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PubMed2002

Intestinal epithelial pathobiology: past, present and future.

The intestinal epithelium serves as one of man's primary interfaces with the outside world. Its importance is illustrated by the fact that the proper functioning of this interface is absolutely essential for human health, and even modest perturbations in its function may lead to diarrhoea, constipation, malnutrition, dehydration, infectious disease or chronic intestinal inflammatory diseases such as Crohn's disease and ulcerative colitis, collectively referred to as inflammatory bowel disease. Both pathogen-induced intestinal inflammation and the active flares of inflammatory bowel disease are histopathologically defined, their sequellae being mediated by neutrophils that migrate across the intestinal epithelium, forming a crypt abscess. Classically, the intestinal epithelium has been thought of primarily as a barrier, and indeed this is a very important aspect of its function, but the intestinal epithelium is also a highly interactive barrier. This chapter will summarize some of the basic research conducted over the past 15 years that has revealed basic insights into how the epithelium participates in the formation of a crypt abscess and how it plays a role in causing the characteristic clinical manifestations that ensue. In addition, the chapter will discuss how this research has resurrected the 'old', yet newly emerging, concept that physiological malfunction of the intestinal epithelium can be the primary defect that leads to the innate and adaptive immune dysregulation mediating inflammatory bowel disease.

Cell Movement↗
PubMed2001

Endogenous PPAR gamma mediates anti-inflammatory activity in murine ischemia-reperfusion injury.

BACKGROUND & AIMS: Peroxisome proliferator-activated receptor gamma (PPAR gamma) is a nuclear receptor whose activation has been linked to several physiologic pathways including those related to the regulation of intestinal inflammation. We sought to determine whether PPAR gamma could function as an endogenous anti-inflammatory pathway in a murine model of intestinal ischemia-reperfusion (I/R) injury. METHODS: PPAR gamma-deficient and wild-type mice were examined for their response to I/R procedure. Treatment with a PPAR gamma-specific ligand was also performed. RESULTS: In a murine model of intestinal I/R injury, we observed more severe injury in PPAR gamma-deficient mice and protection against local and remote tissue injury in mice treated with a PPAR gamma-activating ligand, BRL-49653. Activation of PPAR gamma resulted in down-regulation of intercellular adhesion molecule 1 expression by intestinal endothelium and tissue tumor necrosis factor alpha messenger RNA levels most likely by inhibition of the NF-kappa B pathway. CONCLUSIONS: These data strongly suggest that an endogenous PPAR gamma pathway exists in tissues that may be amenable to therapeutic manipulation in I/R-related injuries.

Animals↗
PubMed2006

Effects of serotonin transporter inhibition on gastrointestinal motility and colonic sensitivity in the mouse.

Serotonin-selective reuptake transporter (SERT) expression is decreased in animal models of intestinal inflammation and in individuals with inflammatory bowel disease (IBD) or irritable bowel syndrome (IBS), and it is possible that resultant changes in intestinal serotonin signalling contribute to the manifestation of clinical features associated with these disorders. The objective of this investigation was to determine whether inhibition of SERT function leads to changes in gut motility and sensitivity. Mice underwent a 14-day treatment with the SERT inhibitor, paroxetine (20 mg kg(-1)), or vehicle (saline/propylene glycol). Gastrointestinal (GI) transit following charcoal gavage, colonic motility, stool frequency and visceromotor responses to colorectal distension were evaluated. In mice treated with paroxetine, stool output was decreased, upper GI transit was delayed, and colonic sensitivity to a nociceptive stimulus was attenuated. These results demonstrate that reduced SERT function (via pharmacological blockade) significantly alters GI motility and sensitivity in mice, and support the concept that altered SERT expression and function could contribute to symptoms associated with IBS and IBD.

Animals↗
PubMed1992

Indomethacin-induced enteropathy: effect of the drug regimen on intestinal permeability in rats.

To set up and characterize reproducible, long-standing small intestinal inflammation in rats, animals were given three different oral regimens of indomethacin (Ind): a bolus of 10 mg/kg in water and three daily doses of 2, 4, and 8 mg/kg Ind in (a) the drinking water or (b) the standard diet. The effect of Ind on the small intestine was monitored by measuring intestinal permeability (IP). The three-day regimen seemed more suitable than a bolus dose to induce long-standing inflammatory modifications in the rat small intestine and Ind administered in the drinking water gave more consistent modifications of IP and more reproducible results than Ind in food. IP seemed a suitable tool for detecting these inflammatory changes in the small-intestinal physiology. This model could be used to assess the effect of new drugs on inflammation.

Administration, Oral↗
PubMed2026

The complement system in inflammatory bowel disease: from early observations to emerging frontiers.

PURPOSE OF REVIEW: The complement system is one of the most evolutionarily conserved arms of innate immunity and has re-emerged as an important regulator of intestinal inflammation in inflammatory bowel disease (IBD). Early observations from the mid-1970 s such as complement deposition in diseased bowel tissue and elevated serum complement levels in patients with ulcerative colitis and Crohn's disease have evolved into a nuanced understanding of how individual complement components can exert both protective and pathogenic effects in IBD. This review highlights recent advances in complement biology and examines how complement shapes intestinal immune responses, particularly in the setting of ongoing inflammation. RECENT FINDINGS: The complement system consists of more than 60 proteins that act as rapid first responders to infection. Although traditionally considered primarily liver-derived circulating effectors, recent work has demonstrated local synthesis and activation of key complement components at mucosal sites, including the colon. In parallel, genome-wide association studies have identified variants in complement genes associated with severe IBD complications. Collectively, these findings reveal a dichotomous role for complement in IBD, whereby excessive activation promotes inflammation, while impaired function compromises host defense and worsens disease outcomes. SUMMARY: Complement-targeted therapies have been effective in other diseases but have not yet translated to IBD. A deeper understanding of context-dependent protective versus pathogenic complement functions will be essential for developing future therapeutic strategies.

Humans↗
PubMed2000

Mice with a selective deletion of the CC chemokine receptors 5 or 2 are protected from dextran sodium sulfate-mediated colitis: lack of CC chemokine receptor 5 expression results in a NK1.1+ lymphocyte-associated Th2-type immune response in the intestine.

The chemokine receptors CCR2 and CCR5 and their respective ligands regulate leukocyte chemotaxis and activation. To determine the role of these chemokine receptors in the regulation of the intestinal immune response, we induced colitis in CCR2- and CCR5-deficient mice by continuous oral administration of dextran sodium sulfate (DSS). Both CCR2- and CCR5-deficient mice were susceptible to DSS-induced intestinal inflammation. The lack of CCR2 or CCR5 did not reduce the DSS-induced migration of macrophages into the colonic lamina propria. However, both CCR5-deficient mice and, to a lesser degree, CCR2-deficient mice were protected from DSS-induced intestinal adhesions and mucosal ulcerations. CCR5-deficient mice were characterized by a greater relative infiltration of CD4+ and NK1.1+ lymphocyte in the colonic lamina propria when compared to wild-type and CCR2-deficient mice. In CCR5-deficient mice, mucosal mRNA expression of IL-4, IL-5, and IL-10 was increased, whereas that of IFN-gamma was decreased, corresponding to a Th2 pattern of T cell activation. In CCR2-deficient mice, the infiltration of Th2-type T cells in the lamina propria was absent, but increased levels of IL-10 and decreased levels of IFN-gamma may have down regulated mucosal inflammation. Our data indicate that CCR5 may be critical for the promotion of intestinal Th1-type immune responses in mice.

Animals↗
PubMed1997

Pathogenesis and immune mechanisms of chronic inflammatory bowel diseases.

The inflammatory bowel diseases (IBDs) are characterized by intestinal inflammation of unknown etiology. Two distinct disorders, Crohn's disease and ulcerative colitis, have been identified. Three theories of IBD etiology are currently under consideration: 1) reaction to a persistent intestinal infection, 2) existence of a defective mucosal barrier to luminal antigens, and 3) a dysregulated host immune response to ubiquitous antigens. In each of these theories, either pathogenic or resident luminal bacteria constantly stimulate the mucosal and systemic immune systems to perpetuate the inflammatory cascade. Chronicity of inflammation results from an interaction of the persistent stimulus of microbial antigens with genetically determined host susceptibility factors that determine the individual's immune response or mucosal barrier function. The pathogenesis of IBD involves a series of steps, beginning with the breach of the intestinal mucosal barrier by infectious agents or toxins. The defective barrier exposes lamina propria immune cells to the continual presence of resident luminal bacteria, bacterial products, or dietary antigens, which perpetuates the inflammatory cascade. Many immunoregulatory abnormalities are noted in IBD, including the ratio of proinflammatory to immunosuppressive cytokines, selective activation of T(H) lymphocyte subsets, and abnormalities in epithelial antigen presentation. When activated during the initial inflammatory process, macrophages and T lymphocytes secrete a host of cytokines, which recruit other inflammatory cell types, thereby continuing the process. Tissue injury is the net result of the soluble products of the activated inflammatory cells. Knowledge of the pathogenesis in IBD suggests that the ultimate goals of therapy should be to block the proinflammatory mediators toward the proximal, rather than the distal, end of the cascade, to decrease the constant antigenic drive of luminal bacteria, and to correct the dysregulated immune response.

Chronic Disease↗
PubMed2005

Regulatory T cells and intestinal homeostasis.

Murine models of inflammatory bowel disease (IBD) are useful tools for the study of the pathogenesis and regulation of intestinal inflammation. Colitis can be induced in immune-deficient mice following transfer of populations of T cells or following infection with Helicobacter hepaticus and other intestinal pathogens. In these situations, colitis occurs as a result of the absence of a specialized population of regulatory cells, as transfer of CD4(+)CD25(+) T cells prevents disease. Importantly, from a clinical perspective, CD4(+)CD25(+) T cells can also reverse an established colitis. CD4(+)CD25(+) T cells proliferate both in the secondary lymphoid organs and at the site of inflammation, suggesting that regulation occurs both locally and systemically. CD4(+)CD25(+) T cells are not only capable of regulating other T cells but are also capable of suppressing components of the innate immune system. Control of colitis is dependent on the presence of the immunosuppressive cytokines interleukin-10 and transforming growth factor-beta, although their roles are divergent and complex. Regulatory T cells represent one of the host's mechanisms to prevent immune pathology during chronic immune stimulation. Enhancement of regulatory T-cell activity may be useful to control autoreactive T-cell responses and inhibit harmful inflammatory diseases such as asthma and IBD.

Animals↗
PubMed2005

Deficiency in expression of the signaling protein Sin/Efs leads to T-lymphocyte activation and mucosal inflammation.

Our studies have concentrated on elucidating the role of the signaling protein Sin in T-lymphocyte function. We have previously shown that Sin overexpression inhibits T-lymphocyte development and activation. Here we show that Sin-deficient mice exhibit exaggerated immune responses characterized by enhanced cytokine secretion and T-cell-dependent antibody production. Excessive T-cell responses in young mice correlate with spontaneous development of inflammatory lesions in different organs of aged Sin(-/-) mice, particularly the small intestine. The intestinal inflammation is characterized by T- and B-cell infiltrates in the lamina propria, which correlate with crypt enlargement and marked villus expansion and/or damage. Similar to the human intestinal inflammatory disorder Crohn's disease (CD), and in contrast to most mouse models of mucosal inflammation, inflammatory lesions in the gastrointestinal tract of Sin(-/-) mice are restricted to the small bowel. Taken together, these results suggest that Sin regulates immune system and T-lymphocyte function and that immune system dysfunction in the absence of Sin may underlie the pathogenesis of tissue-specific inflammation and enteropathies such as CD.

Adaptor Proteins, Signal Transducing↗
PubMed1995

Oxygen radical scavengers are protective against indomethacin-induced intestinal ulceration in the rat.

Nonsteroidal antiinflammatory drugs (NSAIDs) are widely used and may cause small intestinal inflammation and damage. Reactive oxygen metabolites are involved in various gastrointestinal inflammatory processes, but there is little information about their role in small intestinal mucosal damage induced by NSAIDs. We studied the effect of the oxygen radical scavengers superoxide dismutase (SOD), catalase (CAT), and allopurinol (ALLO) on indomethacin (INDO)-induced intestinal ulceration in the rat. Ulceration was produced by s.c. injection of 30 mg/kg of INDO 30 min after refeeding 24 h-fasted rats. Total ulcer area was measured 24 h after INDO administration. Study groups each consisted of eight animals which received either i.p. CAT, SOD, or both together, at a dosage of 5,000 U/kg each. All drugs were divided into five doses, given once an hour over a 4-h period, starting at the time of INDO injection. Another group received 100 mg/kg ALLO in two doses. Total ulcer area was reduced by SOD from 228 +/- 12 (sq mm, mean +/- SEM) to 153 +/- 12 (p < 0.001), by CAT to 179 +/- 13 (p < 0.01), and by both together to 95 +/- 5 (p < 0.0001). ALLO administration reduced the total ulcer area to 176 +/- 7 (p < 0.003). The protective effect of oxyradical scavengers supports the hypothesis that oxygen radicals are involved in the pathogenesis of INDO-induced small intestinal ulceration in the rat.

Allopurinol↗
PubMed2004

Intestinal interleukin-13 in pediatric inflammatory bowel disease patients.

BACKGROUND: Interleukin-13 (IL-13) is a multifunctional cytokine whose net principle action is to diminish inflammatory responses. Dysregulation of IL-13 production has been proposed to contribute to intestinal inflammation in inflammatory bowel disease (IBD) patients. Previous studies implicate IL-13 in IBD pathogenesis; however, they fail to accurately reflect in vivo intestinal IL-13 production. We evaluate IL-13, IL-6, and IL-1beta elaborations from colonic organ cultures of pediatric IBD patients METHODS: Endoscopic lamina propria biopsies or surgical specimens from pediatric patients with IBD were organ cultured and supernatants evaluated by enzyme-linked immunosorbent assay for IL-1beta, IL-6, and IL-13. RESULTS: IL-13 concentrations were significantly reduced in ulcerative colitis (UC) patients when compared with normal controls (P = 0.002) and Crohn disease (CD) patients (P = 0.001). End-stage UC patients at colectomy had lower intestinal IL-13 production than all other UC patients (P = 0.002). No significant correlation was found between IL-13 concentration and histologic disease severity (P = 0.134). CONCLUSIONS: Diminished intestinal IL-13 production is present in UC patients and wanes further with clinical disease progression. These findings suggest that UC patients may be differentiated from CD patients by intestinal IL-13 quantitation, and UC patients may benefit from IL-13 enhancing therapies.

Adolescent↗
PubMed2006

Molecular mechanism of tumor necrosis factor-alpha modulation of intestinal epithelial tight junction barrier.

A TNF-alpha-induced increase in intestinal epithelial tight junction (TJ) permeability has been proposed to be an important proinflammatory mechanism contributing to intestinal inflammation in Crohn's disease and other inflammatory conditions. Previous studies from our laboratory suggested that the TNF-alpha-induced increase in intestinal TJ permeability was mediated by an increase in myosin light chain kinase (MLCK) protein expression. However, the molecular mechanisms that mediate the TNF-alpha increase in intestinal TJ permeability and MLCK protein expression remain unknown. The purpose of this study was to delineate the intracellular and molecular mechanisms that mediate the TNF-alpha-induced increase in intestinal TJ permeability; using an in vitro intestinal epithelial model system consisting of filter-grown Caco-2 intestinal epithelial monolayers. To examine the molecular mechanisms involved in the TNF-alpha regulation of intestinal TJ barrier, we identified and cloned for the first time a functionally active MLCK promoter region. TNF-alpha treatment of filter-grown Caco-2 monolayers transfected with plasmid vector containing the MLCK promoter region produced an increase in MLCK promoter activity and MLCK transcription. The TNF-alpha-induced increase in MLCK transcription corresponded to a sequential increase in MLCK protein expression, MLCK activity, and Caco-2 TJ permeability. The TNF-alpha-induced increase in MLCK promoter activity was mediated by NF-kappaB activation, and the inhibition of NF-kappaB activation prevented the TNF-alpha-induced increase in promoter activity and the subsequent increase in MLCK protein expression and Caco-2 TJ permeability. The TNF-alpha-induced activation of MLCK promoter was mediated by binding of the activated NF-kappaB p50/p65 dimer to the downstream kappaB binding site (-84 to -75) on the MLCK promoter region; deletion of the kappaB binding site prevented the TNF-alpha increase in promoter activity. Additionally, siRNA silencing of NF-kappaB p65 also prevented the TNF-alpha increase in MLCK promoter activity. In conclusion, our findings indicated that the TNF-alpha-induced increase in intestinal epithelial TJ permeability was mediated by NF-kappaB p50/p65 binding and activation of the MLCK promoter. NF-kappaB p50/p65 activation of the MLCK promoter then leads to a stepwise increase in MLCK transcription, expression and activity, and MLCK-mediated opening of the intestinal TJ barrier.

Caco-2 Cells↗
PubMed2003

Intestinal immune responses in wild-type and Apcmin/+ mouse, a model for colon cancer.

C57BL/6J Apc(Min/+) (Apc(Min/+)) mice spontaneously develop pretumoric adenomas into the intestinal mucosa. We studied the relationship between the intestinal immune responses and adenoma formation in Apc(Min/+) mice and compared Apc(Min/+) mice with their wild-type siblings. Three time points (5, 8, and 15 weeks of age) and three high-fat dietary treatments (a non-fiber control with beef or inulin amendment) were included. The numbers of CD8+ T lymphocytes and tissue macrophages (Mac-1+ cells) per villus in ileal mucosa were determined by immunohistology, and the concentrations of secretory IgA, residual prostaglandin E(2) (PGE(2)), tumor necrosis factor alpha, and interleukin (IL)-12 in ileal contents were analyzed by ELISA. The crypt-villus ratio of the ileal mucosa was determined histologically. An immunostimulation, characterized by an increase in several parameters (PGE(2), IgA, Mac-1, and CD8), was observed in both genotypes between weeks 5 and 8. Most of the adenomas in Apc(Min/+) mice also appeared during the same period of sexual maturation. Females had smaller adenomas than males, and the beef group had fewer and smaller adenomas than the control group at 15 weeks. Females had less IgA and fewer Mac-1+ and CD8+ cells in ileal tissue than males at 15 weeks and more luminal IL-12 than males at 8 weeks. Puberty may have affected both tumorigenesis and intestinal immune responses in the Apc(Min/+) mouse. The beef group showed less luminal IgA and tumor necrosis factor alpha but more IL-12 than the control group. The concentration of PGE(2) correlated positively with the number and size of adenomas and was higher in the Apc(Min/+) mice than in wild-type mice at 15 weeks. IgA and Mac-1 were positively correlated with the size of adenomas at 15 weeks. The positive correlations between tumor size and IgA and between tumor number and size and PGE(2) suggest that a balance toward the Th2 type immune response may affect the pace of tumorigenesis in this model. The general similarity of the intestinal immune responses in both genotypes and the lack of intestinal inflammation in the Apc(Min/+) mice suggest that the mutation in the adenomatous polyposis coli gene does not lead to major alterations in intestinal immune function and that the intestinal immunology does not explain tumorigenesis in the Apc(Min/+) mouse model.

Adenoma↗
PubMed2006

Alterations in intestinal contractility during inflammation are caused by both smooth muscle damage and specific receptor-mediated mechanisms.

AIM: To evaluate motoric intestinal disturbances during inflammation with Trichinella spiralis in rats as an experimental model. METHODS: We examined the changes in worm-positive (jejunum) and worm-free (ileum) intestinal segments of rats infected with T. spiralis. To investigate the relationship between structural and functional changes in smooth muscle, we measured the thickness of the muscle layers of rat jejunum and ileum. Mechanical responses to KCl 30 mmol/L, acetylcholine (ACh) 10(-8)-10(-4) mol/L, substance P (SP) 10(-9)-10(-5) mol/L, and to electrical field stimulation of longitudinal muscle strips in the jejunum and ileum were studied in muscle bath as controls (day 0) and on day 2, 6, 14, 23, and 72 after infection. RESULTS: After T. spiralis infestation, an inflammation of the mucosal and submucosal layers of jejunum was observed, whereas in the worm-free ileum there was not any inflammatory infiltrate. Increase in the smooth muscle thickness of both jejunum and ileum were correlated with increased responses to depolarizing agent KCl and to ACh. However, responses to SP were decreased on day 14-23 after infection in jejunum and from day 6-14 after infection in ileum. Electric field stimulation-induced contractions were transiently decreased in the jejunum (day 2 after infection) but in the ileum the contractile responses were decreased until the end of the study period. CONCLUSIONS: Alterations in intestinal smooth muscle function do not require the presence of the parasite and the absence of histopathological signs of inflammation do not warrant intact motor function. Changes in motor responses after T. spiralis infection are not only due to smooth muscle damage but also to disturbances in specific receptor-mediated mechanisms.

Acetylcholine↗
PubMed2006

Role of interleukin (IL-10) in probiotic-mediated immune modulation: an assessment in wild-type and IL-10 knock-out mice.

While the impact of Bifidobacterium infantis 35624 and other probiotics on cytokines has been shown in established colitis, the effects of B. infantis consumption in pre-inflammation of interleukin (IL)-10 knock-out (KO) mice and on the wild-type (WT) C57Bl/6 mice have not been well demonstrated. The objective of this study was to examine cytokine responses in mucosal and systemic lymphoid compartments of IL-10 KO mice early in disease and to compare with control WT mice. Mice were fed B. infantis or placebo for 5 weeks and culled prior to the onset of chronic intestinal inflammation (12-14 weeks). The spleen, Peyer's patches and intestinal mucosa were removed and stimulated with various bacterial stimuli. Cytokine levels were measured by enzyme-linked immunosorbent assay. While basal intestinal and systemic cytokine profiles of WT and IL-10 KO mice were similar, transforming growth factor (TGF)-beta was reduced in the spleen of IL-10 KO mice. Following probiotic consumption, interferon (IFN)-gamma was reduced in the Peyer's patch of both WT and IL-10 KO mice. Alterations in IFN-gamma in the Peyer's patches of WT mice (enhancement) versus IL-10 KO (reduction) were observed following in vitro stimulation with salmonella. Differential IL-12p40, CCL2 and CCL5 responses were also observed in IL-10 KO mice and WT mice. The cytokine profile of IL-10 KO mice in early disease was similar to that of WT mice. The most pronounced changes occurred in the Peyer's patch of IL-10 KO mice, suggesting a probiotic mechanism of action independent of IL-10. This study provides a rationale for the use of B. infantis 35624 for the treatment of gastrointestinal inflammation.

Animals↗
PubMed1998

[The significance of Helicobacter pylori in medical science].

The discovery of Helicobacter pylori as a dominant cause of gastritis is at least revolutionary both with respect to its clinical consequences as to its contribution to fundamental basic science. The velocity with which basic and clinical experience was accumulated in the H. pylori field has been unsurpassed in medicine. The organism is highly complex and can be divided in two subclasses, a more virulent strain containing the socalled 'pathogenicity island' in addition to vacA and IceA1 antigen and an almost commensal-like subtype. The virulent type in particular is associated with severe inflammation and various clinical disease states. The pathogenesis of duodenal ulcer is well understood. The infection is essentially limited to the antrum causing disturbance of the gastrin homeostasis which is one of the mechanisms leading to enhanced acid production. This constant hyperacidity in the duodenal bulb ultimately leads to development of gastric metaplasia with production of neutral mucus. The latter is essential to allow colonisation with the organism, leading to inflammation, erosion and ultimately ulcer. Curing the infection leads to permanent cure of the ulcer diathesis. The mechanisms that ultimately lead to gastric cancer or gastric Malt lymphoma are less clear. Curing the infection turns out to be more difficult than initially anticipated. Currently the triple therapy (a combination of a proton pump inhibitor with clarithromycin and either amoxycillin or metronidazole), or bismuth triple therapy or bismuth quadruple therapy (a combination of a proton pump inhibitor, bismuth, tetracyclin and metronidazole) are most commonly used. Sadly there is a rising frequency of resistance throughout the world against metronidazole and clarithromycin. Finally increasingly H. pylori infection is considered a model for study of fundamental biological problems such as interaction between organism and host, intracellular signalling in case of infection, evolution of inflammation towards atrophy and cancer etc. Equally interesting is the discovery of novel Helicobacters, such as Helicobacter resistance to bile or Helicobacters responsible for intestinal inflammation.

Duodenal Ulcer↗
PubMed1979

Intestinal uptake of macromolecules. VI. Uptake of protein antigen in vivo in normal rats and in rats infected with Nippostrongylus brasiliensis or subjected to mild systemic anaphylaxis.

Adult Sprague-Dawley rats weighing approximately g were fed bovine serum albumin and sodium bicarbonate by gavage. Serum was obtained at intervals after feeding and tested for immunoreactive bovine serum albumin by radioimmunoassay. Nanogram amounts of immunoreactive bovine serum albumin were detected in serum; peak values were obtained after 4 and 6 hr. The influence of intestinal inflammation on protein uptake was examined in two model systems. Infection of rats with Nippostrongylus brasiliensis was accompanied by partial villous atrophy in the intestinal segments harboring adult worms and mild systemic anaphylaxis in the rat was accompanied by increased intestinal vascular and mucosal permeability. Enhanced uptake of BSA was observed before and shortly after self-cure of infection and during mild systemic anaphylaxis. The molecular size of immunoreactive bovine serum albumin approximated that of the administered bovine serum albumin; no small fragments of bovine serum albumin bearing antigenic determinants were detected.

Anaphylaxis↗
PubMed2004

Initiation and resolution of mucosal inflammation.

Antigens entering the body through the mucosal surface are screened by a highly developed immune system comprised not only of traditional lymphoid cells but also epithelial cells, fibroblasts, and antigen-presenting cells (APCs). For example, in the intestinal tract, gut-associated lymphoid tissue (GALT) is tolerant to the approx 400 separate commensal strains residing mainly in the colon, but also retains the capacity to detect and remove virulent bacteria before they infect systemically. This review summarizes recent work characterizing the molecular mechanisms involved in acute and chronic intestinal inflammation. We will also describe a natural murine pathogen, Citrobacter rodentium, which is being used to explore the host response to enteric pathogens and the resulting immunopathology.

Animals↗