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

Weanling male Lewis Mai F rats and A/J mice were fed semi-purified diets either adequate or deficient in essential fatty acids (EFA) for 50-60 days. After death livers were excised, the lipids were extracted, and the fatty acid profile was determined. Groups of rats and mice were immunized by injection with sheep red blood cells (sRBC) either i.v. or i.p. One group of rats received an injection of sRBC plus Bordetella pertussis organisms. The plaque-forming cell response (PFC) of all groups was determined. Samples of mouse spleens were analyzed for prostaglandin F2 alpha. EFA-deficient rat and mice liver fatty acid profiles showed elevated levels of omega 7 and omega 9 fatty acids and decreased omega 6 fatty acids. The fatty acid profiles of mice differed quantitatively from the rats. As determined by the ratios of 18:0 to 18:2 omega 6 and 18:2 omega 6 to 20:4 omega 6 mice showed a higher delta 9 and a lower delta 6 desaturase activity. When the antigen was injected i.v. the EFA-deficient animals of both species showed an increased PFC response compared to controls, but when it was injected i.p. there was no difference between dietary groups. The PFC response in rats receiving B. pertussis increased dramatically but the difference between dietary groups was abrogated. As had been previously shown in rats the increase in PFC response in the mice immunized by the i.v. route correlated with a decreased synthesis of PGF2 alpha by the spleen.
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PMID:Humoral immunity in essential fatty acid-deficient rats and mice: effect of route of injection of antigen. 631 45

Continued treatment with monoclonal anti-IgD (Ig-5a) from birth in BALB/c mice causes a markedly increased responsiveness to i.v. injected dinitrophenylated ovalbumin (DNP-OVA) with Bordetella pertussis at the age of 8 weeks. The 19S plaque-forming cell (PFC)/spleen response is particularly enhanced, 6-8-fold, but all the other isotypes also show increases of 2-6-fold, including IgA and IgE. Both primary and secondary PFC responses and serum antibody titers are enhanced. After transfer of spleen cells from anti-Ig-treated mice to irradiated recipients the IgM/IgG ratio becomes similar to that of controls. In contrast, the response of anti-IgD-treated mice to i.p. immunization with either 0.2 or 100 micrograms DNP-OVA plus alum is reduced by approximately 80% for each Ig isotype except IgM and remains low upon transfer of spleen cells to recipients. It is concluded that the paucity of B cells in peripheral lymph nodes of the anti-IgD-treated mice causes the low responsiveness to i.p. immunization, but that the IgD- B cells in the spleen are quite able to respond and are, in fact, more responsive than IgD+ B cells. This increased responsiveness, together with the higher IgM/IgG ratios for all Ig isotypes and an otherwise similar order of isotype distribution (gamma 1 greater than gamma 2b greater than gamma 2a = epsilon greater than or equal to alpha) as in controls, suggests that a hyperresponsive, but less mature IgD- B cell population is selectively produced in the spleens of mice treated with anti-IgD from birth.
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PMID:Physiology of IgD. III. Effect of treatment with anti-IgD from birth on the magnitude and isotype distribution of the immune response in the spleen. 660 69

The ability of DTP (diphtheria, tetanus, pertussis) vaccine to stimulate IgG-plaque forming cells (PFC) in mice was markedly inhibited by human leukocyte and mouse fibroblast interferon (IF). This effect of IF was not dose-dependent. The maximum inhibitory effect of human IF was observed on Day 10 after the administration of the vaccine. The inhibition of IgM-PFC was more severe when human IF was used. Although IF abrogated the effect of DTP vaccine on IgG-PFC, at the same time it stimulated PFC in the control group of non-vaccinated animals. The administration of DTP vaccine decreased IgM-PFC on Day 5, the effect was enforced by the addition of both human and mouse IF. IF decreased IgM-PFC in the control group. Small and large doses of DTP suppressed the leukocyte adherance inhibition (LAI) on Day 5 after administration of the vaccine, the effect was not affected by addition of IF. The suppressive effect of DTP was lost on Day 10 when addition of IF increased the percent of LAI in all experimental groups. Thus IF appears to interfere with the effect of DTP and selectively modulate the different immune responses.
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PMID:Interferon as an in vitro modifier of immune responses induced by combined vaccine (DTP) in mice. 668 44

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 role of ion channel activity in the response of rat pituitary lactotrophs and gonadotrophs to dopamine (DA) and GnRH, respectively, was investigated. Single lactotrophs and gonadotrophs were unambiguously identified with the reverse hemolytic plaque assay, and recordings of membrane potential and current were obtained using whole-cell and single-channel patch-clamp techniques. In lactotrophs, DA inhibited spontaneous electrical activity by activating a K+ conductance that hyperpolarized the cells. A 50 pS K+ channel underlies this response and was activated following agonist binding to a D2 type receptor via a "direct" interaction with a pertussis toxin-sensitive G-protein. In gonadotrophs, GnRH triggers rhythmic hyperpolarizations due also to a K+ conductance increase. The K+ channel underlying the GnRH response is an apamin-sensitive, Ca(2+)-activated channel. Although both agonists produce hyperpolarizations in their respective target cells via K+ channel activation, differences in intracellular calcium response probably discriminate the stimulatory (GnRH) and inhibitory (DA) actions on hormone secretion. Each K+ channel type plays a different role in modulating the intracellular Ca2+ levels to yield these actions.
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PMID:Modulation of ion channels underlying excitation-secretion coupling in identified lactotrophs and gonadotrophs. 767

Recent findings indicate that low concentrations of dopamine (DA) stimulate the secretion of prolactin (PRL) in vitro. In this study, we found that low concentrations of the highly-specific DA D2 receptor agonist, quinpirole hydrochloride (LY) stimulate PRL secretion in female rats, assessed by reverse hemolytic plaque assay. Low concentrations of LY (10(-12), 10(-10) M) increased the mean plaque area and increased the fraction of lactotrophs forming large plaques. On the other hand, higher concentrations of LY (10(-8), 10(-6) M) reduced the mean plaque size. Treatment of cells with 10(-6) M LY produced a unimodal distribution of small plaques. Low concentrations of LY (10(-12), 10(-10) M) with TRH (10(-7) M) produced an additive effect on TRH-induced PRL release. Pretreatment of anterior pituitary cells with pertussis toxin (30 ng/ml, 24 h) inhibited the LY-stimulated increase in plaque area. These findings indicate that very low concentrations of DA agonist stimulate the secretion of PRL per cell, and that the stimulatory effects of DA agonist on PRL secretion may be mediated by a pertussis toxin-sensitive G protein.
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PMID:The stimulatory and inhibitory effects of quinpirole hydrochloride, D2-dopamine receptor agonist, on secretion of prolactin as assessed by the reverse hemolytic plaque assay. 810 Sep 80

1. The involvement of guanine nucleotide binding proteins in the coupling of D2 dopamine (DA) receptors to single potassium channels was examined in rat pituitary lactotrophs. 2. Lactotrophs were unambiguously identified by the reverse haemolytic plaque assay (RHPA) and membrane potentials, whole-cell and single channel currents recorded using patch electrode methods. 3. DA or the D2 selective agonist, quinpirole, induced the opening of single K+ channels in cell-attached patches underlying robust hyperpolarizations of membrane potential in single cells. 4. Both whole-cell and single channel responses were independent of Ca2+ or cAMP concentrations. 5. Pertussis toxin (PTX) pretreatment (50-250 ng/ml, 6-12 h) blocked the action of DA on lactotroph membrane potential and uncoupled D2 receptors from single K+ channels in cell-attached patches. 6. Internal dialysis with GDP beta S (guanosine 5'-O-(2-thiodiphosphate) greatly reduced whole-cell responses to DA in a dose-dependent manner. 7. Internal dialysis of lactotrophs with GTP gamma S (guanosine 5'-O-(3-thiotriphosphate) potentiated DA responses in a dose-dependent manner while rendering the responses irreversible at higher doses. 8. DA (100 nM) or quinpirole (10 microM) activated K+ channels in excised outside-out membrane patches that were identical to those identified in cell-attached patches in terms of conductance and gating kinetics. 9. It is proposed that D2 receptors are coupled to non-voltage-dependent K+ channels by G proteins of the Gi/Go class and that this coupling is via a direct, membrane delimited pathway.
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PMID:Guanine nucleotide binding proteins mediate D2 dopamine receptor activation of a potassium channel in rat lactotrophs. 839 73

Monocyte chemoattractant protein-1 (MCP-1) is a C-C chemokine thought to play a major role in recruiting monocytes to the atherosclerotic plaque. Tissue factor (TF), the initiator of coagulation, is found in the atherosclerotic plaque, macrophages, and human aortic smooth muscle cells (SMC). The exposure of TF during plaque rupture likely induces acute thrombosis, leading to myocardial infarction and stroke. This report demonstrates that MCP-1 induces the accumulation of TF mRNA and protein in SMC and in THP-1 myelomonocytic leukemia cells. MCP-1 also induces TF activity on the surface of human SMC. The induction of TF by MCP-1 in SMC is inhibited by pertussis toxin, suggesting that the SMC MCP-1 receptor is coupled to a Gi-protein. Chelation of intracellular calcium and inhibition of protein kinase C block the induction of TF by MCP-1, suggesting that in SMC it is mediated by activation of phospholipase C. SMC bind MCP-1 with a Kd similar to that previously reported for macrophages. However, mRNA encoding the macrophage MCP-1 receptors, CCR2A and B, is not present in SMC, indicating that they possess a distinct MCP-1 receptor. These data suggest that in addition to being a chemoattractant, MCP-1 may have a procoagulant function and raise the possibility of an autocrine pathway in which MCP-1, secreted by SMC and macrophages, induces TF activity in these same cells.
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PMID:Tissue factor is induced by monocyte chemoattractant protein-1 in human aortic smooth muscle and THP-1 cells. 935 21

The gastric mucosa is an important portal of entry for lymphocytic choriomeningitis virus (LCMV) infections. Within hours after intragastric (i.g.) inoculation, virus appears in the gastric epithelia, then in the mesenteric lymph nodes and spleen, and then in the liver and brain. By 72 h i.g.-inoculated virus is widely disseminated and equivalent to intravenous (i.v.) infection (S. K. Rai, B. K. Micales, M. S. Wu, D. S. Cheung, T. D. Pugh, G. E. Lyons, and M. S. Salvato. Am. J. Pathol. 151:633-639, 1997). Pretreatment of mice with a G protein inhibitor, pertussis toxin (PTx), delays LCMV dissemination after i.g., but not after i.v., inoculation. Delayed infection was confirmed by plaque assays, by reverse transcription-PCR, and by in situ hybridization. The differential PTx effect on i.v. and i.g. infections indicates that dissemination from the gastric mucosa requires signals transduced through heterotrimeric G protein complexes. PTx has no direct effect on LCMV replication, but it modulates integrin expression in part by blocking chemokine signals. LCMV infection of macrophages up-regulates CD11a, and PTx treatment counteracts this. PTx may prevent early LCMV dissemination by inhibiting the G protein-coupled chemotactic response of macrophages infected during the initial exposure, thus blocking systemic virus spread.
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PMID:Dissemination of lymphocytic choriomeningitis virus from the gastric mucosa requires G protein-coupled signaling. 976

In lactating rats, suckling renders mammotropes more responsive to prolactin (PRL)-releasing stimuli and less responsive to PRL-inhibiting secretagogues. We have previously shown that a decrease in the activity of protein phosphatase 2A (PP2A) may be responsible for the decrease in responsiveness to the inhibitory secretagogue dopamine (DA). In our present experiments, we have studied the involvement of the adenylate cyclase (AC), stimulatory and inhibitory GTP-binding proteins and also the role of PP2A in the sensitization phenomenon. Pituitary cells obtained from mother rats separated from their pups for 4 h prior to dispersion (non-suckled), suckled for 10 or 30 min after the separation period (suckled) and without separation (continual suckling) were incubated in the presence of different doses of forskolin to activate AC and DA. In a further study, pituitary cells of non-suckled rats were pretreated with cholera toxin (CTX) or pertussis toxin (PTX) and tested for the stimulatory action of forskolin or TRH on PRL release. Ocadaic acid (OA) pretreatment has been used to investigate the involvement of PP2A. Hormone secretion was measured by the reverse hemolytic plaque assay (RHPA). Our results have shown that cells from non-suckled rats were unresponsive to forskolin. A 10-min suckling stimulus sensitizes pituitary mammotropes to respond with a PRL release to a dose-dependent activation of AC by forskolin. This sensitization of AC becomes a permanent feature of the cells when suckling continues for an additional 20 min. We have also found that pituitary mammotropes from non-suckled dams respond to forskolin or TRH with PRL release when they were preincubated with either PTX or the PP2A inhibitor OA. It clearly indicates that the non-responsive pituitary can be shifted to the responsive stage by uncoupling of inhibitory G-protein from its receptor as well as by inhibition of PP2A. This latter finding, consonant with our previous results, suggests that suckling may cause selective changes in the function of G(i) of mammotropes due to a rapid phosphorylation which can remove tonic, GTP-dependent inhibitory function.
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PMID:Inhibition of protein phosphatase 2A (PP2A) mimics suckling-induced sensitization of mammotropes: involvement of a pertussis toxin (PTX) sensitive G-protein and the adenylate cyclase (AC). 1037 12


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