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Marked Infiltration (marked + infiltration)
Selected AbstractsVascular endothelial growth factor (VEGF)-induced angiogenesis in herniated disc resorptionJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 3 2002Hirotaka Haro Abstract Intervertebral disc herniation is a major cause of low back pain and sciatica. Spontaneous resorption of herniated disc (HD) is frequently detected by magnetic resonance imaging (MRI). Marked infiltration by macrophages and neo-vascularization are observed upon histogical examination of HD. In addition, enhanced MRI studies suggest that HD resorption occurs more frequently in those completely exposed to the epidural space and that this correlates with their degree of vascularization. We have postulated that the angiogenic factor, vascular endothelial growth factor (VEGF), may be implicated in the neo-vascularization of HD tissues. Here we demonstrate that VEGF and its receptors VEGFR-1 and VEGFR-2 are expressed in human surgical samples of HD. Using a co-culture system comprised of murine peritoneal macrophages and intervertebral disc tissue as a model of the acute phase of HD developed previously, an increase in macrophage VEGF protein and mRNA expression was observed upon exposure to disc tissue. Tumor necrosis factor alpha (TNF-,) was required for this induction of VEGF. Use of a novel angiogenesis assay revealed that addition of the conditioned media from the co-culture system resulted in an increase of vascular tubule formation. This effect was strongly inhibited by anti-VEGF antibody, but augmented by recombinant VEGF. We conclude that VEGF induction, under the co-culture conditions tested can result in neo-vascularization of intervertebral disc tissue and may thus play a role in the resorption of HD. © 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source] Cross-Primed CD8+ Cytotoxic T cells Induce Severe Helicobacter -associated Gastritis in the Absence of CD4+ T cellsHELICOBACTER, Issue 5 2007Toshiro Fukui Abstract Background:, Although previous studies have reported important roles of CD4+ type1-helper T cells and regulatory T cells in Helicobacter -associated gastritis, the significance of CD8+ cytotoxic T cells remains unknown. To study the roles of CD8+ T cells, we examined the immune response in the gastric mucosa of Helicobacter felis -infected major histocompatibility complex (MHC) class II-deficient (II,/,) mice, which lack CD4+ T cells. Materials and methods:, Stomachs from H. felis -infected wild-type and infected MHC II,/, mice were examined histologically and immunohistochemically. Gastric acidity and serum levels of anti- H. felis antibodies were measured. The expression of pro-inflammatory and anti-inflammatory cytokine, Fas-ligand, perforin, and Foxp3 genes in the gastric mucosa was investigated. Results:,H. felis -infected MHC II,/, mice developed severe gastritis, accompanied by marked infiltration of CD8+ cells. At 1 and 2 months after inoculation, mucosal inflammation and atrophy were more severe in MHC II,/, mice, although gastritis had reached similar advanced stages at 3 months after inoculation. There was little infiltration of CD4+ cells, and no Foxp3 -positive cells were detected in the gastric mucosa of the infected MHC II,/, mice. The expression of the interleukin-1, and Fas-ligand genes was up regulated, but that of Foxp3 was down regulated in the infected MHC II,/, mice. Serum levels of anti- H. felis antibodies were lower in the infected MHC II,/, mice, despite severe gastritis. Conclusions:, The present study suggests that cross-primed CD8+ cytotoxic T cells can induce severe H. -associated gastritis in the absence of CD4+ helper T cells and that Foxp3 -positive cells may have an important role in the control of gastric inflammation. [source] Interleukin-18 overproduction exacerbates the development of colitis with markedly infiltrated macrophages in interleukin-18 transgenic miceJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 8 2003TAKAHIRO ISHIKURA Abstract Background and Aim:, The authors have previously shown that production of interleukin (IL)-18 was increased in the inflamed mucosa of patients with Crohn's disease (CD) and blockade of IL-18 ameliorated the murine model of CD. This demonstrated that IL-18 plays a significant role during intestinal inflammation. However, the initial role of IL-18 during intestinal inflammation was unclear; therefore the susceptibility of IL-18 transgenic (Tg) mice to acute dextran sulfate sodium (DSS)-induced colitis was examined. Methods:, Interleukin-18 Tg and wild-type (WT) mice were fed 2.0% of DSS for 8 days. The total clinical scores (bodyweight loss, stool consistency, and rectal bleeding), colon length and histological scores were assessed. The expressions of surface markers and IL-18 on infiltrating lamina propria mononuclear cells were analyzed immunohistochemistrically. Mesenteric lymph node (MLN) cells were isolated and the expressions of CD4+ T-cell activation markers (CD69, CD25 and IL18R) were analyzed by flow cytometry. Results:, The IL-18 Tg mice exhibited an increased susceptibility to DSS-induced colitis, as shown by significantly increased clinical, histological scores, and more severe colonic shortening compared with WT mice. Immunohistochemical analysis revealed a significant increase of IL-18 production and CD11b+ macrophages but not CD4+ T cells in the inflamed mucosa in DSS-fed IL-18 Tg compared with DSS-fed WT mice. Furthermore, MLN cells revealed no evidence of increased CD4+ T-cell activation in DSS-fed IL-18 Tg. Conclusions:, These findings suggest that IL-18 overproduction in the mucosa plays an important role in the marked infiltration of macrophages and exacerbates colitis in IL-18 Tg mice. [source] Disseminated Mycobacterium avium infection in a dog with chronic diarrhoeaAUSTRALIAN VETERINARY JOURNAL, Issue 5 2000B HORN A 3-year-old Maltese-cross dog presented with a 4-month history of chronic diarrhoea and inappetence. Poorly regenerative anaemia, leukocytosis and hypoproteinaemia were evident on several occasions. Biopsies of stomach, duodenum and colon revealed marked infiltration of mucosae by macrophages containing many acid-fast bacilli. Similar organisms were numerous in a faecal smear. Melaena, haematochezia and severe abdominal pain developed and were unresponsive to therapy. Following euthanasia and necropsy, histiocytic cells containing acid-fast bacilli were found throughout the gastrointestinal tract, mesenteric and peripheral lymph nodes, spleen, liver, kidney and lungs. The organism was identified as Mycobacterium avium by bacterial culture and polymerase chain reaction testing. [source] CD4+ T cells from mice with intestinal immediate-type hypersensitivity induce airway hyperreactivityCLINICAL & EXPERIMENTAL ALLERGY, Issue 10 2007C. Ozdemir Summary Background A subset of food-allergic patients does not only respond clinically with symptoms in the gastro-intestinal tract but also with asthmatic reactions. Objective The aim of this study was to analyse whether CD4+ T cells from mice with intestinal immediate-hypersensitivity reactions to food allergen are involved in the development of experimental asthma. Methods BALB/c mice were intraperitoneally sensitized to ovalbumin (OVA), followed by repeated intra-gastric (i.g.) OVA challenges. Control animals were either sham-sensitized or sham-challenged with phosphate-buffered saline (PBS). Duodenum, jejunum, ileum and colon were histologically examined. CD4+ T cells from mesenteric lymph nodes were transferred from various donor groups into recipient mice that received either OVA or PBS aerosol challenges. Recipients were analysed by measurements of lung function using head-out body-plethysmography and examination of broncho-alveolar lavage and lung histology. Results The highest levels of OVA-specific IgE antibody levels were detected in OVA-sensitized and OVA-challenged mice. Throughout the lower intestinal tract, a marked infiltration with eosinophils was observed, and goblet cell numbers as well as goblet cell area were significantly increased. The villus/crypt ratio was decreased compared with controls. The transfer of CD4+ T cells from mesenteric lymph nodes of OVA-sensitized and OVA-challenged mice triggered airway hyperreactivity and eosinophilic airway inflammation in recipients aerosol challenged with OVA, but not with PBS. Conclusion We conclude that CD4+ T cells from mesenteric lymph nodes of mice with allergen-induced immediate-type hypersensitivity reactions in the gut are able to transfer the phenotype of experimental asthma. [source] | ||||||||||