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)

The data presented in this paper show that different thymus-independent (TI) antigens have a differential capacity of inducing antibody formation in mouse bone marrow, both after primary and secondary intravenous immunization. Primary immunization with certain TI antigens (e.g., lipopolysaccharide [LPS], TNP-LPS, DNP-Ficoll) induces the appearance of antibody-forming cells not only in the spleen, but also in the bone marrow. A single injection of certain other TI antigens (e.g., pneumococci [Pn], TNP-conjugated detoxified LPS [TNP-dLPS], TNP-conjugated Brucella abortus bacteria [TNP-BA] ), on the other hand, induces antibody formation in the spleen only. After secondary immunization with these TI antigens only TNP-BA induces a PFC response in the bone marrow. Pn, TNP-dLPS and TNP-BA, but also DNP-Ficoll, are unable to induce bone marrow antibody formation after secondary injection of the antigen, in spite of the clear-cut secondary type character of the splenic response. Thus, the absence of a bone marrow PFC response after secondary immunization with these antigens is not due to a failure to induce memory B cells. This data implies that either two subpopulations of memory B cells exist, one giving rise to antibody formation in the spleen and the other accounting for the bone marrow response, or that antibody can selectively inhibit the secondary bone marrow antibody response to certain TI antigens.
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PMID:Antibody formation in mouse bone marrow during secondary type responses to various thymus-independent antigens. 698 19

As proteolipid of the myelin sheath and its parent glial membrane may possible interact with bacterial pyrogen (lipopolysaccharide, LPS) during penetration into the brain, we investigated the interaction of LPS with proteolipid derived from the cerebrum of rabbits, rats and chickens. Intravenous administration of LPS (1 microgram/kg) produced a febrile response in rabbits, but not in rats and chickens. Marked hyperthermia was observed in these three species after intracisternal administration of LPS (0.01-0.1 microgram/kg). Dinitrophenol (30 mg/kg s.c.) induced a high fever in these three species tested, particularly in the chickens. The pyrogenicity of LPS given intravenously to rabbits was inactivated by incubation of LPS with proteolipid in vitro. Inactivation effects of proteolipid extracted from the three species was in the order of: chickens, rats and rabbits. In rats, the inactivation effects of proteolipid from the adult animal were more potent than in the case of newborn animals. The febrile response induced by dinitrophenol and leucocytic pyrogen in rabbits, however, was not suppressed by incubation with proteolipid extracted from the rabbit brain. These results suggest that proteolipids do play an important role in the mechanism of penetration of LPS into the brain.
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PMID:Interactions between bacterial pyrogen and proteolipid extracted from the cerebrum (I). 731 Nov 53

Although the nature of the germinal center reaction during responses to T-dependent antigens has been well documented, much less is known regarding the relationship between germinal centers and T-independent antigens. In this study, germinal-center cell proliferation was determined at specific time points in spleens of C3H/HeN mice following immunization with either the type-1, T-independent antigen dinitrophenol-lipopolysaccharide (DNP-LPS), or the type-2, T-independent antigen DNP-Ficoll. A stathmokinetic technique was employed to assess proliferation in terms of germinal center cell birth rate and morphometry was used to measure actual growth and regression of the germinal center cell population. An estimate of the absolute rate of germinal-center (GC) cell proliferation was derived from these two values. In addition, immunohistochemistry was performed to correlate changes in GC cell proliferation with the presence or absence of antigen within GC. Following immunization with both antigens, there was an initial reduction of proliferation within pre-existing germinal centers which manifested as either GC dissociation (DNP-LPS) or a suppression of birth rates (DNP-Ficoll). This was followed by a period of increased GC cell proliferation in animals immunized with DNP-LPS, but not in those exposed to DNP-Ficoll. GC cell proliferation was then measured in mice treated with cyclosporin A from 1 day before to 2 days after immunization with DNP-LPS. In these animals, the expected increase in GC cell birth rates did not take place. Immunohistochemistry showed that DNP-Ficoll and DNP-LPS were present in GC from 1 day after immunization until the end of the experiment on day 7. Treatment with cyclosporin A did not affect the deposition of DNP-LPS in GC. These results show that only some T-independent antigens are able to stimulate GC cell proliferation, and we propose that this is related to their ability to recruit precursors of GC B cells into the GC reaction. In addition, the results indicate that GC proliferation seen in response to a so-called T-independent antigen is at least partly driven by T cell-derived cytokines.
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PMID:Germinal-center cell proliferation in response to T-independent antigens: a stathmokinetic, morphometric and immunohistochemical study in vivo. 762 68

The major psychoactive and immunosuppressive component of marihuana, delta 9-tetrahydrocannabinol (delta 9-THC), was investigated for its effects on primary humoral immune responses in the B6C3F1 mouse strain. Oral administration of 50-200 mg/kg delta 9-THC produced a selective and dose related inhibition of primary humoral immune responses to the T-cell dependent antigen, sRBC, as measured by the antibody forming cell (AFC) response with no inhibitory effect on humoral responses to the T-cell independent antigen, DNP-Ficoll. A similar profile of immune inhibition was observed following in vitro direct addition of delta 9-THC to naive spleen cell cultures sensitized with defined antigens. delta 9-THC produced a marked and dose related inhibition of the in vitro sRBC AFC response while having no inhibitory effects on T-cell independent responses to either DNP-Ficoll or the polyclonal B-cell activator, lipopolysaccharide. This selective inhibition of the sRBC response was not due to a shift in the peak day of response or a direct cytotoxic effect on spleen cells. In vivo kinetic studies demonstrated that inhibition by delta 9-THC of the sRBC response was most pronounced when drug administration occurred at times surrounding antigen sensitization. To further evaluate the direct effect of delta 9-THC on T-cell function, T-cell proliferative responses to stimulation by anti-CD3 monoclonal antibodies were measured. delta 9-THC was found to produce a marked and dose related inhibition of anti-CD3 mAb-induced T-cell proliferation which was cell density dependent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Delta 9-tetrahydrocannabinol selectively inhibits T-cell dependent humoral immune responses through direct inhibition of accessory T-cell function. 828 37

Soluble antigens derived from the H37Ra strain of Mycobacterium tuberculosis (Ra antigen) induced marginal proliferative response in spleen cells from unsensitized mice. The FDNB derivative of this antigen (Ra-DNP), however, had a marked proliferation-inducing effect. An increase in the population of B-cells but a reduction in the T-cell population was noted in Ra-DNP-treated spleen cell cultures. BSA-DNP derivatives used as control had no effect on mouse spleen cell proliferative activity. Moreover, addition of BSA-DNP along with Ra did not improve the proliferative response to the latter, indicating that in order to obtain proliferative activity, DNP residues must be present on Ra antigens themselves. Thymidine incorporation studies using sorted cell populations indicated that B-cells proliferated in response to Ra-DNP. The effect of Ra-DNP was neither blocked by Polymyxin-B treatment, nor retained by an endotoxin removal column, suggesting that lipopolysaccharide was not responsible for the B-cell mitogenic effect of Ra-DNP. As compared to Ra antigen, Ra-DNP derivative was found to bind more efficiently to B-cells as well as to mouse Ig. Additionally, lymph node cells derived from Ra-sensitized mice proliferated significantly better in response to Ra-DNP. These results indicate that FDNB derivatization of Ra antigen renders it more reactive with B-cells, which may in turn be responsible for a better T-cell reactivity of the derivative, since B-cells can act as antigen-presenting cells. It is possible that DNP residues may facilitate the interaction of Ra antigen with B-cells, perhaps through their Ig receptor.
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PMID:B-cell mitogenic effect of dinitrophenyl derivative of Mycobacterium tuberculosis antigens. 833 Mar 18

This paper reports on the selection of individual carp with a high or low antibody response, in combination with reproduction by gynogenesis, in order to develop well-characterised inbred carp lines consisting of practically unlimited numbers of carp with the same genotype. Two homozygous progenies, previously characterised as having a high or low immune response to dinitrophenyl keyhole limpet haemocyanin (DNP-KLH), were immunised with either a T-dependent (DNP-human serum albumin (DNP-HSA)) or T-independent (trinitrophenyl lipopolysaccharide (TNP-LPS)) hapten-carrier complex. In comparison with the antibody response after DNP-KLH immunisation, the response to DNP-HSA was observed to be highly variable and did not differ between the divergently selected progenies. This suggests that the divergent selection for antibody production to DNP-KLH has been carrier-specific. Immunisation with T-independent TNP-LPS induced a very rapid response which differed between the high and low responders, and likely measured changes in the DNP-specific precursor pool of B cells caused by the selection. A number of selected individuals with a high immune response to DNP-KLH were infected with Trypanoplasma borreli, a haemoflagellate parasite of carp, to examine a possible relationship between the increase in immune responsiveness and disease resistance, but no change could be detected. However, individual homozygous carp were able to escape inbreeding depression and survive the infection. Such carp would be likely candidates for gynogenetic reproduction to obtain viable inbred carp lines.
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PMID:Investigations into the ubiquitous nature of high or low immune responsiveness after divergent selection for antibody production in common carp (Cyprinus carpio L.). 857 93

Antibody production to dinitrophenyl-keyhole limpet haemocyanin (DNP-KLH) served as the immune parameter to divergently select carp (Cyprinus carpio L.) to produce high- and low-responder F1 hybrid lines. Antibody production to trinitrophenyl-lipopolysaccharide (TNP-LPS) and to DNP-KLH were similar in magnitude. By contrast, some high-responder lines were low responders to DNP-human serum albumin, and vice versa. Low-responder carp were relatively susceptible to infection with the parasite Trypanoplasma borreli. This suggested that at least one gene with a major influence on resistance differed between the two homozygous parents (69, 85) used to generate the high- and low-responder homozygous families, respectively. The isogenic lines showed no within-line variation in DNA fingerprints, but differed with respect to their MhcCyca-DAB genes.
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PMID:Characterization of isogenic carp (Cyprinus carpio L.) lines with a genetically determined high or low antibody production. 893 71

Interleukin-12 (IL-12) is a pivotal cytokine that has dramatic effects on cell-mediated immunity. It is now becoming increasingly recognized that IL-12 also strongly controls humoral immunity. We have investigated the mechanism by which IL-12 induces alterations in antibody isotype expression by determining the influence of IL-12 on in vitro immunoglobulin (Ig) production in polyclonally activated murine spleen cell cultures. Cells exposed to IL-12 plus lipopolysaccharide or anti-CD40 monoclonal antibody showed dramatically elevated IgG2a and suppressed IgG1 production compared to cells cultured in the absence of IL-12. IL-12 treatment of spleen cell cultures induced expression of gamma2a germ-line transcripts, consistent with initiation of switch recombination to IgG2a. In addition, exposure of limiting dilution cultures to IL-12 increased IgG2a+ cell precursor frequency. All of the above results were dependent on interferon-gamma (IFN-gamma). However, in the absence of IFN-gamma, IL-12 still had significant effects on Ig secretion. Specifically, IL-12 enhanced IgG1 and IgG2b anti-DNP antibody levels in mice containing specific disruptions in the IFN-gamma gene. Our results suggest that IL-12 induces T helper type 1 and natural killer cells to secrete large amounts of IFN-gamma which then causes B cells to switch to IgG2a and IgG3 production. In addition, IL-12 has direct or indirect effects on B cells that are independent of IFN-gamma. The IFN-gamma-independent effects may include enhancement of Ig expression by post-switched cells.
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PMID:Interleukin-12 acts as an adjuvant for humoral immunity through interferon-gamma-dependent and -independent mechanisms. 929 32

We have studied the effect of nitric oxide (NO) and hydrogen peroxide (H(2)O(2)), two reactive oxygen species (ROS) on histamine release (HR) from RBL-2H3 cells, a rat mucosal-type mast cell line. Marked HR was elicited by antigen (DNP-HSA), calcium ionophore A23187, sodium fluoride or phospholipase C, but not with compound 48/80 or 1,2-dioctanoyl-sn-glycerol. The NO-synthase substrate L-arginine and its inactive enantiomer (D-arginine), each on its own, induced a small but significant increase in HR above the basal level. However, the NO-donors (sodium nitroprusside or NaNO(3)) or the NO-synthase inducer lipopolysaccharide did not induce HR. Moreover, methylene blue (MB), which inhibits guanylate cyclase and N(omega)-nitro-L-arginine (L-NA), an inhibitor of NO synthase, were also without effect on either the basal HR or the L-arginine-induced HR. HR induced by A23187, DNP-HSA, sodium fluoride or phospholipase C was markedly reduced by MB, but mildly by L-NA (both at 1-100 microM). H(2)O(2) (0.01-1.0 mM) on its own did not induce HR, but it had a potent inhibitory effect on DNP-HSA- or A23187-induced HR, which was not reversed by L-NA (1-100 microM). Taken together, it seems that neither the stimulatory nor the inhibitory effects of the NO-related compounds on HR can be attributed to NO, but rather to other mechanisms. The inhibition of HR by H(2)O(2) also does not involve NO and suggests a negative feedback regulatory role for the peroxide in the allergic inflammation.
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PMID:Effects of nitric oxide and hydrogen peroxide on histamine release from RBL-2H3 cells. 1172 90

PI3K (phosphoinositide 3-kinase) I(A) family members contain a regulatory subunit and a catalytic subunit. The p110delta catalytic subunit is expressed predominantly in haematopoietic cells. There, among other functions, it regulates antigen receptor-mediated responses. Using mice deficient in the p110delta subunit of PI3K, we investigated the role of this subunit in LPS (lipopolysaccharide)-induced B cell responses, which are mediated by Toll-like receptor 4 and RP105. After injection of DNP-LPS (where DNP stands for 2,4-dinitrophenol), p110delta(-/-) mice produced reduced levels of DNP-specific IgM and IgG when compared with wild-type mice. In vitro, the proliferation and up-regulation of surface activation markers such as CD86 and CD25 induced by LPS and an antibody against RP105 were decreased. We analysed the activation state of key components of the LPS pathway in B cells to determine whether there was a defect in signalling in p110delta(-/-) B cells. They showed normal extracellular-signal-regulated kinase phosphorylation, but anti-RP105-induced protein kinase B, IkappaB (inhibitor of nuclear factor kappaB) and c-Jun N-terminal kinase activation was severely reduced. This demonstrates that the p110delta subunit of PI3K is involved in the LPS response in B cells and may represent a link between the innate and the adaptive immune system.
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PMID:The p110delta subunit of phosphoinositide 3-kinase is required for the lipopolysaccharide response of mouse B cells. 1549 16


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