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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The responsiveness to T-dependent (TD) and T-independent (TI) TNP-antigens of murine splenic B cells previously enriched for antigen-binding cells (ABC) was examined. TNP-TI antigens induced B cell proliferation. TNP-TD antigens did not induce a proliferative response regardless of the physical form or nature of the TNP-TD antigen (e.g., soluble vs particulate, low or high haptenation of carrier, TNP on various insoluble matrices, etc.). TNP-TD antigens were effective in enhancing the response of the TNP-ABC to all concentrations of lipopolysaccharide (LPS) tested, indicating that binding of antigen to surface immunoglobulin alters the LPS responsiveness of the cell. Irradiated, keyhole limpet hemocyanin- (KLH) primed T cells induced a threefold to fourfold greater B cell proliferative response with TNP-KLH than with fluoresceinated KLH (FLU-KLH) or FLU-KLH together with TNP-human serum albumin (TNP-HSA). Therefore, linked recognition appears essential for optimal T cell-mediated B cell proliferation, whereas the induction of B cell proliferation via nonlinked, carrier-activated T cells is a minor component of the response.
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PMID:Activation of antigen-enriched B cells. II. Role of linked recognition in B cell proliferation to thymus-dependent antigens. 660 Feb 45

Lipopolysaccharide-responsive C3H/HeN mice were rendered resistant to a mouse-adapted strain of influenza (Aichi, H(3)N(2)) virus when Propionibacterium acnes was given either intranasally or intraperitoneally several days before virus infection. The time of P. acnes treatment was important since no protection was demonstrated when this agent was given either on the same day as or several days after virus challenge. In contrast, lipopolysaccharide-nonresponsive C3H/HeJ mice were not protected when P. acnes was administered intranasally at any time before infection; however, protection was demonstrated when P. acnes was given by the intraperitoneal route. Depending on the route of inoculation, P. acnes induced several distinctive immunological responses in the lungs of both C3H/HeN and C3H/HeJ mice. Intranasal inoculation was more effective in activating pulmonary macrophages in C3H/HeN than in C3H/HeJ mice. In contrast, intraperitoneal inoculation activated pulmonary natural killer cells in both mouse lines but did not activate pulmonary macrophages.
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PMID:Enhancement of natural resistance to influenza virus in lipopolysaccharide-responsive and -nonresponsive mice by Propionibacterium acnes. 683 17

The data are presented on studying the production of antibodies to influenza A (H3N2) virus by lymphoid cells of the amygdaline tonsils and mediastinal lymph nodes in vitro during stimulation of these cells with influenza virus or lipopolysaccharide of typhoid bacteria.
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PMID:[Production of antibodies to influenza virus A by human lymphoid cells in vitro]. 687 60

Experiments were performed to serve as a basis for analyzing the immune responses of the host to a viral respiratory tract infection. In a comparative study, inbred BALB/c and nude (athymic mice bred on a BALB/c background) mice were infected intranasally with mouse adapted A/Port Chalmers/1/73 influenza virus. Survival was prolonged in the nude mice (16 days vs 10 days for BALB/c mice, t = 3.5, p less than 0.01), but significantly fewer of the nude mice survived 21 days (16% vs 42% of BALB/c mice). In addition, virus persisted longer in the lungs of nude mice (5.8 log10 of infectious virus on day 21 vs no detectable virus in BALB/c mice) and lung pathology progressed more slowly but lasted longer in nude mice, as measured by immunofluorescent and histologic examination of pulmonary tissue. Antibody production was significantly lower and there was no cytotoxic T cell response detected in lymphoid cells prepared from the spleens, peripheral blood, or the lung after the infection of nude mice. A significant increase in the number of lymphocytes isolated from the lung was observed by day 7 (t = 5.8, p less than 0.001) in the BALB/c mice but not until day 14 (t = 4.9, p less than 0.001) in the nude mice. Lymphocytes from nude mice did not respond to influenza virus antigens or Concanavalin A (Con A) but did respond to lipopolysaccharide (LPS), whereas lymphocytes from BALB/c mice responded to all 3 preparations.
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PMID:Recovery from a viral respiratory infection. I. Influenza pneumonia in normal and T-deficient mice. 697 Feb 11

Men exposed to high concentrations of bacterial single-cell protein (Pruteen) dust have complained of "sticky eyes" and influenza-like symptoms. Over four years, surveillance of a work force of 70 men with a programme that included a respiratory health questionnaire, skin prick testing, serum testing for precipitating antibodies, lung function measurements, and chest radiography has shown no evidence of allergic reaction or of exposure-related deterioration in lung function. The symptoms experienced may be attributable to exposure to lipopolysaccharide. The results show that Pruteen can be produced and handled without adverse effects on health, provided that adequate measures are taken to prevent exposure to high concentrations of dust.
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PMID:Lack of allergic reactions in workers exposed to Pruteen (bacterial single-cell protein). 706 35

Aged mice of the CBA/Ca strain, 15 months of age, and A/J mice, 17 months of age, exhibited impaired lymphoblastogenic response to concanavalin A but not to lipopolysaccharide. This defective cellular responsiveness was not accompanied by decreased antibody response to protein antigen or decreased ability to develop delayed hypersensitivity to picryl chloride. An increased susceptibility to influenza virus infection given intranasally was noted in the aged mice as compared with young animals. Such virus infection also impaired the lymphoblastogenic response to mitogens. Surprisingly, the virus infection in aged animals was less lethal after a subsequent infection with a small inoculum of Listeria bacteria.
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PMID:Protective effect of sublethal intraperitoneal Listeria infection secondary to intranasal influenza infection in aged immunodeficient mice. 719 67

This study characterized body temperature (Tb), locomotor activity (Act), and feeding behavior under normal conditions and following injection with lipopolysaccharide (LPS) or inoculation with live influenza virus of transgenic C57/black mice deficient in interleukin-1 beta (IL-1 beta). Tb and Act in freely moving mice were measured by biotelemetry. Mice deficient in IL-1 beta had normal circadian rhythm of Tb but were less active than their control counterparts. Mice injected with LPS (2.5 mg/kg i.p.) responded with a prompt decrease of Tb, which lasted approximately 10 h, followed by a fever in which Tb reached a peak at approximately 24 h postinjection. There was no difference between groups in the early drop of Tb after the LPS; however, the 24-h peak of Tb was lower in IL-1 beta-deficient mice. The anorexic effects of LPS and influenza infection were similar in both groups of mice. In mice given influenza virus (17.5 plaque-forming units, median lethal dose), Tb and Act gradually decreased. The fall of Tb was smaller in the transgenic mice. The mice deficient in IL-1 beta displayed a higher mortality rate due to influenza infection than the control mice. We conclude that deficiency in IL-1 beta results in lower fever following the LPS injection and in impairment of the defense response to infection with influenza.
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PMID:Thermal and behavioral effects of lipopolysaccharide and influenza in interleukin-1 beta-deficient mice. 750 24

The design of an adjuvant for eliciting a thymus-dependent response to LPS, a well-defined thymus-independent antigen, is presented. Hybrid liposomes containing LPS and HA2 peptide from the hemagglutinin protein of influenza virus within the liposome bilayer were prepared (LPS/HA2 liposomes). The HA2 polypeptide contains epitopes recognized by T-helper lymphocytes and T-cytotoxic lymphocytes. Outbred mice immunized with LPS/HA2 liposomes produced anti-LPS-specific IgG responses. IgG subclass analysis indicated that IgG1, IgG2, and IgG3 antibodies were produced by these animals. LPS liposomes (liposomes without HA2) stimulated a T-independent response only. This was demonstrated by the detection of IgG3 but not IgG1 or IgG2 in serum of mice immunized with LPS liposomes. These results support the concept that the simultaneous incorporation into liposomes of a polypeptide with T-cell recognition sites along with a T-independent antigen can lead to the generation of cognate T-cell help for the T-independent antigen. The synthesis and characterization of a neo-lipopolysaccharide T-independent antigen for incorporation in hybrid HA2 liposomes are also presented. Findings are discussed relative to the liposome model used and implications for development of vaccines for use in humans.
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PMID:Liposomes that provide T-dependent help to weak antigens (T-independent antigens). 752 35

Infection of murine PU5-1.8 macrophages and human monocytes by influenza A virus was associated with virus replication, release of tumor necrosis factor-alpha (TNF-alpha) and subsequent cell death. In the presence of small and by itself rather inefficient concentrations of lipopolysaccharide (LPS) or free lipid A (1 to 10 ng/ml), TNF-alpha production of virus-infected macrophages was strongly potentiated. LPS-triggered and enhanced TNF-alpha release from virus-infected macrophages was neither due to increased cell survival nor altered virus replication, potentiated TNF-alpha gene transcription, release of intracellularly stored TNF-alpha or shifts in the kinetics of TNF-alpha secretion. Influenza A virus infection alone induced a massive TNF-alpha mRNA accumulation which, however, was only weakly translated into bioactive TNF-alpha protein. When these virus-primed macrophages were exposed to LPS either simultaneously or up to 4 h after infection, an efficient and high translation into TNF-alpha protein occurred. Although the LPS-induced biochemical pathways leading to an augmented TNF-alpha production by virus-infected macrophages still remains unsolved, the findings suggest that the frequently observed serious clinical complications in the course of combined influenza A virus and bacterial infections may be due, at least in part, to an excessive release of cytokines such as TNF-alpha.
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PMID:The potentiating effect of LPS on tumor necrosis factor-alpha production by influenza A virus-infected macrophages. 768 36

Influenza A virus nucleoprotein (NP) was integrated into immunostimulating complexes (ISCOMs) after attachment of bacterial lipopolysaccharide to the antigen. Oral immunization with these NP-ISCOMs protected mice fully against an otherwise lethal challenge infection with an unrelated influenza virus subtype without the appearance of severe clinical signs or extensive pathological lesions in the lungs. Mice immunized with analogous bovine serum albumine-incorporated ISCOMs all died. After oral immunization, high titers of NP-specific antibodies, particularly IgA, could be detected in the bronchoalveolar fluid and in the blood serum. No cytotoxic lymphocytes could be demonstrated in the spleens or the lungs of vaccinated mice, and no anti-NP antibody-dependent cytolysis of infected host cells was mediated by complement or in the form of an antibody-dependent cell cytotoxicity. However, a vigorous delayed-type hypersensitivity reaction was produced after probing vaccinated animals with purified NP. No comparable protective immunity or antibody response was induced by a strictly intragastric administration of NP-ISCOMs. It appears, therefore, that the general and local immune response in the lungs was primarily stimulated through contact of NP-ISCOMs with the mucous membrane of the oro-pharyngeal cavity and that cytotoxic effects did not play a major role for the establishment of the protective immunity. Partial protection against a lethal challenge was observed in chickens immunized with NP-ISCOMs in the drinking water.
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PMID:Protection of mice against an influenza virus infection by oral vaccination with viral nucleoprotein incorporated into immunostimulating complexes. 771 38


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