Adherence of bacteria to intestinal epithelial cells may be the crucial initiating event for translocation and is normally prevented by both specific (secretory IgA) and nonspecific (mucus, bacterial antagonism, desquamation) mucosal defense mechanisms. The purpose of this study was to examine the effect of dexamethasone administration on mucosal immunity; specifically bacterial adherence and IgA. Twenty Fischer rats were randomly assigned to two groups of 10 animals each. Group I received 0.5 mL saline injection intraperitoneal (IP); and group II, 0.8 mg/150 g body weight dexamethasone IP per day for 2 consecutive days. The cecum, mesenteric lymph nodes, and bile were aseptically collected, and bacterial adherence, bacterial translocation, and IgA concentration were determined. Results indicate that, compared with saline-treated animals, dexamethasone-treated animals had a fall in IgA (54 ± 24 versus 232 ± 41 ng/mg protein), an increase in bacterial adherence (8.2 ± 0.5 versus 3.4 ± 0.6 cfu (log10)/g cecum), and an increased incidence of bacterial translocation to the mesenteric lymph nodes (60% versus 0%). These data suggest that glucocorticoids may promote bacterial translocation by impairment of mucosal IgA synthesis.

The effect of glucocorticoic administration on bacterial translocation : evidence for an acquired mucosal immunodeficient state

Arteriovenous difference measurements in dogs in the late 1960's indicated a substantial net uptake of glutamine by the portal-drained viscera. Subsequent studies demonstrated that the mucosa of the small intestine plays the dominant role in this process. ~ More recently, glutamine has become of considerable interest to clinicians and nutritionists because intestinal glutamine metabolism may be impaired during critical illness, and that this impairment may be associated with altered intestinal function.: The small intestine is the principal organ of glutamine uptake and metabolism in the body. The majority of studies that have measured in vivo glutamine utilization by the bowel have employed regional flux techniques using indwelling acutely or chronically placed arterial and portal venous catheters. Such studies quantitate the net exchange of substrate by the tissue, but do not provide information about the specific metabolic events or the specific cells that contribute to the total net rate of glutamine utilization. Thus, while regional flux studies are hampered by the disadvantage that only a net exchange measurement is calculated, they are also a valuable tool for the investigator interested in learning how organ utilization of a particular substrate changes in vivo during pathophysiologic states. Combined with the other methods that are commonly used to study intestinal glutamine transport and metabolism, in vivo measurements have substantially increased our knowledge of how intestinal glutamine utilization changes during disease states and how these changes are regulated. In this review the author summarizes the importance of glutamine for gut metabolism and discusses the techniques used to study glutamine utilization by the gut mucosa. In addition, the changes in intestinal glutamine metabolism that

Intestinal glutamine metabolism and nutrition

Cytokine control of nutrition and metabolism during critical illness

A novel glutaminase isoform in mammalian tissues.

The role of glutaminase in the small intestine

Lymphocytes in the mesenteric lymph nodes (MLNs) play a key role in protecting the body from the translocation of bacteria through the bowel during catabolic states. Lymphocytes use glutamine for energy and for DNA synthesis and have high levels of the glutaminase (GA) enzyme that regulates intracellular glutamine metabolism. This study tested the hypothesis that the increase in circulating glucocorticoid hormones that occurs in response to stress states regulates MLN lymphocyte GA expression at the molecular level. Adult male rats (n=60) received a single dose of dexamethasone (DEX 0.5 mg/kg intraperitoneally) or saline vehicle (CONT). Ileocolic lymph nodes were excised from anesthetized rats via laparotomy at 2, 4, 12, 24, 48, and 72 hours after injection, and GA activity was assayed in MLN homogenates. A second group of rats received repeated doses of DEX (0.5 mg/kg/d for 4 days). GA activity was assayed in MLN homogenates, and total RNA was extracted for quantitation by Northern hybridization using a phosphorus 32-labeled rat GA cDNA probe. GA activity was increased within 2 hours after a single dose of DEX, with a peak after 4 hours. Kinetic analysis at the 4-hour time point showed an increase in the maximum GA activity (maximal transport velocity [V max ]: 619±107 nmol/mg protein/hr in DEX versus 380±53 nmol/mg protein/hr in CONT, p m ]: 2.28±0.39 mM in DEX versus 2.20±0.36 mM in CONT, p=NS). Repeated doses of DEX resulted in a twofold increase in GA activity (550±125 nmol/mg protein/hr versus, 1,175±40, p

Dexamethasone stimulation of glutaminase expression in mesenteric lymph nodes

Background/Hypothesis: Glutamine is the principal fuel used by lymphocytes. It is hydrolyzed by the glutaminase enzyme, which regulates the rate of intracellular glutamine metabolism. Since lymphocyte glutamine utilization is increased during infection to support cellular proliferation, we hypothesized that endotoxin regulates lymphocyte glutaminase expression at the molecular level. Methods: Adult rats received Escherichia coli endotoxin (one dose of 7.5 mg/kg) or saline. Total RNA from lymphocytes in the ileocolic lymph node chain was extracted for Northern hybridization and labeled with an α–phosphorus 32 rat glutaminase cDNA probe. The mRNA of the constitutively expressed gene β-actin was the control for RNA loading. Quantitation of glutaminase transcripts was determined by densitometric scanning and values were normalized to actin. Glutaminase-specific activity (nanomoles per milligram of protein per hour) and glutaminase kinetic parameters were also determined. Results: Treatment with a single dose of endotoxin resulted in a 53% increase in glutaminase activity at 4 hours. Kinetic analysis showed that the increase in glutaminase activity was due to an 84% increase in V max (maximal enzyme velocity) with no change in K m (enzyme affinity). Endotoxin increased glutaminase mRNA twofold at 2 hours and more than fourfold at 4 hours. The increase in message preceded the increase in activity consistent with gene transcription prior to enzyme biosynthesis. Conclusion/Clinical Relevance: The increase in glutaminase activity provides lymphocytes in the mesenteric lymph nodes with more glutamine for energy and cellular proliferation during times of infection when the gut mucosal barrier may become compromised. (Arch Surg. 1993;128:920-924)

Endotoxin Stimulates Lymphocyte Glutaminase Expression

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Dexamethasone stimulation of glutaminase expression in mesenteric lymph nodes

Endotoxin Stimulates Lymphocyte Glutaminase Expression