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Results for “mucosal immunization”

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At least 271 records · Page 15Linked to original sources
PubMed2001

The multiple roles of major histocompatibility complex class-I-like molecules in mucosal immune function.

The human major histocompatibility complex (MHC) on chromosome 6 encodes three classical class-I genes: human leukocyte antigens (HLA) A, B, and C. These polymorphic genes encode a 43- to 45-kDa cell surface glycoprotein that, in association with the 12-kDa beta2-microglobulin molecule, functions in the presentation of nine amino acid peptides to the T-cell receptor of CD8-bearing T lymphocytes and killer inhibitory receptors on natural killer cells. In addition to these ubiquitously expressed, polymorphic proteins, the human genome also encodes several nonclassical MHC class-I-like, or class Ib, genes that, in general, encode nonpolymorphic molecules involved in various specific immunological functions. Many of these genes, including CD1, the neonatal Fc receptor for IgG, HLA-G, HLA-E, the MHC class-I chain-related gene A, and Hfe, are prominently displayed on epithelial cells, suggesting an important role in epithelial cell biology.

CD8 Antigens↗
PubMed1998

Impairment of the mucosal immune system: IgA and IgM cleavage detected in vaginal washings of a subgroup of patients with bacterial vaginosis.

The integrity of the immunoglobulins in vaginal washings of patients with bacterial vaginosis was examined to answer the question of the lack of immune response against Gardnerella vaginalis cytolysin. Clinically diagnosed patients (n=100) were recruited and their vaginal washings examined by Western blotting. Many showed IgA and IgM partially or extensively degraded. According to the degradation pattern, the patients were subdivided into 4 subsets, from intact (score 0) to completely degraded IgA (score +3). Statistical analysis of the data showed a correlation between IgA degradation and absence of immune response to G. vaginalis cytolysin. The extent of IgA degradation correlated also with the sialidase (but not with the prolidase) activity level. All women showed intact IgG and human serum albumin and no trypsin-like activity. Patients with bacterial vaginosis having high sialidase activity and extensive IgA degradation in their secretions could incur more dangerous infections and adverse pregnancy outcomes.

Adolescent↗
PubMed2004

Humoral and mucosal immunity in protection from natural respiratory syncytial virus infection in adults.

Virus-specific nasal immunoglobulin (Ig) A and serum antibody titers in 67 respiratory syncytial virus (RSV)-infected adults were compared with titers in age-matched uninfected control subjects. Control subjects had significantly higher levels of nasal IgA and serum IgG to the RSV F, Ga, and Gb proteins than infected subjects. Serum neutralizing-antibody titers to group A and B RSV strains were also lower in infected subjects, although differences were not as large. Multivariate analysis found that low RSV-specific nasal IgA was an independently significant risk factor for RSV infection.

Adult↗
PubMed2006

Human oviductal epithelial cells express Toll-like receptor 3 and respond to double-stranded RNA: Fallopian tube-specific mucosal immunity against viral infection.

BACKGROUND: The aim of this study was to evaluate the site-specific immunoregulatory mechanisms against viral infection in human Fallopian tubes. METHODS: We therefore investigated the effects of double-stranded RNA (dsRNA) on the production of interleukin (IL)-6, IL-8 and granulocyte chemotactic protein-2 (GCP-2) by cultured oviductal epithelial cells (OECs) using enzyme-linked immunosorbent assays. Phosphorylation of inhibitor kappaB-alpha (IkappaB-alpha) protein after dsRNA stimulation and the expression of Toll-like receptor (TLR) 3 in these cells were also evaluated by western blot analysis. RESULTS: Polyriboinosinic:polyribocytidylic acid (poly I:C), a synthetic dsRNA that antagonizes TLR3, stimulated the secretion of IL-6, IL-8 and GCP-2 by OECs. Poly I:C-induced production of these cytokines by OECs was inhibited by the pretreatment of these cells with anti-TLR3 antibody. The phosphorylation of IkappaB-alpha protein was detected in OECs after stimulation by poly I:C. The expression of TLR3 was also detected in OECs. CONCLUSION: These results suggest that the epithelial cells of the human Fallopian tube have evolved a unique, site-specific mechanism for recognizing viral infection. TLR3-mediated production of proinflammatory cytokines and chemokines in OECs in response to viral dsRNA may be important for antiviral immunity in the human female reproductive tract.

Adult↗
PubMed1997

Alterations in mucosal immune cell distribution in septic rats.

A reduced cell-mediated immunity in the intestinal mucosa might promote gut barrier failure and bacterial translocation in shock. This study was performed to investigate changes from the normal distribution of cellular components of the immune system within the intestine during sepsis. Intra-abdominal sepsis was induced by cecal ligation and puncture. After 24 h, the animals were killed and specimens were taken from the small bowel. Immunohistochemical stainings were performed on frozen sections using monoclonal antibodies reactive with MHC class II positive cells (OX6), the alpha/beta antigen receptor on T lymphocytes (R73), CD4+ T lymphocytes (W3/25), CD8+ T lymphocytes (OX8), and macrophages (ED1). There was a significant reduction in the number of pan T lymphocytes as well as both CD4+ and CD8+ subsets in the mucosa of the septic rats as compared with sham operated rats (p < .01). In contrast, the populations of MHC class II positive cells and macrophages increased in sepsis (p < .01). We conclude that 24 h after the induction of peritonitis, there is an altered pattern of immunocompetent cells within the intestinal mucosa.

Animals↗
PubMed2005

Defects in mucosal immunity leading to ulcerative colitis.

Evidence accumulated over the last decade demonstrates that what we call 'ulcerative colitis' is actually a heterogeneous group of diseases resulting from different pathogenic mechanisms with a common symptomatic expression. Subgroups of patients with ulcerative colitis can be stratified by presence or absence of serum autoantibodies, which are thought not to be pathogenic but to mark for a distinct disease phenotype. In recent years, animal-based experimental systems have emerged that reflect human ulcerative colitis and have potential to accelerate our understanding of its pathogenesis. Genetic and immunological data from human studies in combination with results from animal model systems are the foundation of a hypothesis, which includes a role for microbial antigen exposure in the initiation, perpetuation, and amplification of the disease. In ulcerative colitis, it appears as though the T-cell response to the antigens is not T-helper (Th) 1 dominant as in the case of Crohn's disease but rather is either Th2 [interleukin (IL)-4, IL-13] or is mediated by specialized cells such as natural killer (NK) T cells (IL-13). Lamina propria T cells from ulcerative colitis patients produce significantly greater amounts of IL-13. Ulcerative colitis is associated with an atypical Th2 response mediated by a distinct subset of NK T cells that produce IL-13 and are cytotoxic for epithelial cells. The way in which this response affects the ultimate cascade of inflammatory events has yet to be determined.

Animals↗
PubMed1999

The intestinal epithelial cell: processing and presentation of antigen to the mucosal immune system.

The immunologic tone of the intestinal tract is one of suppressed or highly regulated responses. While there are several components (intrinsic and extrinsic to the gut-associated lymphoid tissue) responsible for this immunologically suppressed tone, the intestinal epithelial call (IEC) has been proposed as a key player in this process. IECs can take up and process antigen but distinct surface molecules and restriction elements allow them to present these antigens to unique regulatory T cells. These include the expression of the class Ib molecule CD1d as well as a novel CD8 ligand, gp180. These molecules come together to activate a subpopulation of CD8+ regulatory cells whose function is to suppress immune responses in an antigen non-specific fashion most likely through cognate interactions. This form of regulation may be unique to the gut-associated lymphoid tissue which is consistent with the unusual demands upon this part of the immune system.

Animals↗
PubMed2006

Human oviductal stromal fibroblasts, but not oviductal epithelial cells, express Toll-like receptor 4: the site-specific mucosal immunity of the human fallopian tube against bacterial infection.

PROBLEM: To evaluate the site-specific immunoregulatory mechanisms against bacterial infection in the human fallopian tubes. METHOD OF STUDY: We investigated the effects of lipopolysaccharide (LPS) on the production of CXC chemokines by cultured oviductal epithelial cells (OEC) and oviductal stromal fibroblasts (OSF). The expression of Toll-like receptor (TLR) 4 and CD14 protein in OEC and OSF were evaluated. The phosphorylation of the inhibitor kappaB-alpha (IkappaB-alpha) protein after LPS stimulation was also examined. RESULTS: Lipopolysaccharide stimulated the secretion of granulocyte chemotactic protein-2, growth-regulated oncogene-alpha, and epithelial neutrophil activating peptide-78 by OSF, but not by OEC. The phosphorylation of the IkappaB-alpha protein was not detected in OEC after stimulation by LPS, whereas IkappaB-alpha phosphorylation was observed in OSF after stimulation by LPS. The expression of the TLR4 protein and mRNA was detected only in OSF but not in OEC. The expression of CD14 was not detected in either OEC or OSF. CONCLUSION: These results suggest that epithelial cells and fibroblasts in the human fallopian tube have evolved a unique, site-specific mechanism for recognizing Gram-negative pathogens. The lack of TLR4 in OEC may be important for avoiding a state of unnecessary inflammation that could disrupt the epithelial barrier and cause irreversible tubal scarring.

Cells, Cultured↗
PubMed2006

The probiotic bacterium Lactobacillus casei induces activation of the gut mucosal immune system through innate immunity.

The mechanisms by which probiotic bacteria affect the immune system are unknown yet, but many of them are attributed to an increase in the innate or in the acquired immune response. To study the influence of the probiotic bacterium Lactobacillus casei in the expression of receptors involved in the innate immune response, this bacterium was orally administered to BALB/c mice. After, they were sacrificed; the small intestine and intestinal fluids were collected to measure secretory immunoglobulin A (IgA) specific for L. casei. Mononuclear cells from Peyer's patches were isolated to determine the CD-206 and TLR-2 receptors. In histological slices we determined the number of IgA+, CD4+, CD8+, and CD3+ cells and two cytokines (interleulin-5 [IL-5] and IL-6). CD-206 and TLR-2 increased with respect to the untreated control. We did not observe an increase in the T population or in the IL-5-positive cells. IgA+ cells and IL-6-producing cells increased after 7 days of L. casei administration. We did not find specific antibodies against L. casei. The main immune cells activated after oral L. casei administration were those of the innate immune response, with an increase in the specific markers of these cells (CD-206 and TLR-2), with no modification in the number of T cells.

Administration, Oral↗