Lipopolysaccharide (LPS) is the toxic chemical component of the cell wall in all gram-negative bacteria which can activate NF-£eB, also stimulate immune cells to release cytokines. These pro-inflammatory mediators induce systemic acute inflammation, multiple organs dysfunction syndrome¡]MODS¡^and sepsis. LPS could increase the permeability of capillary, and cause the acute formation of numerous endothelial gaps among venular endothelial cells that result in extensive plasma leakage in the inflammatory tissues. Plasma leakage from microvasculature is a hallmark of inflammation. Mammalian intestines have many goblet cells that synthesize mucus and discharge it into the intestinal lumen. The mucus film that covers the surface epithelium facing the lumen of digestive system, is an immune defense that can prevent gastrointestinal epithelium from chemical and physical damage and act as a lubricant. Goblet cells can discharge mucins in response to a wide variety of stimuli, including irritant gases, nerve activation, reactive oxygen species, inflammatory mediators.
This study was aimed to investigate : (1) The degree of plasma leakage and goblet cell secretion in the small intestine of rats after an intravenous injection of a high dose of LPS (15 mg/kg), (2) The effect of £\2-adrenergic receptors antagonist, urethan, on endotoxin-induced plasma leakage and goblet cell secretion. For the study of plasma extravasation in small intestine during endotoxemia, India ink was used as the tracer to mark the inflamed leaky microvessels. The sections of the small intestine 3£gm in thickness were stained with Alcian blue and periodic acid-Schiff reagent to detect glycoproteins of goblet cells. Our results showed that LPS not only caused an increase in plasma leakage but also triggered degranulation of many goblet cells in the small intestine. LPS augment the expression of plasma leakage and mucus secretion for three times. A large amount of extracellular mucus was accumulated between intestinal villi after LPS stimulation. Pretreatment with urethan, the £\2-adrenergic receptor antagonist, significantly inhibited plasma leakage by 40-50% and goblet cell secretion by 25-30% induced by endotoxin. It is concluded that the plasma leakage and goblet cell hypersecretion induced by endotoxin shock was outstanding and associated with activation of £\2-adrenergic receptors.
| Identifer | oai:union.ndltd.org:NSYSU/oai:NSYSU:etd-0827104-215348 |
| Date | 27 August 2004 |
| Creators | Liu, Chia-Ming |
| Contributors | none, Hung-Tu Huang, shiping He |
| Publisher | NSYSU |
| Source Sets | NSYSU Electronic Thesis and Dissertation Archive |
| Language | Cholon |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0827104-215348 |
| Rights | withheld, Copyright information available at source archive |
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