Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A comparison was made of seven recognized adjuvants, Freund's incomplete and complete, alhydrogel, Corynebacterium parvum, Bordetella pertussis, muramyl dipeptide and saponin, administered with BSA or SRBC by the S.C. route of immunization. Strong selectivity as well as differences in potency were revealed in relation to these two antigens. Only FIA, FCA, alhydrogel and MDP promoted the primary response to 50 microgram of BSA, and FIA was significantly superior to FCA. Immunological memory to a low dose (0.5 microgram) of BSA, which did not evoke a primary response with any adjuvant, was potentiated by alhydrogel and by MDP and, relatively poorly, by FIA. Radioimmunoelectrophoresis showed that potentiation of the response with MDP was confined to IgG1, whereas alhydrogel, FIA and FCA stimulated both IgG1 and IgG2. Saponin was outstandingly the best adjuvant for both primary and secondary haemagglutinin responses to SRBC. Of the others, alhydrogel for the primary, and alhydrogel and B. pertussis for the secondary were active to a lesser degree. The results show that the relative potency of adjuvants differs markedly according to the antigen used, and suggest that saponin may be a particularly effective adjuvant for antigens in cell membranes.
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PMID:The comparative selectivity of adjuvants for humoral and cell-mediated immunity. I. Effect on the antibody response to bovine serum albumin and sheep red blood cells of Freund's incomplete and complete adjuvants, alhydrogel, Corynebacterium parvum, Bordetella pertussis, muramyl dipeptide and saponin. 624 82

Specific anti-dinitrophenyl (DNP) response to DNP-conjugated L-glutamine60-L-alanine30-L-tyrosine10 (DNP-GAT) was obtained in GAT-responder mice by using synthetic N-acetylmuramyl-L-alanyl-D-isoglutamine (MDP) as adjuvant. Significant levels of anti-DNP antibodies were observed during a secondary response to DNP-GAT, when both antigen and MDP were used for priming. In this system, MDP was able to prime the carrier-specific T cells but not the hapten specific B cells. The study of the isotypic pattern of the anti-DNP response shows that MDP stimulates only the appearance of specific anti-DNP IgG1 plaque-forming cells. Anti-DNP plaque-forming cells were stimulated in animals primed with DNP-GAT in Freund's complete adjuvant or in Maalox-pertussis and used as control IgG1, IgG2a, and IgG2b.
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PMID:Stimulation of the in vivo dinitrophenyl antibody response to the DNP conjugate of L-glutamic acid60-L-alanine30-L-Tyrosine10 (GAT) polymer by a synthetic adjuvant, muramyl dipeptide (MDP): target cells for adjuvant activity and isotypic pattern of MDP-stimulated response. 696 89

The glycosyl-phosphatidylinositol anchored protein, membrane dipeptidase (EC 3.4.13.19) is released from the surface of 3T3-L1 adipocytes in response to insulin treatment through the action of a phospholipase C. The present study investigates the role of guanine-nucleotide binding proteins (G-proteins) in this process. Treatment of permeabilized 3T3-L1 adipocytes with GTPgammaS did not cause release of membrane dipeptidase into the medium, while GDPbetaS did not inhibit the insulin-stimulated release of membrane dipeptidase. Other activators of G-proteins, including the tetradecapeptide mastoparan, pertussis toxin and AlF3, also caused no significant release of membrane dipeptidase from the surface of the 3T3-L1 adipocytes. From these observations it is concluded that G-proteins are not involved in the insulin-stimulated release of membrane dipeptidase. Although X-Pro aminopeptidase (EC 3.4.11.9) is GPI-anchored in 3T3-L1 adipocytes as shown by digestion with bacterial phosphatidylinositol-specific phospholipase C, it was not released upon insulin treatment of the cells, indicating that only a subset of the GPI-anchored proteins are susceptible to insulin-stimulated release.
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PMID:Insulin stimulates the release of a subset of GPI-anchored proteins in a G-protein independent manner. 1082 37

The purpose was to study the effects of macrophage depletion with liposomal dichloromethylene-diphosphonate (Cl(2)MDP-lip) on inflammation and leukocyte-endothelium interaction in experimental melanin-protein induced uveitis (EMIU). Lewis rats (n = 48) were immunized with melanin-associated protein in complete Freund's adjuvant and pertussis toxin. Control groups received adjuvants without the antigen (n = 12) or no injection (n = 6). Animals received treatment with either CL(2)MDP-lip or empty liposomes (empty-lip) on day -2, 1, 4, 6 and 8. Leukocytes were stained with rhodamine 6G i.v. and intravital fluorescence microscopy (IVM) was performed on day 4, 6, 8 and 10 to quantify leukocyte rolling and arrest. After IVM, the cell count and protein concentration were determined in aqueous humor and plasma levels of TNF-alpha and IFN-gamma were measured by ELISA. In EMIU, leukocyte rolling increased on day 4 (10.0 +/- 1.2 cells min(-1)vs baseline of 5.7 +/- 0.7 cells min(-1), mean +/- S.E.(M.)) and peaked on day 8 (40.8 +/- 4.2 cells min(-1);P < or = 0.05). Leukocyte arrest was increased on day 8 (175.4 +/- 18.2 cells mm(-2)vs baseline of 59.7 +/- 7.1 cells mm(-2);P < or = 0.05) and day 10 (371.7 +/- 30.7 cells mm(-2)). CL(2)MDP-lip prevented leukocyte rolling (day 10: 16.6 +/- 1.8 cells min(-1)vs 30.7 +/- 2.9 cells min(-1); CL(2)MDP-lip vs untreated EMIU;P < or = 0.05) and arrest (day 8: 88.3 +/- 13 cells mm(-2); day 10: 128.5 +/- 12.9 cells mm(-2);P < or = 0.05). Empty-lip had no effect on leukocyte rolling (day 10: 34.8 +/- 4.2 cells min(-1)) or arrest (day 8: 159.3 +/- 12.9 cells mm(-2), day 10: 421.2 +/- 41.6 cells mm(-2)). CL(2)MDP-lip completely suppressed leukocyte emigration (11 +/- 2 cells microl(-1)vs 100 +/- 29 cells microl(-1); CL(2)MDP-lip vs empty-lip;P < or = 0.05) and protein extravasation into aqueous humor (2.7 +/- 0.3 mg ml(-1)vs 14.2 +/- 2.1 mg ml(-1); CL(2)MDP-lip vs empty-lip;P < or = 0.05), abrogated the TNF-alpha response (32.5 +/- 2.7 pg ml(-1)vs 954.9 +/- 216.3 pg ml(-1); CL(2)MDP-lip vs untreated EMIU;P < or = 0.05) and caused an attenuated and delayed elevation of IFN-gamma. CL(2)MDP-lip prevented the inflammatory reaction of EMIU and inhibited the increase of leukocyte-endothelium interaction in iris vessels. Our findings emphasize the pivotal role macrophages play in the initiation of autoimmune disease.
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PMID:Macrophage depletion prevents leukocyte adhesion and disease induction in experimental melanin-protein induced uveitis. 1142 67

The acidic dipeptide N-acetylaspartylglutamate (NAAG) is the most prevalent peptide in the central nervous system. NAAG is a low potency agonist at the NMDA receptor, and hydrolysis of NAAG yields the more potent excitatory amino acid neurotransmitter glutamate. beta-NAAG is a competitive inhibitor of the NAAG hydrolyzing enzyme N-acetylated alpha-linked acidic dipeptidase (NAAG peptidase activity) or glutamate carboxypeptidase II, and may also act as a NAAG-mimetic at some of the sites of NAAG pharmacological activity. Since NAAG has been shown to have neuroprotective characteristics in a number of experimental preparations, it is the purpose of the present study to specifically evaluate the possible efficacy of NAAG and beta-NAAG against NMDA- and hypoxia-induced injury to spinal cord mixed neuronal and glial cell cultures. NAAG (500-1000 microM) protected against NMDA- or hypoxia-induced injuries to spinal cord cultures, and the nonhydrolyzable analog beta-NAAG (250-1000 microM) completely eliminated the loss of viability caused by either insult. Both peptides also attenuated NMDA-induced increases in intraneuronal Ca(2+). Nonspecific mGluR antagonists, pertussis toxin, a stable cAMP analog, and manipulation of NAAG peptidase activity did not by themselves alter cell damage and did not influence the neuroprotective effects of NAAG. NAAG was not protective against kainate- or AMPA-induced cellular injury, while beta-NAAG was partially neuroprotective against both insults. At 2 mM, NAAG and beta-NAAG reduced neuronal survival and increased intraneuronal Ca(2+); these effects were only marginally attenuated by dizocilpine and APV. The results indicate that NAAG and beta-NAAG protect against excitotoxic and hypoxic injury to spinal cord neurons, and do so predominantly by interactions with NMDA and not mGluR receptors.
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PMID:N-acetylaspartylglutamate and beta-NAAG protect against injury induced by NMDA and hypoxia in primary spinal cord cultures. 1457 76