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

We studied the function of submandibular lymph nodes (MLN) in the oral mucosa immune system as compared with that of inguinal lymph nodes (ILN) in the cutaneous one. Primary IgM, IgG and IgA antibody responses in MLN to sheep red blood cells (SRBC) as a model antigen given submucosally occurred more extensively than those in ILN to the antigen injected subcutaneously. Particularly, definite IgA synthesis was seen in MLN but not in ILN. This IgA synthesis was shown to be originated locally in oral submucosal lymphoid tissue or MLN but not in gut-associated lymphoid tissue (GALT). This suggested that the oral mucosal tissue including MLN acts like Peyer's patches in GALT for IgA synthesis. When mice were administered with SRBC and bacterial lipopolysaccharide (LPS) submucosally, the adjuvant effect of LPS was only observed on the capacity of MLN cells for secondary antibody response in vitro. This contrasted to the marked augmentation by LPS of both the primary antibody response in ILN and capacity for in vitro secondary antibody response of ILN cells of mice given SRBC and LPS subcutaneously. The radioactivities detected in the local lymph nodes and other tissues of mice given 51Cr labeled SRBC submucosally or subcutaneously were comparable with each other. MLN, however, contained more Ig+/B220+ B cells and less Thy1+/Ly-1+ T cells than ILN did, and the L3T4/Ly-2 ratio of T cell subpopulations in MLN was lower than that in ILN. Partially corresponding to this observation, the B cell-dependent area was developed more extensively in MLN than in ILN. This difference in cellular composition and organization might in part explain the reason why MLN and ILN display distinct modes of response and sensitivity to the action of LPS.
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PMID:Characterization of antibody responses of local lymph nodes to antigen given under the oral submucosa. 159 28

An attenuated Salmonella typhi strain has been sought as an improved oral typhoid vaccine and as a carrier of protective antigens of other pathogens to make hybrid vaccines. Ideally, such a strain would be safe and induce protective immune responses after a single oral dose. CVD 908 is a mutant of S. typhi wild-type strain Ty2 with recombinant deletions in two genes, aroC and aroD. In phase 1 testing to date, this strain has not produced febrile responses or other significant adverse reactions in adult volunteers given doses of 5 x 10(4) to 5 x 10(7) organisms with sodium bicarbonate. In addition, after just a single oral dose of 5 x 10(7) colony-forming units, this strain induced IgG seroconversion to S. typhi lipopolysaccharide in 83% of vaccinees and stimulated specific IgA-secreting gut-derived lymphocytes in 100% of vaccinees. CVD 908 is a new oral typhoid vaccine that should be further investigated as a carrier for expressing foreign antigens in recombinant vaccine constructs.
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PMID:Clinical acceptability and immunogenicity of CVD 908 Salmonella typhi vaccine strain. 160 47

Monoclonal antibody H3/5-47 was raised against a human melanoma metastasis and recognizes an antigen expressed in the endothelial cells of all normal human organs as assessed by immunohistochemistry. Antigen expression is higher in venous than in capillary or arterial endothelia; capillary endothelia of different microvascular beds, such as skin, lung, gut or liver, may express varying amounts of this antigen. H3/5-47 antigen expression in the endothelia of diseased tissues (inflammatory diseases, neoplasias) largely reflects its expression pattern in normal tissues. As might be anticipated, the highest expression of H3/5-47 antigen is found in resting adult cutaneous and hepatic cavernous venous hemangiomas. In contrast, psoriatic vessels, characterized by hypertrophy and fenestrations, tend to express H3/5-47 antigen at a much lower density. In human umbilical vein endothelial cells, half the single donor cases show no expression of H3/5-47 antigen, while the rest express the antigen at relatively low densities in about half the cells. Treatment with interferon-gamma or thrombin, but not interleukin-1, lipopolysaccharide, endothelial cell growth factor or phorbolester, either enhances or induces de novo expression in cultured human umbilical vein endothelial cells within 24h; maximum expression of H3/5-47 antigen is induced by interferon-gamma within 72 h. H3/5-47 antigen is not similar to other antigens inducible in human umbilical vein endothelial cells such as HLA-DR, ICAM-1, HECA-452, Leu13, MCP-1 or gamma-IP-10. It is not specifically expressed in the endothelium as it may also recognize certain epithelia, peripheral nervous tissue and bone marrow-derived cell populations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Monoclonal antibody H3/5-47 recognizes an inducible cell surface antigen expressed differently in endothelium of normal and diseased tissues and in vitro. 162 58

A 30% burn injury has been previously reported to impair mitogenic response of splenocytes to a B-lymphocyte mitogen and to affect serum levels of serum class-specific immunoglobulin. To further investigate the effect of burn injury on the function of B lymphocytes in gut-associated and systemic immune tissues, we studied class-specific immunoglobulin synthesis by cultured lymphocytes from spleen and mesenteric lymph nodes after burn injury in rats. Male Lewis rats received 30% full-thickness burn injuries, and 4 days later, the animals were killed to remove spleen and mesenteric lymph nodes. The cells from spleen and mesenteric lymph nodes were cultured for 5 days with 25 micrograms/ml of lipopolysaccharide. Concentrations of immunoglobulin G (IgG), IgM, and IgA in the supernatant of each well were then measured with enzyme-linked immunosorbent assay for class-specific immunoglobulin. Synthesis of IgG by lymphocytes from spleen was statistically significantly impaired by burn injury (p less than 0.05), but synthesis of IgG by lymphocytes from mesenteric lymph nodes was not affected. There were no significant differences in IgM and IgA synthesis by lymphocytes from spleen between burned animals and controls. The immunoglobulin synthesis in mesenteric lymph nodes did not differ significantly in burned animals compared with controls. The impaired IgG synthesis by lymphocytes from spleen may contribute to increased risk of infection after burn injury.
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PMID:Immunoglobulin synthesis by cultured lymphocytes from spleen and mesenteric lymph nodes after thermal injury. 175 84

In these studies, the mitogen responsiveness of lymphocytes obtained from local gut-associated lymphoid tissues (GALT) and the spleen were evaluated following a 5-day exposure to 7,12-dimethylbenz(a)anthracene (DMBA) at doses of 50 or 150 mg/kg. Phytohemagglutinin and lipopolysaccharide (LPS) responses were suppressed in all lymphoid tissues studied. However, the LPS response in mesenteric lymph nodes and Peyer's Patches seemed to be the most sensitive indicator of immunotoxicity, indicating that B cells appear to be particularly sensitive to DMBA toxicity in the GALT. These studies demonstrate that both splenic tissues and GALT are important targets of immunotoxicity following oral administration of DMBA. Based upon these and past studies we conclude that the total administered dose of DMBA is a more important determinant of immunotoxicity than the length of exposure.
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PMID:Suppression of local gut-associated and splenic mitogen responsiveness of lymphoid cells following oral exposure of B6C3F1 mice to 7,12-dimethylbenz[a]anthracene. 176 29

Despite continuous exposure to gut-derived endotoxin (lipopolysaccharide) under normal conditions, Kupffer cells (KC) fail to generate detrimental cytokine responses. KC function within a unique microenvironment in which high hepatic arginase activities (25 times greater than those activities in the kidney) result in negligible local L-arginine levels. To evaluate the relevance of this profound arginine deficiency on the physiologic function of KC, the kinetics of tumor necrosis factor (TNF-alpha) production and autoregulatory eicosanoid prostaglandin E2 (PGE2) production were compared in lipopolysaccharide-stimulated KC cultured with (1200 mumol/L) and without (10 mumol/L) L-arginine media. In (+)arginine culture the KC TNF-alpha production peaked early before decreasing as PGE2 production increased. In (-)arginine culture, however, KC TNF-alpha production was significantly (p less than 0.01) reduced, whereas PGE2 production was amplified (p less than 0.01). When cyclooxygenase blockade with indomethacin completely prevented KC production of PGE2 in (-)arginine culture, TNF-alpha production was upregulated (p less than 0.001 vs (-)arginine; p not significant vs (+)arginine). These arginine-specific depression of TNF-alpha responses appeared unique to KC because both TNF-alpha and PGE2 levels increased when peritoneal, pleural, and alveolar macrophages were stimulated by lipopolysaccharide in (-)arginine medium. This PGE2-dependent autoregulation of potentially harmful lipopolysaccharide-induced TNF-alpha responses may reflect an evolutionary adaptation by KC to their local hepatic environment and strategic anatomic position in the portal circuit, which optimally removes endotoxin and naturally protects the host.
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PMID:A biologic basis for limited Kupffer cell reactivity to portal-derived endotoxin. 185 31

Infusing pigs with lipopolysaccharide (LPS) decreases superior mesenteric artery blood flow (Qsma), suggesting that mesenteric hypoperfusion may be responsible for LPS-induced alterations in gut mucosal permeability. To test this hypothesis, we studied four groups of anesthetized swine. Group 1 animals (N = 6) were infused with LPS (250 micrograms/kg over 1 hour beginning at 60 minutes) and continuously resuscitated with Ringer's lactate (48 mL/kg per hour). In group 2 (N = 5), Qsma was decreased by 50% by means of a mechanical occluder to mimic the LPS-induced alterations in Qsma observed in group I. Group 3 (N = 5) was included to document our ability to detect ischemia/reperfusion-induced alterations in mucosal permeability; in these pigs, Qsma was decreased in steps to zero flow (at 150 to 210 minutes) and then perfusion was restored (at 210 to 270 minutes). Pigs in group 4 (N = 6) served as normal controls; these animals were resuscitated with Ringer's lactate at the same rate as in group 1 but were not infused with LPS. To assess mucosal permeability, we measured plasma-to-lumen clearances for two markers, chromium 51-labeled edetic acid monohydrate (EDTA) and urea. Loading and maintenance infusions of the markers were given intravenously, and a 20-cm isolated segment of small intestine was continuously perfused at 2 mL/min with Ringer's lactate at 37 degrees C. Results were expressed as the ratio of the clearances for the two probes (CEDTA/CUREA). In group 3, CEDTA/CUREA was 999% +/- 355% of baseline at 270 minutes. In group 1, CEDTA/CUREA was 572% +/- 235% of baseline at 270 minutes. In groups 2 and 4, however, CEDTA/CUREA did not change significantly from the baseline value over the duration of the study. These data suggest that increased mucosal permeability after LPS is due to factors other than (or in addition to) mesenteric hypoperfusion.
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PMID:Increased intestinal permeability in endotoxic pigs. Mesenteric hypoperfusion as an etiologic factor. 189 58

Superior mesenteric arterial perfusion (Q) decreases and gut intramucosal hydrogen ion concentration, [H+], increases in resuscitated normodynamic endotoxic pigs. The present study tested the hypothesis that these adverse phenomena can be prevented by pretreatment with LY171883, a specific leukotriene (LT) D4/E4 receptor antagonist. Pentobarbital-anesthetized pigs (14-18 kg) were instrumented to permit measurement of Q (ultrasonic flow probe) and [H+] (tonometer). Mesenteric O2 delivery (DO2) and consumption (VO2) were calculated from the O2 contents of arterial and superior mesenteric venous blood. At t = -20 min, groups (N = 6) of pigs were pretreated witH LY171883 (10 mg/kg) or vehicle. At t = 0 min, the pigs were infused over 20 min with lipopolysaccharide (LPS; 150 micrograms/kg) and resuscitated for 2 hr with saline (1.2 ml/kg min). Irrespective of treatment group, mean arterial pressure and systemic vascular resistance index decreased significantly after infusion of LPS. In general, cardiac index (CI) was well preserved, although in controls at t = 20, 100, and 120 min, CI decreased significantly with respect to the t = 0 min value. Normal mesenteric Q and DO2 were maintained in the LY171883 group, whereas, in controls, these parameters decreased significantly. Mesenteric VO2 increased transiently but significantly in controls; this phenomenon was abrograted by the LT receptor antagonist. In controls, intramucosal [H+] increased by almost threefold; this adverse effect was significantly ameliorated by LY171883. These data suggest that decreased mesenteric Q and increased intramucosal [H+] may be mediated by LT in this porcine endotoxic shock model.
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PMID:LY171883 preserves mesenteric perfusion in porcine endotoxic shock. 197 68

Insertion mutations were constructed in cloned pmi and rfc genes of Salmonella typhimurium, and these mutations were recombined (singly) into the chromosome of mouse-virulent S. typhimurium C5, displacing the wild-type alleles. Phage sensitivity profiles, lipopolysaccharide analysis, and DNA blotting all confirmed that the replacement events had occurred. The mutations were complemented by plasmid-borne wild-type alleles, as judged by the restoration of wild-type phage plaquing profiles and lipopolysaccharide production (both mutants) and the restoration of pmi-encoded enzyme production (pmi mutant). The virulence, persistence, and immunizing capacities of the mutants fed to mice were compared with those of the wild-type strain and complemented mutants. Both mutants were much reduced in virulence, with the rfc mutant being avirulent even at 10(9) bacteria per mouse. This mutant was also avirulent at up to 10(6) bacteria per mouse when administered intraperitoneally. Both the rfc and pmi mutant strains persisted in the Peyer's patches of the gut after feeding and were capable of colonizing the deeper tissues of the mice from such initial infective foci. Both mutant strains were effective as live oral vaccines (10(7) bacteria or more) against oral S. typhimurium challenge (10(4) 50% lethal doses; 6 x 10(8) bacteria) in mice.
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PMID:Mutations at rfc or pmi attenuate Salmonella typhimurium virulence for mice. 199 12

The purpose of this study was to support the hypothesis that cytokines such as interleukin-1, tumor necrosis factor and interleukin-6 are released by macrophages or monocytes within 1 to 2 hr of phagocytosis of circulating, gut-derived bacterial lipopolysaccharide translocated by acute liver injury. Time courses of fever, neutrophilia and low blood-zinc levels generally attributed to cytokines were quantified after partial (67%) hepatectomy of rats under ether anesthesia. These acute phase responses in hepatectomized rats were compared with those after intravenous injection of exogenous endotoxin and human natural interleukin-1. Fever commenced 30 min after interleukin-1 injection, 4 hr after exogenous lipopolysaccharide injection and 6 hr after 67% liver resection. Similarly, rectal temperatures were significantly elevated in recipient rats 30 min after intravenous administration of donor plasma from hepatectomized animals, indicating that cytokines, not lipopolysaccharide, elicited the febrile response. Neutrophilia was present 1, 2, and 4 hr after interleukin-1 injection, lipopolysaccharide injection and hepatectomy, respectively. Furthermore, the reduction in plasma zinc, which depends on cellular metallothionein synthesis, occurred 4 hr after interleukin-1 administration and 6 hr after lipopolysaccharide injection or partial hepatectomy. Donor plasma from hepatectomized rats also elicited neutrophilia at 1 hr and low blood-zinc levels 4 hr after injection in recipient animals. The timing of these responses, just as for the fever, implies that cytokines and not lipopolysaccharide in the donated plasma elicited the neutrophilia and hypozincemia. Evidence was reviewed that interleukin-1, tumor necrosis factor and interleukin-6 function as hepatotrophic factors and have been identified in the circulation of humans with liver damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute phase responses after acute liver injury by partial hepatectomy in rats as indicators of cytokine release. 211 49


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