Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of vitamin A deficiency on the mitogen response of splenic B and T lymphocytes was determined in adult vitamin A-deficient rats. Female weanling Brown Norway/Billingham-Rijswijk (BN/BiRij) and Sprague-Dawley rats were fed a semipurified, essentially vitamin A-free diet, which resulted in clinical symptoms of vitamin A deficiency and severely decreased plasma retinol contents at the age of about 17 and 41 wk for BN/BiRij and Sprague-Dawley rats, respectively. A lower B cell proliferative response after stimulation with lipopolysaccharide in combination with dextran sulfate was observed in vitamin A-deficient rats of both strains, but the T cell proliferative response after concanavalin A stimulation was unchanged. The lower B cell mitogen response was not associated with changes in the cellular composition of the spleen (as analyzed with monoclonal antibodies specific for the various subsets of T and B cells and of macrophages). We suggest that the age at which clinical symptoms of vitamin A deficiency are induced may be an important determinant for the immunological variables affected.
 ...
PMID:Mitogen response of B cells, but not T cells, is impaired in adult vitamin A-deficient rats. 194 Dec 60

Although the antibody response of vitamin A-deficient rats immunized with pneumococcal polysaccharide (SSS-III) was barely detectable, coimmunization with SSS-III plus 2 or 20 micrograms of Pseudomonas aeruginosa lipopolysaccharide (LPS) resulted in an anti-SSS-III response that was equal to or greater than that of vitamin A-sufficient rats immunized only with SSS-III. Doses of 2 and 20 micrograms of LPS, but not 0.1 and 0.5 micrograms, produced significant adjuvanticity, and LPS functioned as an adjuvant when given concomitantly with SSS-III (day 0) or up to 3 days later. Thus, vitamin A deficiency per se does not preclude the anti-SSS-III response, and LPS or factors released in response to LPS, even after initiation of the response to SSS-III, may substantially enhance antibody production to this thymus-independent, type 2 antigen.
 ...
PMID:The antibody response of vitamin A-deficient rats to pneumococcal polysaccharide is enhanced through coimmunization with lipopolysaccharide. 810 80

Reduced antibody response to tetanus toxoid (TT) was previously demonstrated during vitamin A deficiency but the response to bacterial lipopolysaccharide (LPS) was normal. We addressed whether anti-TT IgG responses are enhanced in vitamin A-sufficient and deficient rats by immunization with LPS plus TT. Antibody responses in vitamin A-sufficient and deficient rats increased significantly after coimmunization (LPS + TT) compared with the response of rats immunized with TT alone. In additional studies, recombinant tumor necrosis factor-alpha (TNF-alpha) also significantly increased the anti-TT IgG concentrations. Because pretreatment with anti-TNF before coimmunization or immunization with TT alone markedly reduced the anti-TT IgG responses, we infer TNF to be a mediator of both the adjuvanticity of LPS and the unstimulated response to TT. In conclusion, vitamin A-deficient rats can be stimulated to respond to TT by coimmunization with LPS or by treatment with TNF.
 ...
PMID:Antibody response against tetanus toxoid is enhanced by lipopolysaccharide or tumor necrosis factor-alpha in vitamin A-sufficient and deficient rats. 814 39

Morbidity and mortality due to viral infections are major health concerns, particularly when individuals are vitamin A deficient. Vitamin A deficiency significantly impairs mucosal IgA, a first line of defense against virus at its point of entry. Previous reports have suggested that CD11c(Hi) dendritic cells (DCs) of the gastrointestinal tract produce retinaldehyde dehydrogenase (ALDH1A), which metabolizes vitamin A precursors to retinoic acid to support normal mucosal immunity. Given that the upper respiratory tract (URT) and gastrointestinal tract share numerous characteristics, we asked if the CD11c(Hi) DCs of the URT might also express ALDH1A. To address this question, we examined both CD11c(Hi) test cells and CD11c(Lo/neg) control cells from nasal tissue. Surprisingly, the CD11c(Lo/neg) cells expressed more ALDH1A mRNA per cell than did the CD11c(Hi) cells. Further evaluation of CD11c(Lo/neg) populations by PCR and staining of respiratory tract sections revealed that epithelial cells were robust producers of both ALDH1A mRNA and protein. Moreover, CD11c(Lo/neg) cells from nasal tissue (and a homogeneous respiratory tract epithelial cell line) enhanced IgA production by lipopolysaccharide (LPS)-stimulated splenocyte cultures in the presence of the retinoic acid precursor retinol. Within co-cultures, there was increased expression of MCP-1, IL-6, and GM-CSF, the latter two of which were necessary for IgA upregulation. All three cytokines/chemokines were expressed by the LPS-stimulated respiratory tract epithelial cell line in the absence of splenocytes. These data demonstrate the autonomous potential of respiratory tract epithelial cells to support vitamin A-mediated IgA production, and encourage the clinical testing of intranasal vitamin A supplements in vitamin A deficient populations to improve mucosal immune responses toward respiratory tract pathogens and vaccines.
...
PMID:Respiratory tract epithelial cells express retinaldehyde dehydrogenase ALDH1A and enhance IgA production by stimulated B cells in the presence of vitamin A. 2446 50

Vitamin A is a critical micronutrient for regulating immunity in many organisms. Our previous study demonstrated that gestational or early-life vitamin A deficiency decreases the number of immune cells in offspring. The present study aims to test whether vitamin A supplementation can restore lymphocyte pools in vitamin A-deficient rats and thereby improve the function of their intestinal mucosa; furthermore, the study aimed to identify the best time frame for vitamin A supplementation. Vitamin A-deficient pregnant rats or their offspring were administered a low-dose of vitamin A daily for 7 days starting on gestational day 14 or postnatal day 1, day 14 or day 28. Serum retinol concentrations increased significantly in all four groups that received vitamin A supplementation, as determined by high-performance liquid chromatography. The intestinal levels of secretory immunoglobulin A and polymeric immunoglobulin receptor increased significantly with lipopolysaccharide challenge in the rats that received vitamin A supplementation starting on postnatal day 1. The rats in this group had higher numbers of CD8+ intestinal intraepithelial lymphocytes, CD11C+ dendritic cells in the Peyer's patches and CD4+CD25+ T cells in the spleen compared with the vitamin A-deficient rats; flow cytometric analysis also demonstrated that vitamin A supplementation decreased the number of B cells in the mesenteric lymph nodes. Additionally, vitamin A supplementation during late gestation increased the numbers of CD8+ intestinal intraepithelial lymphocytes and decreased the numbers of B lymphocytes in the mesenteric lymph nodes. However, no significant differences in lymphocyte levels were found between the rats in the other two vitamin A supplement groups and the vitamin A-deficient group. In conclusion, the best recovery of a subset of lymphocytes in the offspring of gestational vitamin A-deficient rats and the greatest improvement in the intestinal mucosal immune response are achieved when vitamin A supplementation occurs during the early postnatal period.
...
PMID:Vitamin A supplementation in early life enhances the intestinal immune response of rats with gestational vitamin A deficiency by increasing the number of immune cells. 2550 94