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PubMed2004

Expression of opioid receptors during peripheral inflammation.

Opioid receptors (OR) and their mRNA are present in the central and peripheral nervous system of mammals. In this review we examine the behavioral effects of opioids and the expression of their receptors during peripheral inflammation in two experimental models: the rat paw and the mouse intestine. Inflammation increased the antinociceptive (paw) and the inhibitory effects of opioids in the gut (transit, permeability and plasma extravasation) by interaction with OR located at peripheral sites. Based on agonist efficacy, micro > delta >> kappa-OR mediate the antinociceptive and antitransit effects of opioids during inflammation. Intestinal permeability is modulated by delta = micro >> kappa-OR, while kappa > delta >> micro-OR are involved in the inhibition of plasma extravasation. Intestinal inflammation increased the transcription of micro and delta-OR (but not kappa) genes in the gut, thus explaining the enhanced antitransit and antisecretory effects of micro and delta-OR agonists; however, the increased inhibitory effects of kappa-OR agonists on plasma extravasation could result from post-transcriptional regulation of the receptor. Similarly, the increased expression of peripheral micro-OR observed in the rat paw during inflammation, occurs at post-transcriptional levels and is related to an increased axonal transport from the dorsal root ganglia to peripheral terminals. The sites and mechanisms implicated in the increased transcription of micro and delta-OR during intestinal inflammation are under investigation.

Analgesics↗
PubMed2001

Inflammation enhances mu-opioid receptor transcription and expression in mice intestine.

Opioid receptors (ORs) and their mRNA are present in the central and peripheral nervous systems of mammals and in different peripheral tissues, including the gut. Using a model of croton oil-induced (CO) intestinal inflammation in mice, we have shown a 6-fold increase in the potency of the antitransit and antisecretory effects of mu-OR agonists, mediated by peripheral ORs. We postulate that the enhanced effects are mediated by an increase in the expression of intestinal OR. We used jejunum (stripped of the mucosal layer) from mice with CO-induced intestinal inflammation and, as control subjects, saline-treated animals (SS). We evaluated the quantity of mu-OR mRNA determined by a competitive reverse-transcriptase polymerase chain reaction; the levels of mu-OR protein by Western blot immunoassay, and the localization and number of cells expressing mu-OR using immunohistochemistry. The results show a significant increase of mu-OR mRNA (7.7-fold) and receptor protein (3-fold) during intestinal inflammation. Inflammation also induced a 64.3% increase in the number of neurons expressing mu-OR immunoreactivity in the myenteric plexus but not in the submucosal plexus. Our results show that intestinal inflammation enhances the transcription and translation of mu-OR mRNA, thus explaining the increased potency of mu-opioids during inflammation.

Animals↗
PubMed1999

Gastric cardia inflammation and intestinal metaplasia: associations with reflux esophagitis and Helicobacter pylori.

Gastric cardia inflammation and intestinal metaplasia are the subjects of recent investigation. Some authors have found associations with gastroesophageal reflux disease, whereas others have identified relationships with Helicobacter pylori (HP). We studied 150 consecutive patients who underwent upper endoscopy, had normal gastroesophageal anatomy, and had biopsies of the antrum, cardia, and lower esophagus, to evaluate relationships between reflux esophagitis, cardia inflammation, intestinal metaplasia, and HP gastritis. Forty-two patients had HP infection. Cardia inflammation was significantly related to esophageal squamous inflammation in the non-HP-infected patient group and to antral inflammation and cardia HP infection in the HP-infected patient group. The differences between the patient groups was most apparent in the patients with moderate or marked inflammation. Twenty-seven percent of patients had cardia intestinal metaplasia that was related to cardia inflammation. Cardia inflammation and intestinal metaplasia probably have multiple causes. Pathologists should refrain from applying the term Barrett's esophagus for biopsies procured from the cardia that show intestinal metaplasia in patients with a normal squamocolumnar junction.

Adolescent↗
PubMed2006

Autoimmune-mediated intestinal inflammation-impact and regulation of antigen-specific CD8+ T cells.

BACKGROUND & AIMS: Few data exist regarding mechanisms of mucosal CD8+ T-cell reactivity to epithelial-specific antigen. To dissect the immunologic mechanisms underlying CD8+ T-cell dysregulation, reactivity to a self-antigen expressed in intestinal epithelium of mice bearing a major histocompatibility complex class I-restricted T-cell receptor specific for this antigen was studied. In addition, antigen-specific regulatory CD4+ T cells induced in vivo were tested to control these autoreactive CD8+ T cells. METHODS: Transgenic VILLIN-HA mice were mated with CL4-TCR transgenic mice. Alternatively, adoptive transfer of CL4-TCR transgenic CD8+ T cells into VILLIN-HA transgenic mice was performed to mimic spontaneous encounter of neoantigen. Mucosal CD8+ T cells were characterized under different conditions of tolerance, immunopathology, and active immunosuppression. RESULTS: Transgenic CD8+ T cells from VILLIN-HA x CL4-TCR transgenic mice preferentially migrated and expanded in mucosal lymphoid tissues. Although transgenic CD8+ T cells showed signs of T-cell activation, they failed to cause tissue damage. This was accompanied by the induction/expansion of CD4+ and CD8+, Foxp3-expressing T cells. In contrast, adoptive transfer of naive transgenic CD8+ T cells from CL4-TCR transgenic mice into VILLIN-HA transgenic mice induced severe intestinal inflammation with poor clinical course of disease. Transgenic CD8+ T cells secreted vigorous amounts of proinflammatory cytokines like interferon gamma/tumor necrosis factor alpha. Strikingly, this acute wasting disease was significantly ameliorated by cotransfer of antigen-specific regulatory CD4+ T cells. CONCLUSIONS: Epithelial-specific antigen expression is sufficient to trigger severe antigen-specific CD8+ T-cell-mediated intestinal inflammation; this might be controlled by antigen-specific regulatory T cells under physiological conditions.

Animals↗
PubMed2003

A murine model of chronic inflammation-induced intestinal fibrosis down-regulated by antisense NF-kappa B.

BACKGROUND & AIMS: To elucidate extracellular matrix (ECM) changes underlying intestinal fibrosis, a frequent complication of inflammatory bowel disease, we developed a murine model of chronic colitis associated with intestinal fibrosis. METHODS: Chronic inflammation was established by weekly intrarectal administration of trinitrobenzene sulfonic acid (TNBS). In 2 variations of the model an antisense oligonucleotide for nuclear factor kappa B (NF-kappa B) p65 was given prophylactically or therapeutically to block chronic inflammation-associated fibrosis. Colonic inflammation and fibrosis were determined by histology. Total collagen level was estimated by hydroxyproline quantification. Colonic expression of collagens (Col1a2, Col3a2), ECM remodeling genes (matrix metalloproteinase [MMP]-1, -3, and tissue inhibitor of matrix metalloproteinase [TIMP]-1), and inflammation-modulating cytokines (tumor necrosis factor alpha [TNF-alpha], interferon gamma [IFN-gamma], transforming growth factor beta 1 [TGF-beta 1], and insulin-like growth factor 1 [IGF-1]) were assessed by semiquantitative reverse-transcription polymerase chain reaction. Control and TNBS-treated colonic mesenchymal cells were characterized by morphology, phenotype, and functional response to TNF-alpha and IFN-gamma. RESULTS: Colons of TNBS-treated mice contained acute and chronic inflammatory infiltrates, increased collagen, fibrogenic tissue architecture, and increased expression of TNF-alpha, TGF-beta 1, IGF-1, Col1a2, MMP-1, and TIMP-1. Colonic mesenchymal cells from TNBS-treated mice were also morphologically distinct from those of the control mice, with increased TIMP-1 expression in response to IFN-gamma treatment. Fibrosis persisted for 2-4 weeks after cessation of the TNBS treatment. In mice given NF-kappa B antisense prophylactically, 67% were fibrosis-free, whereas of those treated after establishing chronic inflammation, 43% were free of fibrosis. CONCLUSIONS: Extended TNBS treatment of mice yielded chronic intestinal inflammation-associated fibrosis with extensive fibrogenic ECM changes that could be counteracted by specific blockade of NF-kappa B.

Animals↗
PubMed1996

Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4(+) TH1-like responses.

We have characterized the progressive stages of chronic intestinal inflammation that develops spontaneously in specific pathogen-free (SPF) mice with a targeted disruption in the IL-10 gene (IL-10-/-). Our longitudinal studies showed that inflammatory changes first appear in the cecum, ascending and transverse colon of 3-wk-old mutants. As the disease progressed, lesions appeared in the remainder of the colon and in the rectum. Some aged IL-10-/- mice also developed inflammation in the small intestine. Prolonged disease with transmural lesions and a high incidence of colorectal adenocarcinomas (60%) was observed in 6-mo-old mutants. Mechanistic studies have associated uncontrolled cytokine production by activated macrophages and CD4+ Th1-like T cells with the enterocolitis exhibited by IL-10-/- mice. A major role for a pathogenic Th1 response was further suggested by showing that anti-IFNgamma antibody (Ab) treatment significantly attenuated intestinal inflammation in young IL-10-/- mice. When weanlings were treated with IL-10, they failed to develop any signs of intestinal inflammation. Interestingly, IL-10 treatment of adults was not curative but did ameliorate disease progression. Our studies have also shown that inheritable factors strongly influence the disease susceptibility of IL-10-/- mice. In 3-mo-old mutants, intestinal lesions were most severe in IL-10-/- 129/SvEv and IL-10-/- BALB/c strains, of intermediate severity in the IL-10-/- 129 x C57BL/6J outbreds, and least severe in the IL-10-/- C57BL/6J strain.

Aging↗
PubMed2006

A defect in epithelial barrier integrity is not required for a systemic response to bacterial antigens or intestinal injury in T cell receptor-alpha gene-deficient mice.

BACKGROUND AND AIMS: Genetically induced disruption of the intestinal epithelial barrier leads to development of intestinal inflammation. In the interleukin-10 gene-deficient inflammatory bowel disease (IBD) mouse model, for instance, a primary defect in intestinal epithelial integrity occurs before the development of enterocolitis. In humans, a causal role for epithelial barrier disruption is still controversial. Although studies with first-degree relatives of IBD patients suggests an underlying role of impaired barrier function, a primary epithelial barrier defect in IBD patients has not been confirmed. The purpose of this article is to examine whether a primary epithelial barrier disruption is a prerequisite for the development of intestinal inflammation or whether intestinal inflammation can develop in the absence of epithelial disruption. We examined the intestinal epithelial integrity of the T cell receptor (TCR)-alpha gene-deficient mouse model of IBD. MATERIALS AND METHODS: In vivo colonic permeability, determined by mannitol transmural flux, was assessed in 6-week-, 12-week-, and 25-week-old TCR-alpha gene-deficient and wild-type control mice using a single-pass perfusion technique. Mice were scored for intestinal histological injury and intestinal cytokine levels measured in organ cultures. Systemic responses to bacterial antigens were determined through 48-h spleen cell cultures stimulated with sonicate derived from endogenous bacterial strains. RESULTS: In contrast with previous findings in the interleukin-10 gene-deficient IBD model, TCR-alpha gene-deficient mice did not demonstrate evidence of primary intestinal epithelial barrier disruption at any age, despite developing a moderate to severe colitis within 12 weeks. A rise in intestinal interferon (IFN)-gamma levels preceded the onset of mucosal inflammation and then correlated closely with the degree of intestinal inflammation and injury. Spleen cells from TCR-alpha gene-deficient mice released IFN-gamma in response to stimulation with endogenous luminal bacterial antigens, a finding that suggests that the systemic response to bacterial antigens occurred independently of epithelial barrier disruption. CONCLUSIONS: Intestinal inflammation and a systemic response to bacterial antigens can develop in the absence of a measurable disruption of intestinal permeability.

Age Factors↗
PubMed2005

Intestinal inflammation-induced growth retardation acts through IL-6 in rats and depends on the -174 IL-6 G/C polymorphism in children.

Inflammatory diseases frequently impair linear growth. Crohn's disease inhibits growth in up to one third of affected children. In rats with trinitrobenzenesulphonic acid-induced colitis, 40% of growth impairment is attributable to inflammation, with the rest being due to undernutrition. In transgenic mice without inflammation, raised IL-6 retards growth, suppressing insulin-like growth factor (IGF)-I. We hypothesized that IL-6, induced by intestinal inflammation, suppresses growth and inhibits IGF-I expression. Therefore, an anti-IL-6 Ab was given to rats with trinitrobenzene-sulphonic acid colitis. The Ab did not improve nutrient intake or decrease inflammation compared with untreated disease controls, but it significantly restored linear growth (P = 0.023) and increased IGF-I (P = 0.05). In humans, the IL-6 -174 G/C promoter polymorphism affects IL-6 transcription, with the GG genotype inducing the greatest IL-6 levels. Because IL-6 is increased in Crohn's disease, we further hypothesized that growth failure would vary with the IL-6 -174 genotype. At diagnosis, among 153 children with Crohn's disease, those with the IL-6 GG genotype were more growth-retarded than those with the GC or CC genotypes (height SD score, -0.51 vs. -0.10; P = 0.031). Also, the patients with the IL-6 GG genotype had higher circulating levels of C-reactive protein, an IL-6-induced product (36 vs. 18 mg/dl, P = 0.028). However, their risk of developing Crohn's disease was similar to other genotypes when compared with 351 healthy controls (P = 0.7). Thus, the IL-6 -174 genotype mediates growth failure in children with Crohn's disease.

Animals↗
PubMed2002

Endometriosis is associated with an altered profile of intestinal microflora in female rhesus monkeys.

BACKGROUND: The intestinal microflora provide a strong defence against intestinal pathogens, and may be altered in inflammatory conditions that impact the gut, such as endometriosis. Therefore, intestinal bacteria shed from rhesus monkeys with endometriosis were compared with age-matched healthy controls. A second study assessed the prevalence of intestinal inflammation in female monkeys to determine whether endometriosis is associated with an increased likelihood of intestinal inflammation. METHODS: Differential and selective agars were used to enumerate total and Gram-negative aerobic and facultatively anaerobic bacteria, as well as Lactobacilli, from female monkeys with or without endometriosis. In addition, the prevalence of intestinal inflammation in monkeys with or without endometriosis was determined in a retrospective analysis of necropsy reports. RESULTS: Monkeys with endometriosis had a significantly different profile of shed microflora. Endometriosis was associated with lower Lactobacilli concentrations and higher Gram-negative bacteria concentrations. Moreover, there was a higher prevalence of intestinal inflammation in monkeys with endometriosis in comparison to healthy controls. CONCLUSIONS: Endometriosis is associated with an altered profile of intestinal microflora in rhesus monkeys. Although the exact mechanisms linking endometriosis and the microflora are unknown, it is possible that the microflora were affected by endometriosis-associated intestinal inflammation.

Animals↗
PubMed2001

Th1-type responses mediate spontaneous ileitis in a novel murine model of Crohn's disease.

We describe here the immunologic characterization of a new mouse strain, SAMP1/Yit, which spontaneously develops a chronic intestinal inflammation localized to the terminal ileum. The resulting ileitis bears a remarkable resemblance to human Crohn's disease. This strain of mice develops discontinuous, transmural inflammatory lesions in the terminal ileum with 100% penetrance by 30 weeks of age. The intestinal inflammation is characterized by massive infiltration of activated CD4+ and CD8alpha(+)TCRalphabeta(+) T cells into the lamina propria and is accompanied by a dramatic decrease in the intraepithelial lymphocyte CD8alpha(+)TCRgammadelta(+)/CD8alpha(+)TCRalphabeta(+) ratio. The results of adoptive transfer experiments strongly suggest that CD4+ T cells that produce a Th1-like profile of cytokines, e.g., IFN-gamma and TNF, mediate the intestinal inflammation found in SAMP1/Yit mice. In addition, pretreatment of adoptive transfer recipients with a neutralizing anti-TNF antibody prevents the development of intestinal inflammation, suggesting that TNF plays an important role in the pathogenesis of intestinal inflammation in this model. To our knowledge, these data provide the first direct evidence that Th1-producing T cells mediate intestinal inflammation in a spontaneous animal model of human Crohn's disease.

Adoptive Transfer↗
PubMed2000

In vivo changes in the intestinal reflexes and the response to CCK in the inflamed small intestine of the rat.

Functional motor changes and morphological alterations have been associated with intestinal inflammation. The aim of our study was to evaluate functional alterations of intestinal reflexes and of the responses to CCK in the Trichinella spiralis model of intestinal inflammation. Rats were prepared with strain gauges and electrodes in the small intestine to evaluate spontaneous motor activity, the ascending contraction of the peristaltic reflex, and the motor responses to CCK-8 infusion. Infected animals showed increased motor activity at the duodenum and jejunum but not at the ileum. Ascending contraction was increased in both duodenum and ileum. Ascending excitation after N(omega)-nitro-L-arginine was still increased as well as the residual response after atropine. Response to CCK-8 during intestinal inflammation was changed in the jejunum, in which it turned from the inhibition shown in healthy animals to excitation. NADPH-diaphorase staining did not show any changes between distribution and density of positive neurons in either healthy or infected animals. In conclusion, intestinal inflammation induces functional changes in the motor activity that could explain the abnormal motor responses observed in inflammatory disorders.

Animals↗
PubMed2006

Gram-negative bacteria aggravate murine small intestinal Th1-type immunopathology following oral infection with Toxoplasma gondii.

Oral infection of susceptible mice with Toxoplasma gondii results in Th1-type immunopathology in the ileum. We investigated gut flora changes during ileitis and determined contributions of gut bacteria to intestinal inflammation. Analysis of the intestinal microflora revealed that ileitis was accompanied by increasing bacterial load, decreasing species diversity, and bacterial translocation. Gram-negative bacteria identified as Escherichia coli and Bacteroides/Prevotella spp. accumulated in inflamed ileum at high concentrations. Prophylactic or therapeutic administration of ciprofloxacin and/or metronidazole ameliorated ileal immunopathology and reduced intestinal NO and IFN-gamma levels. Most strikingly, gnotobiotic mice in which cultivable gut bacteria were removed by quintuple antibiotic treatment did not develop ileitis after Toxoplasma gondii infection. A reduction in total numbers of lymphocytes was observed in the lamina propria of specific pathogen-free (SPF), but not gnotobiotic, mice upon development of ileitis. Relative numbers of CD4(+) T cells did not differ in naive vs infected gnotobiotic or SPF mice, but infected SPF mice showed a significant increase in the frequencies of activated CD4(+) T cells compared with gnotobiotic mice. Furthermore, recolonization with total gut flora, E. coli, or Bacteroides/Prevotella spp., but not Lactobacillus johnsonii, induced immunopathology in gnotobiotic mice. Animals recolonized with E. coli and/or total gut flora, but not L. johnsonii, showed elevated ileal NO and/or IFN-gamma levels. In conclusion, Gram-negative bacteria, i.e., E. coli, aggravate pathogen-induced intestinal Th1-type immunopathology. Thus, pathogen-induced acute ileitis may prove useful to study bacteria-host interactions in small intestinal inflammation and to test novel therapies based on modulation of gut flora.

Animals↗
PubMed2003

The role of cryptopatch-derived intraepithelial lymphocytes in the development of chronic ileocecitis.

Lympho-haemopoietic progenitors residing in murine gut cryptopatches (CPs) have been shown to generate intestinal extrathymic intraepithelial lymphocytes (IELs). However, the role of CPs in the development of intestinal inflammation remains unclear. To investigate the role of CPs in the development of intestinal inflammation, we examined SAMP1/Yit mice, which spontaneously develop a chronic intestinal inflammation localized to the terminal ileum and cecum. Here, we showed the sharp correlation between the disease onset and the decreased number of CPs, resulting in decreased number of both thymus-independent IELs including T-cell receptor gammadelta+ (TCRgammadelta+) and CD8alphaalpha+TCRalphabeta+ cells but not thymus-dependent CD8alphabeta+TCRalphabeta+ and CD4+TCRalphabeta+ cells in SAMP1/Yit mice. These data provide the first suggestion that thymus-independent IELs derived from CP might play protective role against the onset and the development of intestinal inflammation.

Animals↗
PubMed1998

Experimental colitis induced by dextran sulphate sodium in mice: beneficial effects of sulphasalazine and olsalazine.

BACKGROUND: Animal models of inflammatory bowel disease are artificial and more or less representative of human disease. However, the dextran sulphate sodium (DSS) induced intestinal inflammation model has recently been shown to fulfil some pathological criteria for an adequate experimental model. AIM: To determine whether this form of experimental intestinal inflammation responds to established therapy used for human inflammatory bowel disease. METHODS: DSS was used to induce intestinal inflammation in conventional Balb/c mice and athymic nu/nu CD-1(BR) mice, and the well-documented 5-aminosalicylic acid (5-ASA) based anticolitis drugs sulphasalazine (SASP) and olsalazine (OLZ) were used to study therapeutic effects. Parameters which have been shown to reflect DSS-induced intestinal inflammation (body weight, colon length, spleen weight, diarrhoea, and rectal bleeding) were measured in the Balb/c mice. RESULTS: Significant amelioration was seen on these parameters after different treatment protocols. Survival in nu/nu CD-1 mice was studied, and after 16 days a death rate of 50% was noted in the DSS group. SASP (100 mg/kg/day) and OLZ (50 mg/kg/day) significantly prolonged the survival to 29 and 38 days, respectively. SASP and OLZ showed a dose-dependent effect in the range between 10 and 100 mg/kg/day, doses closely corresponding to those used in humans. CONCLUSIONS: SASP and OLZ are able to ameliorate the DSS-induced intestinal inflammation. The dose-response patterns suggested that the active therapeutic moiety for the two drugs appears to be mainly the liberated 5-ASA molecule.

Aminosalicylic Acids↗
PubMed1989

Increase in permeability and phospholipase A2 activity of colonic mucosa in Crohn's colitis.

Patients with Crohn's colitis were investigated regarding the relationship between intestinal inflammation, mucosal activity of phospholipase A2 and intestinal permeability to different-sized polyethylene glycols (PEG). Mucosal specimens for phospholipase A2 were obtained at colonoscopy and PEG (590-942 daltons) were deposited in the descending colon. Colonic absorption was measured as urinary output of deposited PEG. Colonic absorption of PEG was higher in these patients, even when the colitis was in remission at colonoscopy, than in ileal Crohn's disease or control patients. Mucosal phospholipase A2 activity was increased in active colitis, but in the patients with endoscopic remission it was at the same level as in the controls or in the patients with ileal Crohn's disease. The observations suggest that increased intestinal permeability may be a primary factor in activation of mucosal phospholipase A2 activity and in intestinal inflammation.

Adolescent↗
PubMedDate not supplied

Pancreatic protease inhibition during shock attenuates cell activation and peripheral inflammation.

Intestinal ischemia contributes to shock-induced multiple organ failure. Our recent evidence suggests that pancreatic proteases may be involved in the formation of inflammatory activators within an ischemic intestine. These inflammatory mediators are released early into the circulation and may contribute to the severe systemic inflammatory response syndrome (SIRS) during shock. We examined the impact of intra-intestinal pancreatic protease inhibition on acute intestinal ischemia-induced hypotension, the formation of activating factors for cardiovascular cells, as well as cremaster muscle cell death and intestinal injury by intravital microscopy. Male Wistar rats were divided into four groups: (1) a sham group; and experimental groups with 100 min of superior mesenteric artery occlusion (2) without (SMAO group), and (3) with intestinal lavage using Krebs-Henseleit solution (LAV group), or (4) lavage using the protease inhibitor gabexate mesilate in Krebs-Henseleit solution (FOY group, 0.37 mM). Intestinal ischemia and reperfusion-induced hypotension upon reperfusion was accompanied by a significant increase in the level of neutrophil-activating factors in the intestine and plasma. During reperfusion, a significant increase in leukocyte-endothelium interactions in postcapillary venules and parenchymal cell death were observed in the cremaster muscle in LAV and SMAO animals suggesting peripheral neutrophil cell activation. Intra-intestinal pancreatic protease inhibition resulted in a stable blood pressure throughout the experiment. Cell activation, leukocyte-endothelial interactions and cell death in the cremaster muscle were almost completely abolished in the FOY group. In addition, ischemia-induced intestinal mucosal injury was attenuated with intestinal pancreatic protease inhibition. These results indicate that intestinal pancreatic protease inhibition significantly attenuates intestinal ischemia-induced shock by reducing SIRS and gut injury.

Abdominal Muscles↗
PubMed1999

Weaning anorexia may contribute to local inflammation in the piglet small intestine.

Compromising alterations in villus-crypt structure are common in pigs postweaning. Possible contributions of local inflammatory reactions to villus-crypt alterations during the weaning transition have not been described. This study evaluated local inflammatory responses and their relationship with morphological changes in the intestine in 21-d-old pigs (n = 112) killed either at weaning (Day 0) or 0.5, 1, 2, 4 or 7 d after weaning to either milk- or soy-based pelleted diets. Cumulative intake averaged <100 g during the first 2 d postweaning, regardless of diet. During this period of weaning anorexia, inflammatory T-cell numbers and local expression of the matrix metalloproteinase stromelysin increased while jejunal villus height, crypt depth and major histocompatibility complex (MHC) class I RNA expression decreased. Upon resumption of feed intake by the fourth d postweaning, villus height and crypt depth, CD8(+) T cell numbers, MHC class I RNA expression and local expression of stromelysin returned to Day 0 values. Together the results indicate that inadequate feed intake during the immediate postweaning period may contribute to intestinal inflammation and thereby compromise villus-crypt structure and function.

Animals↗