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PubMed2002

Interactions between the microbiota and the intestinal mucosa.

The intestinal microflora can be considered as a postnatally aquired organ composed of a large diversity of bacterial cells that can perform different functions for the host. This organ is highly exposed to environmental influences and thus modulated in its composition and functions by external factors, such as nutrition. Specific components of the intestinal microflora, including lactobacilli and bifidobacteria, have been associated with beneficial effects on the host, such as promotion of gut maturation and integrity, antagonisms against pathogens and immune modulation. In addition, the microflora seem to play a significant role in the maintenance of intestinal immune homeostasis and prevention of inflammation. At the present time, the contribution of intestinal epithlial cell in the first line of defence against pathogenic bacteria and microbial antigens has been recognized, in contrast, the interactions of intestinal epithelial cells with commensal bacteria are less understood. The present work summarizes the increasing scientific attention for mechanisms of the innate immune response of the host to different components of the autochthonous microflora and suggests a potential role for selected probiotic bacteria in the regulation of intestinal inflammation.

Bifidobacterium↗
PubMed2004

Impairment of small intestinal protein assimilation in patients with end-stage renal disease: extending the malnutrition-inflammation-atherosclerosis concept.

BACKGROUND: Protein malnutrition is a common finding in renal disease. Recently, we showed that impaired protein assimilation (digestion and absorption) may contribute to protein malnutrition in nondiabetic patients with chronic renal failure. OBJECTIVE: The aim of the present study was to evaluate whether these findings can be extended to the dialysis population. Moreover, relations with indexes of the malnutrition-inflammation-atherosclerosis (MIA) syndrome were investigated. DESIGN: Protein assimilation was evaluated in 24 healthy control subjects and in 40 patients with end-stage renal disease (ESRD; 14 treated with peritoneal dialysis and 26 with hemodialysis) by means of a [13C]protein breath test, quantification of the generation rate of p-cresol, or both methods. Both approaches provide reliable information on the efficiency of protein assimilation. Breath test results were expressed as the maximum percentage recovery per hour of the administered dose of 13C (%max) and as the cumulative percentage recovery at the end of the test (%cum end). Several indexes of nutritional status, inflammation, and atherosclerosis were assessed. RESULTS: Compared with the control subjects, ESRD patients had significantly lower breath-test derived indexes of protein assimilation [%max=3.75 +/- 0.30 compared with 4.90 +/- 0.25, P=0.006; %cum end=12.41 (5.74-23.22) compared with 16.87 (9.42-22.99), P=0.020] and a higher 24-h p-cresol generation rate corrected for dietary protein intake [3.89 (0.48-11.60) compared with 2.81 (0.21-11.20) mg p-cresol/g urea nitrogen; P=0.028]. The presence of impaired protein assimilation was associated with indexes of the MIA syndrome. CONCLUSION: Our study provides evidence that protein assimilation is impaired in ESRD patients. Moreover, this disorder is associated with the severity of the MIA syndrome.

Adult↗
PubMed1991

Chronic gastritis: progression of inflammation and atrophy in a six-year endoscopic follow-up of a random sample of 142 Estonian urban subjects.

To study the prevalence and course of chronic gastritis (CG), 142 adult subjects collected at random from an Estonian urban area were endoscopically and bioptically examined at a six-year interval. The histology of the antral and corpus mucosae was evaluated by grading gastritis without ("superficial gastritis"; SG) and with atrophy ("atrophic gastritis"; AG) into mild, moderate and severe categories. A total of 135 (95%) and 139 (98%) subjects showed CG in the 1st and 2nd examinations, respectively. The CG healed in one subjects (0.7%), and in 5 out of 7 subjects with normal stomach in the 1st examination the CG started during the follow-up. No change in the severity of CG was seen in 24% of subjects with gastritis in the 1st examination. The main trend of CG was a slow, "one-step progression" in severity of inflammation and appearance of atrophy and intestinal metaplasia. Inflammation progressed significantly, especially in the young age groups and in the antrum in particular. The prevalence of AG increased linearly with age in corpus (mean annual risk 1.25%). Parietal cell antibodies (PCA) were found in 2 subjects in the 1st examination, and a further 2 subjects developed these antibodies later. Three of four PCA-positive subjects belonged to a subgroup of 8 elderly subjects who had corpus AG at both examinations and who also showed normal or normalizing mucosa in the antrum. It is concluded that CG is a slowly progressive disease advancing with time and, once started, rarely healing spontaneously.

Adolescent↗
PubMed2001

Mycobacterium avium subspecies paratuberculosis triggers intestinal pathophysiologic changes in beige/scid mice.

We investigated whether infection of beige/scid mice with Mycobacterium avium subspecies paratuberculosis can induce intestinal pathophysiologic changes. Six-week-old beige/scid mice were inoculated intraperitoneally with M. paratuberculosis, then were killed 32 weeks after inoculation when the small intestine was evaluated for physiologic and morphologic abnormalities. All infected mice developed clinical disease. The lamina propria of the intestine from infected mice was mildly infiltrated with mononuclear cells containing acid-fast bacteria, and had significantly increased villus width. In vitro physiologic studies in Ussing chambers indicated that M. paratuberculosis infection caused significant abnormalities in intestinal transport parameters. Baseline short circuit current and potential difference were abnormally high in tissues from infected, compared with control mice, indicative of increased ion secretion. Baseline conductance was significantly decreased in infected mice, suggesting that intestinal tissue from infected mice was less permeable to ions. The change in short circuit current following transmural electrical and glucose stimulation was significantly reduced in intestines from infected mice, suggesting that inflamed intestine had neural and/or epithelial cell damage. We conclude that infection of beige/scid mice with M. paratuberculosis triggers significant intestinal pathophysiologic changes consistent with chronic inflammation. These functional abnormalities may contribute to the pathogenesis of the wasting syndrome seen in bovids with paratuberculosis. This animal model provides evidence that T cell-independent mechanisms are sufficient to cause mucosal pathophysiologic changes and inflammation in response to a specific pathogen, and may be of relevance to inflammatory bowel disease in humans.

Animals↗
PubMed1998

Brain Fos expression and intestinal motor alterations during nematode-induced inflammation in the rat.

Brain-gut interactions and intestinal motility were studied during pulmonary and jejunal inflammation induced by Nippostrongylus brasiliensis. Jejunal electromyographic activity was continuously recorded from day 1 before to day 28 after infection. Expression of c-fos was assessed in the brain by immunohistochemistry, and myeloperoxidase (MPO) activity was determined in lung and intestine on days 1,7,14, 21, and 28 postinfection. The cyclic intestinal motor pattern was replaced by an irregular activity from day 4, corresponding to larvae migration to the intestine, to day 14. c-fos was expressed in the caudal nucleus of the solitary tract (NTS) and lateral parabrachial nucleus (LPB) on day 1 (lung stage of N. brasiliensis) and in the medial part of the NTS, the LPB, and locus ceruleus on day 7. Pulmonary and intestinal MPO activity was increased from days 1 to 21 postinfection. During N. brasiliensis infection, c-fos expression indicates that specific and different brain nuclei are activated at the onset of pulmonary and intestinal inflammation, which is associated with motor disorders.

Animals↗
PubMed2006

Polymeric diet alone versus corticosteroids in the treatment of active pediatric Crohn's disease: a randomized controlled open-label trial.

BACKGROUND & AIMS: Nutritional therapy has been reported to have an almost equivalent efficacy of corticosteroids in achieving clinical remission in active Crohn's disease (CD). However, the effects of both treatments on intestinal mucosal inflammation rarely are reported. In a randomized controlled trial in children with active CD we compared the efficacy of nutritional therapy alone or corticosteroids on clinical variables and intestinal mucosal healing. METHODS: In a prospective, 10-week open-label trial, children with active, naive CD were randomized to orally polymeric formula alone or oral corticosteroids. The clinical activity index and nutritional and activity serum variables were evaluated at week 0 and then every 2 weeks; intestinal mucosal inflammation was assessed through endoscopy and histology at weeks 0 and 10. Primary efficacy outcomes were clinical remission and mucosal healing. RESULTS: Of the 37 children randomized, 19 received polymeric formula and 18 received corticosteroids. At week 10, on an intention-to-treat basis, the proportion of patients achieving clinical remission was comparable between the 2 groups (polymeric formula: 15/19 [79%; 95% confidence interval (CI), 56%-92%]; corticosteroid group: 12/18 [67%; 95% CI, 44%-84%]; P = .4; not significant). On the contrary, the proportion of children showing mucosa healing was significantly higher in the polymeric (14/19; 74%; 95% CI, 51%-89%) than the corticosteroid group (6/18 [33%; 95% CI, 16%-57%]; P < .05). At week 10 both endoscopic and histologic scores significantly decreased only in the polymeric group (P < .001). CONCLUSIONS: In children with active and recently diagnosed CD, a short course of polymeric diet is more effective than corticosteroids in inducing healing of gut inflammatory lesions.

Administration, Oral↗
PubMed2003

Prevention of gut inflammation by Bifidobacterium in dextran sulfate-treated gnotobiotic mice associated with Bacteroides strains isolated from ulcerative colitis patients.

Indigenous Bacteroides strains are closely associated with the occurrence and exacerbation of ulcerative colitis (UC). In this study, we aimed to clarify the effect of Bifidobacterium strains, another major member of colonic bacteria, on the development of gut inflammation using gnotobiotic mouse models associated with Bacteroides strains isolated from UC patients. Dextran sulfate (DSS) administration induced inflammation in the large intestine, in particular of the cecum, in the gnotobiotic mice associated with three strains of Bacteroides vulgatus, judging from the myeloperoxidase activity, occult blood score, and IgG leakage into the intestinal contents. However, the severity of the inflammation was greatly reduced in the gnotobiotic mice associated with both B. vulgatus and Bifidobacterium strains. The severity of the cecal inflammation was well correlated with the concentration of succinic acid in the cecum. Bacteriologically, the density of B. vulgatus strain A (BV-A) greatly decreased and the predominant strain changed from BV-A to BV-B on additional association with Bifidobacterium strains. Among gnotobiotic mice associated with a single B. vulgatus strain, the severity of cecal inflammation in BV-A-associated mice was greater than that in BV-B-associated mice. Each Bifidobacterium strain produced compound(s) more effectively inhibiting the growth of BV-A than BV-B in in vitro culture. Taken together, these results suggest that the severity of DSS-induced gut inflammation is closely associated with a particular B. vulgatus strain, and that Bifidobacterium strains may repress exacerbation of intestinal inflammation through growth inhibition of the B. vulgatus strain.

Animals↗
PubMed1998

Review article: bone and joint diseases in inflammatory bowel disease.

The intestinal and articular systems are closely linked in inflammatory bowel disease. Clinical and immunological studies support an important aetio-pathogenetic link between intestinal and articular inflammation. There is increasing evidence for a negative link between bone mass density and intestinal inflammation. This paper will focus on the prevalence, aetio-pathogenesis and treatment of arthritis (peripheral, sacroiliitis and spondylitis) and osteoporosis in inflammatory bowel disease.

Animals↗
PubMed2005

Intestinal dysmotility in inflammatory bowel disease: mechanisms of the reduced activity of smooth muscle contraction.

Inflammation suppresses intestinal motility, which secondarily induces abnormal growth of intestinal flora. Disturbance of this flora plays a role in the pathogenesis of mucosal inflammation, which in turn aggravates the intestinal dysmotility. Therefore, it is important to know the mechanism of alteration in motor function in the inflamed intestine. Recent studies have shown molecular mechanisms responsible for the motility disorder in the inflamed gut. These include an increase in the activity of myosin light-chain phosphatase and an alteration of ion channel activity in smooth muscle cells.

Animals↗
PubMed1999

Malnutrition modifies pig small intestinal inflammatory responses to rotavirus.

Infectious diarrheal diseases and malnutrition are major causes of child morbidity and mortality. In this study, malnutrition was superimposed on rotavirus infection in neonatal piglets to simulate the combined intestinal stress of viral enteritis in malnourished infants. Two-day-old piglets were assigned to three treatment groups as follows: 1) noninfected, fully nourished; 2) infected, fully nourished; and 3) infected, malnourished. Intestinal indices of inflammation were monitored over the subsequent 2-wk period. Intestinal damage and diarrhea were observed within 2 d of rotavirus infection and began to subside in nourished piglets by d 9 but persisted through d 16 postinfection in malnourished piglets. Rotavirus upregulated small intestinal expression of major histocompatibility complex (MHC) class I and class II genes; malnutrition intensified MHC class I gene expression and suppressed MHC class II expression. Jejunal CD4(+) and CD8(+) T-lymphocyte numbers were elevated for infected, nourished piglets on d 2, 9 and 16 postinfection. Malnutrition did not significantly affect the local expansion of T cell subsets in response to rotavirus. Intestinal prostaglandin E2 (PGE2) concentrations were elevated early after rotavirus infection independent of nutritional state. By d 9, PGE2 concentrations returned to baseline in infected, nourished piglets but remained elevated in malnourished piglets, corresponding to diarrhea observations. Together, the results identify intestinal indices of inflammation that are modulated by malnutrition and prompt reconsideration of current models of rotavirus pathophysiology.

Animals↗
PubMed1991

Bechet's colitis: a differential diagnosis in inflammations of the large intestine.

A previously well 39 year old woman presented with severe localized and painful anorectal ulceration. There were no other associated symptoms apart from arthritis of the hips and fingers. In the absence of definitive tissue diagnosis, a presumptive diagnosis of Crohn's disease was made. After a period of progression, the inflammation and ulceration subsided with conservative therapy. Following a relatively symptom-free period of 7 years, painful ulceration recurred in the same segment of bowel, which was refractory to steroid therapy but responded to defunctioning of the rectum. Upon excision of the defunctioned rectum, multiple discrete ulcers developed in the remaining colon, with a fistula from the distal sigmoid colon to the midline wound. The patient simultaneously developed painful apthous ulceration of the mouth and throat, and pustules appeared on the perianal skin and trunk for the first time. A colectomy was performed, with good results. The pathology of the colonic lesions is described. The characteristic appearance of these lesions, together with associated 'major' and 'minor' clinical criteria, enabled a diagnosis of Bechet's disease to be made. Although there is some overlap, particularly in the distribution of this condition with Crohn's colitis, the pathologic appearances in Bechet's colitis are relatively distinct. A diagnosis of Bechet's colitis should not be excluded in a patient presenting with atypical inflammatory bowel disease, even if associated clinical criteria are not simultaneously present.

Adult↗
PubMed1991

Refeeding enhances intestinal repair during an acute enteritis in infant rabbits subjected to protein-energy malnutrition.

We examined the effects of refeeding during an acute bacterial enteritis on small intestinal repair in infant rabbits subjected to protein-energy malnutrition and in noninfected and infected dietary controls. Malnutrition was induced by litter expansion at 7 d of age. Randomly selected litters from both dietary groups were infected on d 17 with Yersinia enterocolotica. Inflammation and intestinal damage were observed in the jejunum and ileum at the "acute stage" of infection in 23-d-old animals from both dietary groups, as evidenced by an inflammatory infiltrate, blunted villi, and reduced disaccharidase activities. In addition, ileal glucose-stimulated Na+ absorption was depressed. On d 24, a 7-d period of ad libitum refeeding of breast milk and rabbit feed was initiated in randomly selected litters of infected-malnourished animals and all dietary controls. Mucosal repair was nearly complete at 31 d of age in infected dietary controls and in the infected-malnourished animals that were refed, as demonstrated by the recovery of segmental mucosal mass and ileal glucose-stimulated Na+ transport in association with the resolution of inflammation and diarrhea. Only mucosal disaccharidase activities remain depressed. In contrast, in 31-d-old infected-malnourished animals subjected to ongoing nutrient deprivation, severe intestinal damage persisted as evidenced by increased mortality, ongoing intestinal inflammation, mucosal hypoplasia, depressed disaccharidase activities, and reduced glucose-stimulated Na+ transport. We conclude that a refeeding regimen introduced during an acute bacterial enteritis is well tolerated and promotes recovery of intestinal mass, structure, and function in malnourished infant rabbits and dietary controls.

Animals↗
PubMed2003

Interferon-gamma augments CARD4/NOD1 gene and protein expression through interferon regulatory factor-1 in intestinal epithelial cells.

Although intestinal epithelial cells appear to be functionally hyporesponsive to normal intestinal flora, human intestinal epithelial cells can respond to enteroinvasive bacteria and induce an inflammatory response. This initial inflammatory response leads to the recruitment of polymorphonuclear leukocytes to the affected site in vitro and in vivo. CARD4/NOD1 is a potential cytosolic receptor for peptidoglycan in mammalian cells that resembles pathogen-resistant proteins of plants. In this context, CARD4/NOD1 is a candidate for a recognition protein of intracellular bacteria or peptidoglycan in intestinal epithelial cells. In this study, we demonstrate that CARD4/NOD1 is constitutively expressed in intestinal epithelial cell lines and isolated primary intestinal epithelial cells. Interferon-gamma (IFN gamma), which is a potent pro-inflammatory cytokine in intestinal mucosal inflammation, activates CARD4/NOD1 mRNA transcription in a time- and dose-dependent manner and results in augmentation of CARD4/NOD1 protein in SW480 cells. Promoter analysis of CARD4/NOD1 indicates that interferon regulatory factor-1 (IRF-1) binding motif (-791 to -782) is essential for the effect of IFN gamma. Nuclear extracts from SW480 cells treated with IFN gamma show specific binding of oligonucleotides corresponding to this IRF-1-binding motif, which was supershifted by anti-IRF-1 antibody in electrophoretic mobility shift assay. Overexpression of IRF-1 protein activates the CARD4/NOD1 promoter but not the deletion mutant of the IRF-1-binding site in a co-transfection assay of IRF-1 expression plasmid with CARD4/NOD1 promoter. These studies suggest that the Th1 cytokine, IFN gamma, activates CARD4/NOD1 transcription and regulate innate immune mechanisms in the condition of intestinal mucosal inflammation.

Adaptor Proteins, Signal Transducing↗
PubMed2000

Evidence of chronic inflammation in morphologically normal small intestine of cystic fibrosis patients.

Cystic fibrosis (CF) is caused by mutations in the CF transmembrane conductance regulator gene and characteristically leads to prominent lung and pancreatic malfunctions. Although an inflammatory reaction is normally observed in the CF airways, no studies have been performed to establish whether a chronic inflammatory response is also present in the CF intestine. We have investigated whether immunologic alterations and signs of inflammation are observed in CF small intestine. Fourteen CF, 20 negative, and four disease controls underwent duodenal endoscopy for diagnostic purposes. Two CF patients were rebiopsied, one after 3 mo of an elemental diet and the other after 2 wk of pancreatic enzyme withdrawal. In three CF and 10 controls, in vitro small intestine organ cultures were also performed. Expression of ICAM-1, IL-2 receptor, IL-2, IFN-gamma, CD80, and transferrin receptor was studied by immunohistochemistry before and after in vitro organ culture. In CF small intestine, an increased number of lamina propria mononuclear cells express ICAM-1 [mean 114 (SD 82.8), p < 0.001 versus controls], CD25 [20.2 (18.7), p < 0.01], IL-2 [23.6 (13.7), p < 0.05], and IFN-gamma [19 (15.9), p < 0.05], whereas villus enterocytes highly express transferrin receptor. Reduced expression of immunologic markers was observed after 24 h of in vitro culture in all three CF patients as well as in the patient kept on elemental diet for 3 mo. These results indicate that chronic inflammation is observed in CF duodenum and suggest that the perturbation of local mucosal immune response may contribute to the overall clinical picture in CF patients.

Adolescent↗
PubMed2003

NAD+ ameliorates inflammation-induced epithelial barrier dysfunction in cultured enterocytes and mouse ileal mucosa.

In the course of other experiments, we serendipitously observed that extracellular nicotinamide adenine dinucleotide (NAD+) ameliorated the development of epithelial hyperpermeability when monolayers of Caco-2 enterocyte-like cells were incubated with cytomix, a mixture containing interferon-gamma, interleukin-1beta, and tumor necrosis factor-alpha. We sought to characterize the effects of NAD+ on inflammation-induced epithelial barrier dysfunction using Caco-2 monolayers that were exposed to cytomix in the absence or presence of NAD+ or other purine-containing molecules. Paracellular barrier function measured as the apical-to-basolateral passage of fluorescein isothiocyanate-conjugated dextran (mol. wt. approximately 4000) was preserved in a concentration-dependent manner when immunostimulated Caco-2 cells were exposed to extracellular NAD+. Incubation with NAD+ prevented cytomix-induced derangements in the expression and localization of the tight junction proteins occludin and zonula occludens-1 in Caco-2 cells. Treatment of cytomix-stimulated cells with NAD+ also blocked nuclear factor-kappaB (NF-kappaB) activation, inducible nitric-oxide synthase induction, and increased production of nitric oxide (NO.). Ileal mucosal permeability to fluorescein isothiocyanate-dextran mol. wt. approximately 4000 was increased in mice 18 h after lipopolysaccharide (endotoxin) injection, but treatment of endotoxemic mice with NAD+ ameliorated the development of gut mucosal hyperpermeability. Thus, extracellular NAD+ seems to ameliorate inflammation-induced intestinal epithelial barrier dysfunction by inhibiting NF-kappaB activation and increased NO. production.

Animals↗