Hand-assisted laparoscopic live-donor nephrectomy.
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Adult↗
Biomedical subjects
J Alverdy
Publications and source records attributed to J Alverdy.
Surgical stress shifts the intestinal Escherichia coli population to that of a more adherent phenotype: role in barrier regulation.
BACKGROUND: We have shown that the combination of surgical stress and starvation in mice is associated with a defect in epithelial permeability and increased numbers of mucosa-associated Escherichia coli in the cecum. The aim of this study was to determine the specific role of mucosa-associated E coli on epithelial barrier dysfunction in this model. METHODS: Cecal E coli were harvested from mice 48 hours after a sham operation (control mice) or after a 30% surgical hepatectomy with only water provided ad libitum (short-term starvation) after the surgical procedure. Strains were tested for their ability to adhere to and alter the transepithelial electrical resistance (TEER) of cultured young adult mouse colon epithelial cells. TEER changes were further characterized by mannitol fluxes to confirm a defect in paracellular permeability. RESULTS: Strains of cecal E coli harvested from hepatectomy-starved mice adhered to and altered the permeability of young adult mouse colon cells, whereas E coli from the cecum of control mice were less adherent and had no effect on epithelial permeability. The effect of the strains harvested from mice after hepatectomy on the TEER of young adult mouse colon cells was inhibited by mannose and reversed by ciprofloxacin. CONCLUSION: The combination of surgical stress and short-term starvation is associated with a greater abundance of adherent and barrier-altering strains of E coli in the mouse cecum.
Animals↗
Quality of life and psychosocial adjustment in patients after Roux-en-Y gastric bypass: a brief report.
BACKGROUND: While Roux-en-Y gastric bypass (RYGBP) appears to be the most effective procedure for weight loss in morbidly obese patients, objective outcome data regarding quality of life (QoL) and psychosocial status following surgery are lacking. METHODS: The present study examined the effects of RYGBP in 32 morbidly obese subjects on a variety of outcome measures including QoL and psychosocial functioning. Assessments were conducted before surgery, 1 to 3 weeks post-surgery, and at 6-month follow-up. RESULTS: In addition to weight loss, results show significant improvements in health-related QoL, depression, and self-esteem, as well as a significant reduction in eating pathology following surgery. Results also show that neither the presence of binge-eating disorder nor clinical depression predicted poorer outcome post-surgery. CONCLUSION: RYGBP results in a dramatic reduction in weight, and marked improvements in health-related QoL, depression, self-esteem, and eating pathology, including binge-eating in the short term. These findings need to be replicated in a larger cohort of patients and followed for a longer time before we can reach more definitive conclusions regarding the psychosocial outcome in RYGBP.
Activities of Daily Living↗
Laparoscopic intracavitary debridement of peripancreatic necrosis: preliminary report and description of the technique.
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Acute Disease↗
Gut-derived sepsis occurs when the right pathogen with the right virulence genes meets the right host: evidence for in vivo virulence expression in Pseudomonas aeruginosa.
OBJECTIVE: To define the putative role of the PA-I lectin/adhesin, a binding protein of Pseudomonas aeruginosa, on lethal gut-derived sepsis after surgical stress, and to determine if this protein is expressed in vivo in response to physical and chemical changes in the local microenvironment of the intestinal tract after surgical stress. SUMMARY BACKGROUND DATA: Previous work from the authors' laboratory has established that lethal gut-derived sepsis can be induced after the introduction of P. aeruginosa into the cecum of mice after a 30% hepatectomy. This effect does not occur when P. aeruginosa is introduced into the cecum of sham operated control mice. Previous experiments further established that the mechanism of this effect is due to the presence of the PA-I lectin/adhesin of P. aeruginosa, which induces a permeability defect to a lethal cytotoxin of P. aeruginosa, exotoxin A. METHODS: Three strains of P. aeruginosa, one lacking functional PA-I, were tested in two complementary systems to assess virulence. Strains were tested for their ability to adhere to and alter the permeability of cultured human colon epithelial cells, and for their ability to induce mortality when injected into the cecum of mice after a 30% hepatectomy. To determine if PA-I is "in vivo expressed" when present in the cecal environment after hepatectomy, strains were retrieved from the cecum of sham-operated and hepatectomy-treated mice 24 and 48 hours after their introduction into the cecum and their PA-I expression was assessed. RESULTS: Results indicated that PA-I plays a putative role in lethal gut-derived sepsis in the mouse, because strains lacking functional PA-I had an attenuated effect on cultured human epithelial cells, and were nonlethal when injected into the cecum of mice after 30% surgical hepatectomy. Furthermore, surgical stress in the form of hepatectomy significantly altered the intestinal microenvironment, resulting in an increase in luminal norepinephrine associated with an increase in PA-I expression in retrieved strains of P. aeruginosa. Co-incubation of P. aeruginosa with norepinephrine increased PA-I expression in vitro, suggesting that norepinephrine plays a role in the observed response in vivo. CONCLUSIONS: Lethal gut-derived sepsis may occur when intestinal pathogens express virulence determinants in response to environmental signals indicating host stress. In this regard, the PA-I lectin/adhesin of P. aeruginosa appears to be a specific example of in vivo virulence expression in colonizing pathogens in the intestinal tract in response to surgical stress.
Adhesins, Bacterial↗
Continuous enteral nutrition attenuates pulmonary edema in rats exposed to 100% oxygen.
Adult rats exposed to hyperoxia develop anorexia, weight loss, and a lung injury characterized by pulmonary edema and decreased lung liquid clearance. We hypothesized that maintenance of nutrition during hyperoxia could attenuate hyperoxia-induced pulmonary edema. To test this hypothesis, we enterally fed adult male Sprague-Dawley rats via gastrostomy tubes and exposed them to oxygen (inspired O(2) fraction >0.95) for 64 h. In contrast to controls, enterally fed hyperoxic animals did not lose weight and had smaller pleural effusions and wet-to-dry weight ratios (a measure of lung edema) that were not different from room air controls. Enterally fed rats exposed to hyperoxia had increased levels of mRNA for the Na(+)-K(+)-ATPase alpha(1)- and beta(1)-subunits and glutathione peroxidase. These findings suggest that maintenance of nutrition during an oxidative lung injury reduces lung edema, perhaps by allowing for continued expression and function of protective proteins such as the Na(+)-K(+)-ATPase.
Animals↗
The impact of morbid obesity on oxygen cost of breathing (VO(2RESP)) at rest.
Oxygen consumption dedicated to respiratory work (V O(2RESP)) during quiet breathing is small in normal patients. In the morbidly obese, at high minute ventilations, VO(2RESP) is greater than in normal patients, but VO(2RESP) during quiet breathing in these patients is not known. We postulated that such patients have increased VO(2RESP) at rest which may predispose them to respiratory failure when additional respiratory workloads are imposed. We measured baseline VO(2) in morbidly obese patients immediately prior to gastric bypass surgery and again after intubation, mechanical ventilation, and paralysis, and compared their change in VO(2) to nonobese patients scheduled for elective abdominal surgery. Baseline VO(2) was higher in the obese patients compared with control patients (354.6 versus 221.4 ml/min; p = 0.0001) and the change in VO(2) from spontaneous breathing to mechanical ventilation was significant in the obese patients (354.6 versus 297.2 ml/min; p = 0.0002) but not the control patients (221.4 versus 219.8 ml/min; p = 0.86). We conclude that morbidly obese patients dedicate a disproportionately high percentage of total VO(2) to conduct respiratory work, even during quiet breathing. This relative inefficiency suggests a decreased ventilatory reserve and a predisposition to respiratory failure in the setting of even mild pulmonary or systemic insults.
Adult↗
Cholecystokinin modulates mucosal immunoglobulin A function.
BACKGROUND: We have established that mucosal immunoglobulin A (IgA) production is highly dependent on cholecystokinin release and is markedly suppressed by glucocorticoids. The purpose of the present study was to examine the role of cholecystokinin on the functional responsiveness of the mucosal IgA system in glucocorticoid treated rats. METHODS: A total of 24 Fischer rats were assigned to three groups of 8 animals each. Animals were injected with vehicle (CON), dexamethasone (DEX) (0.08 mg/150 g), or DEX (0.08 mg/150 gm) and ARL1294KF (500 ng twice daily), a novel and potent long-acting cholecystokinin agonist (DEX+CCK). Animals were treated for 48 hours and killed. Duodenum was harvested, and the total mucosal concentration of cholecystokinin was measured by radioimmunoassay. Mucosal IgA was assayed by quantitation of immunoreactive cells in the ileum. Bacterial adherence was evaluated by quantitative culture of vigorously washed stripped cecal mucosa. Transepithelial electrical resistance, a measure of tight junction permeability, was assessed by mounting strips of adjacent cecal mucosa in Ussing chambers. RESULTS: Glucocorticoid administration resulted in a statistically significant (p < 0.001) decrease in duodenal cholecystokinin, decreased IgA, and impaired mucosal immunity (increased bacterial adherence and decreased tissue resistance). Cholecystokinin administration preserved mucosal immune function in DEX-treated rats. CONCLUSIONS: Cholecystokinin may play an important role in maintaining the functional responsiveness of mucosal immunity during catabolic stress.
Animals↗
Whole gut washout for severe sepsis: review of technique and preliminary results.
BACKGROUND: The purpose of this study was to determine the safety and feasibility of whole gut washout for severe sepsis in human beings. METHODS: High-volume polyethylene glycol-3500 was administered to patients with severe sepsis. Body temperature, white blood cell count, and ventilatory indexes were recorded 24 hours before and 24 hours after whole gut washout. RESULTS: A significant decrease in febrile response was observed after gut washout with polyethylene glycol. Improvements in PaO2, positive end-expiratory pressure, and peak airway pressure were observed. The washout was well tolerated in all but one patient. CONCLUSIONS: High-volume whole gut washout for severe sepsis appears safe in critically ill patients and may offer some promise in reducing enterogenic inflammation after catabolic stress.
Adolescent↗
Enteropathogenic Escherichia coli adherence to intestinal epithelial monolayers diminishes barrier function.
The mechanism by which enteropathogenic Escherichia coli (EPEC) causes diarrhea remains elusive. Several alterations within the host cell have been demonstrated to occur following EPEC attachment including increases in intracellular Ca2+ concentration and rearrangement and phosphorylation of several cytoskeletal proteins. The consequences of these intracellular perturbations on host cell function, however, have not been determined. The aim of this study was to examine the effect of EPEC adherence on intestinal epithelial barrier function. T84 cell monolayers were infected with either wild-type EPEC or a nonadherent isogenic derivative. Transepithelial electrical resistance, a measure of barrier function, decreased 33.5 +/- 6.4% after a 6-h incubation with the wild-type strain. Electron microscopy revealed ultrastructurally normal cells, and lactate dehydrogenase release assays failed to demonstrate cytotoxicity. Dual 22Na+ and [3H]mannitol flux studies localized the permeability defect to tight junctions. In addition, cumulative flux of the paracellular marker mannitol was four- to fivefold greater across monolayers infected with wild-type EPEC. Sequestration of intracellular calcium stores by dantrolene completely abrogated the resistance drop associated with EPEC attachment. These data demonstrate that adherence of EPEC to intestinal epithelial cell monolayers disrupts tight junction barrier function via a calcium-requiring event.
Bacterial Adhesion↗
The effect of dexamethasone administration on rat intestinal permeability: the role of bacterial adherence.
BACKGROUND/AIMS: Previous studies have shown that dexamethasone administration to rats results in diminution of biliary secretory immunoglobulin A concentration and alters intestinal barrier function to bacteria. The aims of this study were to examine and characterize the effect of dexamethasone on intestinal permeability and to determine the possible influence of bacterial adherence to the mucosa in this process. METHODS: Groups of adult Fisher rats were studied, and the effects of dexamethasone administration and bowel decontamination on bacterial adherence and intestinal permeability were determined in various bowel segments. RESULTS: Dexamethasone administration was associated with a significant increase in bacterial adherence to the mucosa, which was most pronounced in the cecum (4.33 +/- 0.2 colony forming units (cfu) (log10) per gram of mucosa for control vs. 6.23 +/- 0.2 for dexamethasone). This was accompanied by significant alterations in intestinal permeability as measured by a decrease in transepithelial electrical resistance (49.5 +/- 4.1 omega.cm2 for control vs. 25.4 +/- 2.5 omega.cm2 for dexamethasone). Dual sodium-mannitol flux analysis showed this defect to be predominantly paracellular. Antibiotic decontamination of the intestine completely abrogated the intestinal permeability defect observed in this model. CONCLUSIONS: Bacterial-mucosal cell interactions may be responsible for alterations in intestinal permeability after dexamethasone administration.
Animals↗
The effect of nutrition on gastrointestinal barrier function.
The tightly adherent monolayer of epithelial cells that line the luminal side of the intestine provides a dynamic and highly regulated barrier to the passive transport of macromolecules. The presence of both nutrients and microbes within the gastrointestinal lumen impose a dichotomous task to this epithelial barrier. Several lines of evidence suggest that conditions created in modern intensive care units (ICUs) dysregulate the discriminatory function of the epithelial barrier. Alterations in intestinal barrier function may result in permeation of autotoxic macromolecules of immense size and diversity that normally reside in the gut lumen. It is becoming increasingly recognized that artificial nutritional support of the critically ill patient may result in significant alterations in epithelial barrier function. The causes and consequences of diet-induced alterations in the gastrointestinal barrier will be discussed. Future strategies in the development of more physiological diets for the critically ill will likely involve the addition of neural, hormonal, and growth factors as stimulants for enhancement of barrier function.
Animals↗
The importance of the mucosal immune system.
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Critical Illness↗
The effect of glucocorticoid administration on bacterial translocation. Evidence for an acquired mucosal immunodeficient state.
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 intraperitoneally (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 micrograms/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.
Animals↗
Biliary secretory IgA levels in rats with protein-calorie malnutrition.
Malnutrition is a recognized cause of failure of host defense mechanisms. In the past 5 years, it has been demonstrated that the gut, long known to have significant morphologic changes with protein calorie malnutrition (PCM), is an immune organ affected by malnutrition. To assess the role of biliary immunoglobulin A (S-IgA), part of the barrier to bacterial invasion from the gastrointestinal tract, the following study was performed. Seventy-eight Fisher female inbred rats weighing 110-130 g were randomly separated into two groups. The control rats were fed standard rat chow. The experimental rats were fed a 2% agar protein depletion (PCM) diet (USP XV). The biliary tract of the rat was cannulated with Silastic tubing and bile flow and rat secretory immunoglobulin A (S-IgA) was sampled at intervals. S-IgA was measured by the Elisa method. Total bile protein was measured by micro-Kjeldahl. Bile was collected from the rats on day 0, 7, 14, 21, 29, 36, 42, and 49. During the study, the weight of rats fed the PCM diet decreased from 127.4 +/- 14.5 g at day 0 to 83 +/- 2.6 g on day 37. Control rats gained weight from 124.4 +/- 14.5 g at day 0 to 153.6 +/- 3.8 g at day 37. Total biliary protein at day 0 was 2.52 +/- .05 mg/ml and at day 36 was 2.51 +/- 11 mg/ml for PCM rats and 2.57 +/- 10 mg/ml for control rats. Normal rats and control rats both had an initial increase of S-IgA from 2.74 +/- 73 mg/ml on day 0 to 5.75 +/- 1.75 mg/ml on day 37. Both PCM and control rats demonstrated an increase in S-IgA levels despite significant loss of weight in the experimental group. Similarly, total biliary protein was not decreased in either group. The results suggest that gut immune system is preserved despite significant protein calorie malnutrition.
Animals↗
The effect of parenteral nutrition on gastrointestinal immunity. The importance of enteral stimulation.
Secretory IgA (S-IgA), an immunoglobulin present in secretions, prevents the adherence of bacteria to mucosal cells and is the principle component of the gut mucosal defense system. The purpose of this study was to determine whether the route of nutrient administration affects S-IgA. Twenty-five female Fisher rats were randomized into three groups. Groups I and II were fed an isonitrogenous, isocaloric standard hyperalimentation solution, Group I intravenously and Group II via a gastrostomy. Group III (control) was fed rat chow and water ad lib. Since bile is one of the principle sources of S-IgA, animals had biliary T-tubes placed for sampling of bile every 4 days. At day 16, Group I animals were fed rat chow and water for an additional 8 days. S-IgA was measured by the ELISA immunoassay. Results indicated at day 16 that the S-IgA level in mg/ml of Group I was 1.1 +/- 0.2, while the S-IgA in Groups II and III was 2.2 +/- 0.6 and 2.2 +/- 0.26, respectively. Furthermore, the S-IgA level in Group I after 8 days of enteral feeding rose to 1.8 +/- 0.4. The difference in S-IgA levels between enterally and parenterally fed rats suggests that an important defense barrier is compromised during parenteral hyperalimentation. Rats fed the same nutrients by gastrostomy maintained S-IgA levels better than rats fed the same nutrients intravenously. The rapid return to normal levels after resumption of enteral feeding suggests that the intraluminal presence of foodstuffs is essential for maintenance of S-IgA.
Animals↗
Effect of immunonutrition on virulence strategies in bacteria.
A coevolutionary balance exists between bacteria within the mammalian gastrointestinal tract and the lining epithelia. Recent advances in the molecular detection of bacteria have demonstrated that under normal circumstances, the lining mucosal epithelium in the gastrointestinal tract is sterile. Under conditions of stress and dietary alteration however, the probability of bacteria adhering to and altering epithelial function is a reflection of the virulence tactics of the resident bacteria balanced against the innate mucosal defense system. This pathologic event may be caused in part by the adaptive response of intestinal bacteria to their changing environment and food supply. Accustomed to a warm climate and a constant and predictable food supply, bacteria exposed to luminal nutrient starvation and a catabolically stressed host may express virulence determinants that can harm the host. The causes and consequences of bacterial adherence to host intestinal epithelia during stress and dietary manipulation are discussed.
Bacteria↗