP group.
- Significantly higher TNF-α mRNA expression in the brain of the PLSP group.
- Upregulated NLRP3 inflammasome expression in both pancreas and brain of PLSP rats; altered BDNF and NGF mRNA levels.
Conclusions:
- Acute pancreatitis induces morphological changes in microglia, indicative of an activated phenotype.
- AP may trigger neuroinflammation, impacting the hippocampus.
