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Results for “mucosal immunization”

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At least 919 records · Page 51Linked to original sources
PubMed1993

Anthranoids and the mucosal immune system of the colon.

The mechanism of action of anthranoids in general and of sennosides at the cellular level is not precisely known. Pseudomelanosis or pseudolipofuscinosis, a condition characterized by the accumulation of pigmented macrophages in the lamina propria, is one of the well-known effects of these products. It is most probably the result of an interaction between apoptotic epithelial cells and the lamina propria cellular infiltrate. Treatment of cell suspensions of intestinal epithelial cells and of human intestinal epithelial cells in culture with rhein anthrone, the active compound of sennosides, demonstrates a direct influence of the drug on these epithelial cells. Low doses induce alterations in cellular shape and organelles consistent with increased metabolism. High doses induce apoptotic changes. The interaction between the epithelial cells and cells of the monocyte/macrophage lineages induces also the release of prostaglandins of the E series as shown by experiments on cell cultures of epithelial cells and peripheral blood cells. An increase of PGE2 release to about 140% of the control value is noted following administration of low doses of rhein anthrone to a combination of human intestinal epithelial cells and human peripheral blood mononuclear cells. This finding indicates that rhein anthrone is activating cellular components of the intestinal immune system and may by this pathway induce secretion and motility.

Animals↗
PubMed1991

Mucosal immunity in primary glomerulonephritis: II. Study of the serum IgA subclass repertoire to food and airborne antigens.

IgA specific for 7 food and 6 airborne antigens were sought in the serum of 30 adult patients with IgA mesangial nephropathy (IgA GN), 23 with membranous nephropathy (MGN), 20 with idiopathic nephrotic syndrome (INS), 11 with membranoproliferative GN (MPGN) and 22 healthy controls by means of an enzyme-linked immunoassay. The IgA subclass was determined using monoclonal antibodies. Increased levels of IgA specific for gliadin, bovine serum albumin (BSA), ovalbumin, lysozyme and alpha-lactalbumin were found in IgA GN, while increased levels of IgA to BSA, ovalbumin, lysozyme and alpha-lactalbumin were observed in MGN; IgA specific for alpha-lactalbumin were increased in INS, and MPGN patients had reduced levels of IgA to BSA and increased levels of IgA to beta-lactoglobulin and alpha-lactalbumin. These specific IgA to food antigens were restricted to the IgA1 subclass. Patients with IgA GN had significantly increased levels of IgA specific for Dermatophagoides pteronyssinus (DP) and Dactil while the MGN group showed increased levels of IgA specific for DP, feathers, Dactil and mold. INS patients had increased levels of IgA specific for DP, feathers, Dactil, mold and dog hairs, while MPGN patients had increased levels of IgA specific for feathers, Dactil, dog hairs and mold. All these specific IgA to airborne antigens were restricted to the IgA1 subclass. Patients with the four types of primary glomerulonephritis had decreased IgA specific for cat hairs which were of both the IgA1 and IgA2 subclasses. We conclude that anomalies of the IgA repertoire to environmental antigens are also encountered in primary glomerulonephritis other than IgA GN.

Adult↗
PubMed1993

Mucosal immunity in primary glomerulonephritis. III. Study of intestinal permeability.

To study the specificity of gut hyperpermeability in primary glomerulonephritis, we investigated intestinal permeability by means of 51Cr-EDTA testing in 20 healthy individuals and in 30 patients with Immunoglobulin A nephropathy (IgA GN), 25 with idiopathic nephrotic syndrome (INS) and 20 with immune complex glomerulonephritis (IC-GN; membranous+membranoproliferative glomerulonephritis). Gut permeability was statistically increased in each patient group versus the controls [controls: 2% (0.4-3.9); IgA GN: 3.25% (0.7-17.70); INS: 3.71% (0.82-10); IC-GN: 3.40% (0.30-16); results are median (range); p < 0.005, nonparametric Mann-Whitney test]. An increase in intestinal permeability exceeding the upper limit of control values (95th percentile) was observed in 36% of IgA GN, 60% of INS and 50% of IC-GN patients. We conclude that intestinal permeability is frequently increased in primary glomerulonephritis and may also be increased in types of glomerulonephritis other than IgA GN.

Adult↗
PubMed1984

Mucosal immunity.

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Glomerulonephritis, IGA↗
PubMed1995

Interleukin-4 is required for the induction of lung Th2 mucosal immunity.

Aerosol antigen challenge of ovalbumin-sensitized mice induced an eosinophilic airway inflammation that was dependent on interleukin (IL)-5 and CD4+, but not CD8+, T lymphocytes. The involvement of the Th2 phenotype of CD4+ T cells was supported by demonstrating that FACS-sorted purified lung T cells from sensitized, but not control, mice produced IL-4, IL-5, and IL-10 after activation of the CD3/TCR complex. To determine the role of IL-4 in this process, we used mice in which the gene for IL-4 was deleted by homologous recombination. Antigen challenge of IL-4 gene-targeted mice resulted in a marked attenuation of eosinophilic inflammation and IL-5 secretion. To more fully understand the time when IL-4 was involved, we administered a neutralizing anti-IL-4 antibody (11B11) either immediately before antigen challenge or during immunization. Inhibition of IL-4 before antigen challenge had little effect on antigen-induced eosinophil infiltration. However, when 11B11 was administered during immunization, there was a marked reduction in eosinophil infiltration. Cross-linking of the CD3/TCR complex of FACS-sorted lung T cells revealed that only when anti-IL-4 was administered during immunization was there an inhibition of T cell-derived IL-5 and IgE production. These results suggest that IL-4 is central both to the induction of a local Th2 response and to the development of eosinophilic inflammation of the lung. Moreover, we suggest a sequential involvement of IL-4 and IL-5, with IL-4 committing naive T cells to a Th2 phenotype which upon activation by aerosol provocation secrete IL-5, resulting in eosinophil accumulation.

Animals↗
PubMedDate not supplied

Alteration of mucosal immunity after long-term ingestion of an elemental diet in rats.

The effects of an elemental diet on lymphocyte transport in intestinal lymph and immune responses of gut-associated lymphoid tissue were investigated in rats. The control animals were fed a conventional diet. After 4 week of feeding, the total calorie intake and body weight gain showed no differences between the two groups. The number and total area of Peyer's patches and the ratio of height of villi to height of crypt showed no significant differences between the two groups. The rate of lymph flow in intestinal lymphatics showed no significant change in treated animals compared with the control rats. However, an elemental diet induced a significant decrease in lymphocyte flux in intestinal lymphatics compared with that in control rats. Lymphocyte subsets in intestinal lymph revealed a significant decrease in CD3-positive cells, especially CD4-positive cells in the elemental diet-treated group. A significant decrease in the number of immunoglobulin A-containing cells and a decreased CD4/CD8 ratio in T-cell subsets were observed in the lamina propria of ileal mucosa in the elemental diet-treated group by morphometric analysis in the immunohistochemical study. Specific antibody-secreting cells in intestinal lymph were also investigated after rats were intraduodenally primed with cholera toxin and challenged with the same toxin after an interval of 2 weeks. No significant difference was seen between the two groups in any of the numbers of anti-cholera toxin immunoglobulin-secreting cells in any immunoglobulin A, immunoglobulin G, or immunoglobulin M class as determined by the enzyme-linked immunospot assay.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Development of intestinal mucosal immunity in fetal life and the first postnatal months.

Nine premature infants who were either stillborn or who died shortly after delivery (gestational age, 24-32 wk), eight full-term infants who died during the first 3 postnatal wk, and four infants who died in the postneonatal period were studied by immunohistochemistry for duodenal expression of secretory component (SC) and epithelial HLA class I and II determinants and for the presence of IgA-, IgM-, and IgG-producing immunocytes. Only small amounts of SC appeared before the 29th gestational wk, but thereafter it increased rapidly; 1 wk after birth, SC showed an adult distribution pattern. Epithelial class I was expressed throughout the period investigated, whereas class II (HLA-DR) determinants were absent on the duodenal villi until 1 wk after birth. HLA-DP and -DQ were not expressed by the epithelium. No IgA immunocytes were seen before 1 wk after birth, whereas a few IgM- and IgG-producing cells were present throughout the period studied. The intense epithelial HLA-DR expression from the 2nd postnatal wk, along with SC and the appearance of IgA immunocytes, suggests that the intestinal immune system is modulated in response to environmental factors shortly after birth.

Antibody-Producing Cells↗
PubMed2006

Lack of mucosal immune reconstitution during prolonged treatment of acute and early HIV-1 infection.

BACKGROUND: During acute and early HIV-1 infection (AEI), up to 60% of CD4(+) T cells in the lamina propria of the lower gastrointestinal (GI) tract are lost as early as 2-4 wk after infection. Reconstitution in the peripheral blood during therapy with highly active antiretroviral therapy (HAART) is well established. However, the extent of immune reconstitution in the GI tract is unknown. METHODS AND FINDINGS: Fifty-four AEI patients and 18 uninfected control participants underwent colonic biopsy. Forty of the 54 AEI patients were followed after initiation of antiretroviral therapy (18 were studied longitudinally with sequential biopsies over a 3-y period after beginning HAART, and 22 were studied cross sectionally after 1-7 y of uninterrupted therapy). Lymphocyte subsets, markers of immune activation and memory in the peripheral blood and GI tract were determined by flow cytometry and immunohistochemistry. In situ hybridization was performed in order to identify persistent HIV-1 RNA expression. Of the patients studied, 70% maintained, on average, a 50%-60% depletion of lamina propria lymphocytes despite 1-7 y of HAART. Lymphocytes expressing CCR5 and both CCR5 and CXCR4 were persistently and preferentially depleted. Levels of immune activation in the memory cell population, CD45RO+ HLA-DR+, returned to levels seen in the uninfected control participants in the peripheral blood, but were elevated in the GI tract of patients with persistent CD4+ T cell depletion despite therapy. Rare HIV-1 RNA-expressing cells were detected by in situ hybridization. CONCLUSIONS: Apparently suppressive treatment with HAART during acute and early infection does not lead to complete immune reconstitution in the GI mucosa in the majority of patients studied, despite immune reconstitution in the peripheral blood. Though the mechanism remains obscure, the data suggest that there is either viral or immune-mediated accelerated T cell destruction or, possibly, alterations in T cell homing to the GI tract. Although clinically silent over the short term, the long-term consequences of the persistence of this lesion may emerge as the HIV-1-infected population survives longer owing to the benefits of HAART.

Acute Disease↗