Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Intestinal barrier”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources
PubMed1978

A study of endotoxemia in ulcerative colitis and Crohn's disease. I. Clinical study.

Endotoxin (lipopolysaccharide, LPS) and LPS antibody in the blood were studied in 61 cases of ulcerative colitis (U.C.) by radioimmunoassay. Lysozyme (LZM) concentration was also studied by the turbidimetric method. As a result, it was found that the blood LPS value as well as serum LZM concentration reflects the clinical observations. The case of endotoxemia in the active phase group showed a positive correlation between the LPS value and LZM concentration. LPS antibody which could not be detected in many cases of the active phase, had a high titer in cases of remission with a long history of the disease. These results would suggest that in U.C. with damaged intestinal mucosal barrier, LPS originating from intestinal flora enters into the blood and aggravates the disease and further that this invading LPS releases LZM into the blood. The same studies were performed on 7 cases of Crohn's disease and the same result was obtained.

Adolescent↗
PubMed1982

The permeability of the plasma-lymph barrier of the small intestine of various species to macromolecules.

The filtration coefficients of polyvinylpyrrolidone (PVP) of molecular weight 10,000-110,000 were measured at the plasma-lymph barrier of the upper small intestine of rabbits, rats and cats. For this purpose the animals were given intravenous injections or infusions of PVP in such a way as to produce a constant blood level; PVP concentrations were measured in lymph obtained by cannulating the mesenteric duct and also in the plasma. In these species low molecular weight PVP had a filtration coefficient of 0.85-0.64, while high molecular weight PVP (MW 110,000) either had a very low filtration coefficient - 0.22 - or was not detectable in the intestinal lymph. The three species, representing herbivores, omnivores and carnivores, showed no differences in the penetration behavior of PVP, i.e., in the permeability of the plasma-lymph barrier to macromolecules.

Animals↗
PubMed1979

[Effect of tetracycline group antibiotics on the barrier properties of the small intestine epithelium].

The effect of 5 tetracyclines on the barrier and transport properties of the small intestine epithelium was studied. The barrier properties were estimated by a change in the ionic selectivity and conductivity of the epithelium, as well as by enterocyte linkage. The current of the short circuit served the characteristics of the Na transport system state. Dimethylchlortetracycline, methacycline and oxytetracycline in concentrations of 10(-7) g/ml decreased the epithelium conductivity and increased the cell linkage. Tetracycline and methacycline in concentrations of 10(-9) g/ml had an analogous effect. The effect was observed 10--20 minutes after the start of incubation with the substance. No effect on the current of the short circuit was observed within the concentrations of 10(-4) to 10(-9) g/ml. It is suggested that the decreased conductivity and increased linkage are due to adsorption of the tetracycline molecules in the region of close cell contacts.

Animals↗
PubMed2001

Jejunal luminal nitric oxide during severe hypovolemia and sepsis in anesthetized pigs.

OBJECTIVE: Lowered gut blood perfusion and the associated intestinal mucosal barrier dysfunction is considered important in the pathophysiology leading to critical illness. Intestinal mucosal nitric oxide formation has been attributed a key role in the regulation of epithelial permeability and other properties of the intestinal mucosal barrier. This study was performed to delineate intestinal mucosal NO formation during hypovolemia or sepsis, both of which are associated with intestinal hypoperfusion. MATERIALS AND METHODS: Seventeen pigs were subjected to 2 h of severe hypovolemia (bleeding induced) or sepsis (systemic infusion of live Escherichia coli) or no treatment (controls). Jejunal mucosal NO production was monitored by a tonometer. Mesenteric blood flow was measured as portal venous blood flow by an ultrasonic transit time flowmeter probe, and oxygen delivery and consumption were calculated from regional blood samples. RESULTS: Intestinal perfusion and oxygen delivery were reduced by the same order of magnitude in both groups. Jejunal mucosal NO production and oxygen consumption decreased markedly in the hypovolemia group but remained stable in the group subjected to septic shock. CONCLUSIONS: These data suggest that blood loss inhibits jejunal mucosal NO production as part of a general downregulation of nonvital organs. Sepsis represents a more complex stress condition with activation/maintenance of host defense mechanisms as reflected by maintained jejunal mucosal NO production despite reduced gut blood perfusion.

Analysis of Variance↗
PubMed2002

Intestinal infection with Giardia spp. reduces epithelial barrier function in a myosin light chain kinase-dependent fashion.

BACKGROUND & AIMS: Giardiasis causes malabsorptive diarrhea, and symptoms can be present in the absence of any significant morphologic injury to the intestinal mucosa. The effects of giardiasis on epithelial permeability in vivo remain unknown, and the role of T cells and myosin light chain kinase (MLCK) in altered intestinal barrier function is unclear. This study was conducted to determine whether Giardia spp. alters intestinal permeability in vivo, to assess whether these abnormalities are dependent on T cells, and to assess the role of MLCK in altered epithelial barrier function. METHODS: Immunocompetent and isogenic athymic mice were inoculated with axenic Giardia muris trophozoites or sterile vehicle (control), then assessed for trophozoite colonization and gastrointestinal permeability. Mechanistic studies using nontransformed human duodenal epithelial monolayers (SCBN) determined the effects of Giardia on myosin light chain (MLC) phosphorylation, transepithelial fluorescein isothiocyanate-dextran fluxes, cytoskeletal F-actin, tight junctional zonula occludens-1 (ZO-1), and MLCK. RESULTS: Giardia infection caused a significant increase in small intestinal, but not gastric or colonic, permeability that correlated with trophozoite colonization in both immunocompetent and athymic mice. In vitro, Giardia increased permeability and phosphorylation of MLC and reorganized F-actin and ZO-1. These alterations were abolished with an MLCK inhibitor. CONCLUSIONS: Disruption of small intestinal barrier function is T cell independent, disappears on parasite clearance, and correlates with reorganization of cytoskeletal F-actin and tight junctional ZO-1 in an MLCK-dependent fashion.

Actins↗
PubMed2001

Redox regulation of endothelial barrier integrity.

Intestinal ischemia-reperfusion is associated with the generation of reactive oxygen metabolites as well as remote, oxidant-mediated lung injury. Oxidants elicit endothelial redox imbalance and loss of vascular integrity by disorganizing several junctional proteins that contribute to the maintenance and regulation of the endothelial barrier. To determine the specific effect of redox imbalance on pulmonary vascular barrier integrity, microvascular permeability was determined in lungs of animals subjected to chemically induced redox imbalance. The effect of redox imbalance on microvascular permeability and endothelial junctional integrity in cultured lung microvascular cells was also determined. Whole lung and cultured pulmonary endothelial cell permeability both increased significantly in response to chemical redox imbalance. Thiol depletion also resulted in decreased endothelial cadherin content and disruption of the endothelial barrier. These deleterious effects of intracellular redox imbalance were blocked by pretreatment with exogenous glutathione. The results of this study suggest that redox imbalance contributes to pulmonary microvascular dysfunction by altering the content and/or spatial distribution of endothelial junctional proteins.

Animals↗
PubMed1998

Impedance analysis for the determination of epithelial and subepithelial resistance in intestinal tissues.

The barrier function of the intestinal wall plays a key role in body homeostasis and defense against noxious agents. Conventional Ussing chamber techniques determine the overall transmural resistance but do not differentiate epithelial and subepithelial tissues. The barrier function, however, resides in the epithelial cell layer only. Transmural impedance analysis can solve this problem, if adequate models are applied. We show that: (i) epithelial and subepithelial impedances are additive, (ii) the epithelium proper can be represented by a very general electrical model, which demonstrates short-circuiting at high frequencies (due to cell membrane capacitances), and (iii) the reactance of subepithelial tissue can be described phenomenologically. Using an empirical expression for description of the subepithelial impedance, the present method allows the determination of the epithelial and the subepithelial resistance. This was exemplified in rat ileum, which defied adequate impedance analysis so far. Of the transmural DC resistance of 61 +/- 5 omega.cm2 (n = 8) the subepithelial contribution was 28 +/- 2 omega.cm2 and the epithelial resistance was 33 +/- 4 omega.cm2.

Animals↗
PubMed2026

Intestinal blood vessel-associated macrophages and gut-vascular barrier dysfunction in cirrhosis.

BACKGROUND: Bacterial translocation in cirrhosis can trigger infection and hepatic decompensation, leading to systemic inflammation, organ failure and increased mortality. These infections often originate from the gastrointestinal tract after bacteria breach the intestinal barrier and disseminate to systemic sites. OBJECTIVE: In this study, we explore the mechanisms underlying intestinal barrier dysfunction in cirrhosis using an experimental cirrhosis model and patient-derived intestinal biopsies. DESIGN: We developed a murine model of cirrhosis through chronic administration of carbon tetrachloride for up to 20 weeks. We investigated both the intestinal epithelial and vascular compartments and performed single-cell transcriptomic profiling of myeloid cells isolated from cirrhotic mice and from individuals with compensated and decompensated cirrhosis. RESULTS: Our findings indicate that bacterial translocation in cirrhosis is the result of failure at multiple checkpoints, including aberrant epithelial cell death, vascular barrier damage and dysfunction of gut-vascular macrophages. In a preclinical model of cirrhosis, macrophages exhibited increased levels of monocyte-attracting chemokines, reduced bacterial clearance and impaired interactions with blood vessels. Importantly, depleting vascular-lining macrophages resulted in bacterial translocation to systemic sites, even in the absence of experimental liver disease. Transcriptional profiling of macrophages from duodenal biopsies of patients with cirrhosis indicated similar dysregulation of pathways supporting blood vessels and elevated expression of chemokines. CONCLUSIONS: This study emphasises the critical role of intestinal macrophages in preventing the dissemination of luminal bacteria and highlights the multifaceted breakdown of the intestinal barrier in cirrhosis and the importance of the gut-vascular barrier.

Animals↗
PubMed1989

Interferon-gamma directly affects barrier function of cultured intestinal epithelial monolayers.

Although epithelia, which often are in intimate contact with lymphoid cells, may bear receptors for various cytokines, it is unclear whether cytokines directly effect epithelial function. We examine the effects of the cytokine interferon (IFN) on barrier function of cultured monolayers of the T84 human intestinal epithelial cell line. Gamma IFN, in concentrations and exposures required to show its other biological effects, directly affects such monolayers. Monolayer resistance is substantially diminished by gamma IFN. Such effects were not due to cytotoxicity as judged morphologically and by LDH assays. Solute fluxes and dual Na+-mannitol flux analysis indicate that the resistance decrease is due to an effect of gamma IFN on tight junction permeability. The effects of gamma IFN on monolayer barrier function were not duplicated by the cytokines interleukin 1, interleukin 2, or tumor necrosis factor. We speculate that such products of activation of lymphoid cells might influence barrier function of intestinal, and perhaps other epithelia in disease states.

Cell Line↗
PubMed2003

The mycotoxin fumonisin B1 alters the proliferation and the barrier function of porcine intestinal epithelial cells.

Fumonisin B1 (FB1) is a mycotoxin produced by Fusarium verticillioides (formerly F. moniliforme), a fungus that commonly contaminates maize. FB1 causes toxicological effects in laboratory and domestic animals including pigs. Because the gastrointestinal tract represents the first barrier met by exogenous food compounds, the purpose of this study was to investigate the effects of FB1 on IPEC-1, a porcine intestinal epithelial cell line. We first verified that low concentrations of FB1 did not exert any cytotoxic effect on IPEC-1. Indeed, significant LDH release was only observed for FB1 concentrations greater than 50 and 700 microM on proliferating and nonproliferating cells, respectively. We then demonstrated that FB1 inhibits proliferation of IPEC-1. Fluorescence-activated cell sorting (FACS) analysis of the cell cycle indicated that FB1 blocks the proliferation of intestinal cells in the G0/G1 phase. Similar results were obtained with LLC-PK1, a renal porcine epithelial cell line, which is considered to be a good model for studying FB1 in vitro effects. We have also assessed the effects of FB1 on the integrity of the barrier formed by the intestinal epithelium. We demonstrated that FB1 decreases the transepithelial electrical resistance (TEER) of IPEC-1 in a time- and dose-dependent manner. This effect was only noticed after a long exposure (8-12 days of treatment). FB1 induced the TEER decrease independently of the cell differentiation stage, and this effect was partially reversible. Taken together, our data indicate that FB1 alters the proliferation and the barrier function of intestinal cells. These results may have implications for humans and animals consuming FB1-contaminated food or feed.

Animals↗
PubMed1989

Food allergy: facts and fiction.

Hypersensitivity reactions to dietary products are especially common in the pediatric population, yet food allergy as a distinct clinical entity remains poorly defined. The clinicopathologic features of this syndrome can vary considerably from patient to patient; no reliable diagnostic laboratory tests are available, and some of the treatment regimens are controversial. The pathogenesis of this condition is not well understood. An important factor is the role of the intestinal mucosal barrier in the regulation of uptake of dietary antigen from the intestinal tract. Recently, significant differences have been observed between the features of the immature newborn and the mature adult intestinal mucosal barriers. These findings may be of fundamental importance to the pathogenesis of food allergy and are currently an area of intense research.

Aging↗
PubMed2001

Extraperitoneal approach reduces intestinal and renal dysfunction in elective abdominal aortic aneurysm repair.

BACKGROUND: Intestinal mucosal barrier dysfunction observed in patients undergoing transperitoneal abdominal aortic aneurysm (AAA) repair may contribute to the development of the systemic inflammatory response syndrome and dysfunction of various organs. The aim of this study is to investigate whether an extraperitoneal approach reduces intestinal mucosal barrier and renal dysfunction in elective infrarenal AAA repair. METHODS: Twenty patients admitted for elective infrarenal AAA repair were randomized into either the transperitoneal approach (n=10) or the extraperitoneal approach (n=10). Intestinal permeability was measured preoperatively, and at day 1 and day 3 after surgery using the lactulose/mannitol test by calculating the differential urinary excretion ratio of the two sugars after oral administration. Renal dysfunction was assessed by measuring the urinary albumin/creatinine ratio (ACR) at the same time points. RESULTS: Intestinal permeability was significantly increased in the transperitoneal group at day 1 [0.124+/-0.035 (mean+/-s.e.m.)] compared to the preoperative level (0.020+/-0.003), (p=0.001) and to the extraperitoneal group at day 1 (0.025+/-0.008), (p<0.05) which showed no change in comparison with the preoperative level (0.020+/-0.003). The ACR was also significantly increased in the transperitoneal group at day 1 (16.69+/-5.12) compared to the preoperative level (5.71+/-2.89), (p<0.05) and to the extraperitoneal group at day 1 (4.33+/-1.49), (p<0.05) which showed no significant change at any of the times examined. No correlation was observed between the lactulose/mannitol ratio and the albumin/creatinine ratio, or between age, operating time, aortic clamping time, amount of blood lost or blood transfused. CONCLUSIONS: These results support the suggestion that minimising intestinal manipulation using an extraperitoneal approach in AAA repair preserves intestinal mucosal barrier and renal glomerular functions.

Aged↗
PubMed1996

Regulation of the mucosal epithelial barrier.

Rapid re-sealing of the intestinal epithelial barrier is initially accomplished by migration of viable epithelial cells from the wound edge into the denuded area ('restitution') and only later by cell proliferation. Whereas proliferation of intestinal epithelial cells has been studied intensively, much less is known about the pivotal initial phase of cell migration. Restitution appears to be modulated by peptide growth factors/cytokines, extracellular matrix molecules, and luminally secreted products of mucus-producing cells (schematically summarized in Figure 1). Recent work has demonstrated that various cytokines (TGF-beta 1, TGF-alpha, EGF, IL-1 beta, IFN-gamma, basic FGF, KGF and HGF) present in the intestinal mucosa enhance intestinal epithelial restitution, presumably by mediating its effects through the basolateral pole of the epithelial monolayer. In addition to their effects on cell adhesion, differentiation, and spatial organization, the extracellular matrix molecules on which intestinal epithelial cells reside also have the potential to stimulate intestinal epithelial cell migration. The basement membrane components fibronectin and collagen type IV may be especially important. Finally, trefoil factors, a recently identified family of peptides which are secreted onto the luminal surface where they form the visco-elastic mucus layer through interaction with mucin glycoproteins, also promote the important process of restitution through a pathway distinct from that used by factors acting at the basolateral cell surface.

Animals↗
PubMed2026

Probiotic Lacticaseibacillus casei 2S-1 Attenuates Escherichia coli-Induced Enteritis via Gut Microbiota Modulation and Host Gene Regulation.

Maintaining gut microbial homeostasis is crucial for host health, whereas infection with Escherichia coli (E. coli) is a major contributor to intestinal inflammation and microbial dysbiosis. Recent research has focused on probiotic strategies for managing enteric inflammatory disorders. Previous studies have shown that beneficial microorganisms show protection through modulating host immune responses, enhancing intestinal epithelial barrier integrity, and inhibiting pathogenic bacteria. To evaluate the prophylactic effectiveness of a recently isolated strain, Lacticaseibacillus casei 2S-1, in a murine model of E. coli-induced enteritis, this study focuses on interactions within the microbiota-intestinal-immune axis, together with host transcriptional responses and pathway enrichment associated with oxidative stress and mitochondrial function. In vitro analysis of probiotic features, including growth dynamics, acidogenic capacity, and tolerance to acidic and bile salt environments, as well as genetic safety profiling, followed the methodical isolation and taxonomic identification of L. casei 2S-1. A preventive intervention protocol was established, and a murine model of enteritis was induced by exposure to E. coli. Histopathological analyses were performed to observe in vivo safety and protective efficacy. Changes in gut microbial structure were characterized by 16S rRNA gene sequencing, while host responses were identified by intestinal immunohistochemistry and transcriptome profiling. L. casei 2S-1 showed probiotic properties. In vitro analyses showed that the strain exhibited tolerance to acidic and bile salt conditions, and its untreated culture supernatant showed antimicrobial activity against pathogenic bacteria. Its safety profile was supported by genomic analysis, which verified the lack of virulence-associated genes and antibiotic resistance factors. In vivo, L. casei 2S-1 pretreatment reduced mortality and intestinal inflammation, modulated gut microbial composition, and preserved intestinal barrier-associated protein expression in infected mice. This study provides experimental evidence supporting the prophylactic effects of L. casei 2S-1 and its associations with gut microbiota modulation and host transcriptional responses, providing a foundation for further investigation of probiotic-based preventive strategies against intestinal infections.

Animals↗
PubMed1997

Epithelial cell kinase-B61: an autocrine loop modulating intestinal epithelial migration and barrier function.

Epithelial cell kinase (Eck) is a member of a large family of receptor tyrosine kinases whose functions remain largely unknown. Expression and regulation of Eck and its cognate ligand B61 were analyzed in the human colonic adenocarcinoma cell line Caco-2. Immunocytochemical staining demonstrated coexpression of Eck and B61 in the same cells, suggestive of an autocrine loop. Eck levels were maximal in preconfluent cells. In contrast, B61 levels were barely detectable in preconfluent cells and increased progressively after the cells reached confluence. Caco-2 cells cultured in the presence of added B61 showed a significant reduction in the levels of dipeptidyl peptidase and sucrase-isomaltase mRNA, markers of Caco-2 cell differentiation. Cytokines interleukin-1beta (IL-1beta), basic fibroblast growth factor, IL-2, epidermal growth factor, and transforming growth factor-beta modulated steady-state levels of Eck and B61 mRNA and regulated Eck activation as assessed by tyrosine phosphorylation. Functionally, stimulation of Eck by B61 resulted in increased proliferation, enhanced barrier function, and enhanced restitution of injured epithelial monolayers. These results suggest that the Eck-B61 interaction, a target of regulatory peptides, plays a role in intestinal epithelial cell development, migration, and barrier function, contributing to homeostasis and preservation of continuity of the epithelial barrier.

Adenocarcinoma↗
PubMedDate not supplied

Effect of oral genistein and isoflavone-free diet on cecal flora and bacterial translocation in antibiotic-treated mice.

BACKGROUND: There are several reports indicating that the isoflavone genistein may augment the integrity of the intestinal epithelial barrier as well inhibit bacterial internalization by cultured enterocytes. We speculated that oral genistein might enhance the integrity of the intestinal epithelial barrier as monitored by the extraintestinal dissemination of intestinal bacteria. METHODS: Mice were treated with oral antibiotics to induce cecal bacterial overgrowth accompanied by bacterial translocation of antibiotic-resistant enterobacteria, especially Escherichia coli. These mice were divided into separate groups that included chow-fed mice orally inoculated either with saline, vehicle, or genistein, and mice fed isoflavone-free diet and orally inoculated with either saline, vehicle, or genistein. Intestinal bacterial overgrowth was monitored by quantitative culture of excised ceca and bacterial translocation was monitored by quantitative culture of draining mesenteric lymph nodes. RESULTS: Mice fed the isoflavone-free diet had decreased populations of cecal bacteria compared with chow-fed mice, and bacterial translocation was reduced in chow-fed mice compared with mice fed isoflavone-free diet. However, bacterial translocation was similar in mice given oral genistein compared with appropriate control mice. CONCLUSIONS: Oral genistein had no noticeable effect on bacterial translocation in this model. However, the isoflavone-free diet had an antibacterial effect on cecal flora, and the isoflavone-free diet was associated with decreased numbers of cecal bacteria and decreased incidence of bacterial translocation.

Administration, Oral↗
PubMed2005

Mechanism of TNF-{alpha} modulation of Caco-2 intestinal epithelial tight junction barrier: role of myosin light-chain kinase protein expression.

TNF-alpha plays a central role in the intestinal inflammation of various inflammatory disorders including Crohn's disease (CD). TNF-alpha-induced increase in intestinal epithelial tight junction (TJ) permeability has been proposed as one of the proinflammatory mechanisms contributing to the intestinal inflammation. The intracellular mechanisms involved in the TNF-alpha-induced increase in intestinal TJ permeability remain unclear. The purpose of this study was to investigate the possibility that the TNF-alpha-induced increase in intestinal epithelial TJ permeability was regulated by myosin light-chain kinase (MLCK) protein expression, using an in vitro intestinal epithelial model system consisting of the filter-grown Caco-2 intestinal epithelial monolayers. TNF-alpha (10 ng/ml) produced a time-dependent increase in Caco-2 MLCK expression. The TNF-alpha increase in MLCK protein expression paralleled the increase in Caco-2 TJ permeability, and the inhibition of the TNF-alpha-induced MLCK expression (by cycloheximide) prevented the increase in Caco-2 TJ permeability, suggesting that MLCK expression may be required for the increase in Caco-2 TJ permeability. The TNF-alpha increase in MLCK protein expression was preceded by an increase in MLCK mRNA expression but not an alteration in MLCK protein degradation. Actinomycin-D prevented the TNF-alpha increase in MLCK mRNA expression and the subsequent increase in MLCK protein expression and Caco-2 TJ permeability, suggesting that the increase in MLCK mRNA transcription led to the increase in MLCK expression. The TNF-alpha increase in MLCK protein expression was also associated with an increase in Caco-2 MLCK activity. The cycloheximide inhibition of MLCK protein expression prevented the TNF-alpha increase in MLCK activity and Caco-2 TJ permeability. Moreover, inhibitors of MLCK, Mg(2+)-myosin ATPase, and metabolic energy prevented the TNF-alpha increase in Caco-2 TJ permeability, suggesting that the increase in MLCK activity was required for the TNF-alpha-induced opening of the Caco-2 TJ barrier. In conclusion, our results indicate for the first time that 1) the TNF-alpha increase in Caco-2 TJ permeability was mediated by an increase in MLCK protein expression, 2) the increase in MLCK protein expression was regulated by an increase in MLCK mRNA transcription, and 3) the increase in Caco-2 TJ permeability required MLCK protein expression-dependent increase in MLCK activity.

Antimetabolites↗
PubMed2005

Effect of acute alcohol ingestion prior to burn injury on intestinal bacterial growth and barrier function.

Previous studies from our laboratory have shown that acute alcohol (EtOH) ingestion prior to burn injury enhances intestinal bacterial translocation. This study tested if increased intestinal bacterial translocation in alcohol and burn injured rats is due to an overgrowth in intestinal bacteria. We determined if the translocation was accompanied with alterations in intestinal permeability and immune cell population. Rats (225-250 g) were gavaged with alcohol to achieve a blood EtOH level in the range of 100 mg/dl prior to burn or sham injury (25% total body surface area). Two days after injury, we found that acute alcohol ingestions prior to burn injury results in a significant increase in bacterial counts in small intestine. The increase in intestinal bacterial counts accompanied a significant increase in intestinal permeability. Finally, immunohistochemical analysis revealed a substantial (p<0.05) loss of both T cell and dendritic cells in intestine of alcohol and burn injured rats compared with intestine of rats receiving either burn or sham injury. Altogether, results presented in this manuscript suggest that increase in intestinal bacterial growth along with alterations in intestinal permeability and immune status contribute to the increase in bacterial translocation observed in alcohol and burn injured rats.

Animals↗