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)

A low-toxic lipopolysaccharide (BP-LPS) was isolated from killed Bordetella pertussis (Tohama strain). LD50 of BP-LPS was about 0.8 mg/mouse which was about 10-fold higher than the LD50 of E. coli-LPS(80 micrograms/mouse). Toxicity measured by decrease in body weight of BP-LPS-injected mice was similarly low. BP-LPS had strong antitumor activities against various murine syngeneic tumors, and its systemic administration caused clear regression of such as MM46 mammary carcinoma and Meth A fibrosarcoma. It is noteworthy that a tolerable dosage of BP-LPS (375 micrograms/mouse) showed clear antitumor activity against MH134 hepatoma, which is known to be insusceptible to usual types of BRM including bacterial LPS. These findings suggest that BP-LPS is a promising candidate as an antitumor agent for clinical use. Biological activities of BP-LPS were examined and compared with those of toxic LPS extracted from Escherichia coli and other enterobacteria. Activation or stimulation of macrophages and lymphocytes by these LPS, including TNF induction, was found to be similar. However, activation of human or murine neutrophils, as estimated by neutrophil-adherence assay in vitro, though induced by all other toxic LPS tested, was not induced by BP-LPS. This inability of BP-LPS to activate neutrophils is assumed to be related to its low toxicity.
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PMID:BRM activities of low-toxic Bordetella pertussis lipopolysaccharides. 141 7

The intracerebroventricular (i.c.v.) injection of antisera directed against different sequences of Gs alpha to mice enhanced the antinociceptive potency of the opioids morphine, beta h-endorphin-(1-31) and of the alpha 2-agonist clonidine when studied 24 h later in the tail-flick test. The activity of DAGO, DADLE, DPDPE and [D-Ala2]-Deltorphin II remained unchanged after that treatment. Cholera toxin (0.5 microgram/mouse, i.c.v.), agent that impairs the receptor regulation of Gs transducer proteins promoted comparable changes in the supraspinal analgesia induced by these substances. Six days after a single i.c.v. injection (0.5 microgram/mouse) of pertussis toxin the antinociceptive activity of all the opioids and clonidine appeared diminished. It is concluded that opioids and clonidine promote analgesia after binding to receptors functionally coupled to Gi/G(o) proteins, moreover, the activity of morphine, beta-endorphin and clonidine in this test seems to be counteracted by a process involving activation of Gs alpha transducer proteins.
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PMID:Intracerebroventricular injection of antibodies directed against Gs alpha enhances the supraspinal antinociception induced by morphine, beta-endorphin and clonidine in mice. 144 47

An acellular pertussis vaccine was prepared from pertussis vaccine concentrates by eliminating the cells by centrifugation and subsequent acid precipitation. SDS-PAGE analysis indicated the presence of 17 clearly defined bands including the subunits of pertussis toxin. The acellular preparation was detoxified with glutaraldehyde and lost its undesirable effects (leukocytosis-promoting activity, histamine-sensitizing activity and decrease in weight gain) but retained a very good protective activity (PD50 approximately 2 micrograms protein/mouse). Sera from mice immunized with this preparation indicated an antibody response against the A protomer of pertussis toxin.
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PMID:Characterization and detoxification of an easily prepared acellular pertussis vaccine. Antigenic role of the A protomer of pertussis toxin. 157 19

Cholera toxin, an agent that impairs the function of Gs transducer proteins, was injected (0.5 microgram/mouse, icv) and the antinociceptive activity of opioids and clonidine was studied 24h later in the tail-flick test. In these animals, an enhancement of the analgesic potency of morphine, beta-endorphin and clonidine could be observed. Cholera toxin did not modify the antinociception evoked by the enkephalin derivatives DAGO and DADLE. Pertussis toxin that catalyses the ADP ribosylation of alpha subunits of Gi/Go regulatory proteins was given icv (0.5 microgram/mouse). This treatment reduced the analgesic effect of opioids and clonidine. However, while the analgesia elicited by DAGO, DADLE and clonidine was greatly decreased, the effect of morphine and beta-endorphin was reduced to a moderate extent. It is concluded that Gi/Go regulatory proteins functionally coupled to opioid and alpha 2 receptors are implicated in the efficacy displayed by opioids and clonidine to produce supraspinal analgesia. Moreover, these two receptors are susceptible to regulation by a process that might involve a Gs protein.
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PMID:Cholera toxin and pertussis toxin on opioid- and alpha 2-mediated supraspinal analgesia in mice. 185 Apr 93

We used the alkylating agent N-ethylmaleimide in order to investigate G-proteins linked to release-modulating prejunctional receptors of sympathetic nerves in mouse atria incubated with [3H]-noradrenaline. The receptors tested were facilitatory beta-adrenoceptors and angiotensin II receptors and inhibitory neuropeptide Y receptors. In order to evaluate the specificity of the N-ethylmaleimide treatment, we tested N-ethylmaleimide against the second messenger pathways that are linked to beta-adrenoceptors (adenylate cyclase) and angiotensin II (protein kinase C). The results show that a 60-min preincubation with N-ethylmaleimide (3 microM) abolished the facilitatory effect of isoprenaline (0.1 microM) and angiotensin II (0.1 microM) on the stimulation-induced release of noradrenaline and reduced the inhibitory action of neuropeptide Y (0.3 microM). N-ethylmaleimide had no effect on the stimulatory action of either phorbol dibutyrate (0.01, 0.1 microM), forskolin (10 microM), or a combination of 8-bromo adenosine-3'5'-monophosphate (90 microM) and 3-isobutyl-1-methylxanthine (100 microM). However, at a higher concentration (10 microM), N-ethylmaleimide reduced the facilitatory effect of phorbol dibutyrate (0.1 microM) and the combination of 8-bromo adenosine-3',5'-monophosphate (90 microM) and 3-isobutyl-1-methylxanthine (100 microM). This suggests that N-ethylmaleimide at 3 microM but not 10 microM was selective for receptor-mediated modulation of noradrenaline release without directly affecting the adenylate cyclase (forskolin, 8-bromo adenosine-3',5'-monophosphate + 3-isobutyl-1-methylxanthine) or protein kinase C (phorbol dibutyrate) transduction pathways. In atria from mice pretreated with pertussis toxin (1.5 micrograms/mouse), N-ethylmaleimide preincubation (1 and 3 microM) resulted in a more pronounced reduction of the inhibitory action of neuropeptide Y (0.3 microM). The nature of this interaction is unclear. Since N-ethylmaleimide has been shown in other studies to inactivate G-proteins, the inhibitory effect of N-ethylmaleimide on prejunctional beta-adrenoceptors, angiotensin II receptors and neuropeptide Y receptors of sympathetic nerves may suggest that G-proteins are involved with these receptors, although other effects of N-ethylmaleimide on the receptor coupling processes cannot be ruled out. Moreover, it appears that the concentration of N-ethylmaleimide used is critical since a higher concentration (10 microM) resulted in non-specific effects on signal transduction mechanisms in the present experimental conditions.
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PMID:Prejunctional beta-adrenoceptors, angiotensin II and neuropeptide Y receptors on sympathetic nerves in mouse atria are linked to N-ethylmaleimide-susceptible G-proteins. 217 55

In this study we report that treatment with recombinant human interleukin-1 beta (rIL-1 beta) (10 U per mouse, intraperitoneally) significantly increased the number of inflammatory macrophages in the peritoneal cavity of mice treated with pertussis toxin (PT) (1 micrograms per mouse, intravenously). The administration of rIL-1 beta in a single intraperitoneal dose (10 U per mouse) 1 or 2 days before challenge with PT did not prevent the decrease in the number of inflammatory macrophages in the peritoneal cavity of mice. On the other hand, the simultaneous administration of rIL-1 beta and PT, as well as the administration of rIL-1 beta 24 h after injection of PT, significantly counteracted the inhibitory effect of PT on inflammatory peritoneal macrophages.
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PMID:Effects of recombinant human interleukin-1 beta on accumulation of inflammatory peritoneal macrophages in mice treated with pertussis toxin. 225 36

1. Mouse atria were incubated with [3H]-noradrenaline, and the outflow of radioactivity due to electrical field stimulation (5 Hz, 60 s) was used as an index of noradrenaline release. Angiotensin II (0.01 and 0.1 microM) significantly enhanced the stimulation-induced (S-I) outflow of radioactivity. 2. Phorbol 12-myristate 13-acetate (0.001, 0.03, 0.1 and 1.0 microM), a protein kinase C activating phorbol ester, significantly enhanced the S-I outflow of radioactivity. When angiotensin II (0.1 microM) was present with the concentration of phorbol 12-myristate 13-acetate that was maximally effective in increasing the S-I outflow (0.1 microM), the enhancement of S-I outflow produced by angiotensin II was maintained. 3. Polymyxin B (70 microM), an inhibitor of protein kinase C, significantly inhibited the S-I outflow. Polymyxin B also inhibited the enhancement of the S-I outflow produced by angiotensin II (0.1 microM). 4. In another series of experiments mice were injected with pertussis toxin (1.5 micrograms per mouse), 4 days before their atria were removed. The effectiveness of pertussis toxin pretreatment was determined indirectly using carbachol. Carbachol caused a concentration-dependent fall in both the rate and force of beating of isolated spontaneously beating atria from mice pretreated with vehicle. This effect of carbachol was not seen with atria from mice pretreated with pertussis toxin. 5. Pertussis toxin pretreatment did not alter the enhancement of the S-I outflow of radioactivity produced by angiotensin II (0.01 and 0.1 microM). 6. These results suggest that angiotensin II receptor modulation of noradrenaline release is not mediated through either a pertussis toxin sensitive guanine nucleotide-binding protein or activation of protein kinase C.
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PMID:Effect of phorbol ester and pertussis toxin on the enhancement of noradrenaline release by angiotensin II in mouse atria. 272 Feb 95

1. The alpha 2-adrenoceptor agonist clonidine (0.03 and 0.1 mumol/l) significantly inhibited stimulation-induced overflow of radioactivity from mouse isolated atria preincubated with [3H]-noradrenaline. This effect of clonidine was blocked by idazoxan (0.3 mumol/l) but not prazosin (0.3 mumol/l), indicating that an alpha 2-adrenoceptor was involved. 2. In some experiments mice were injected with pertussis toxin (1.5 micrograms/mouse) 4 days before their atria were removed and subsequently incubated with [3H]-noradrenaline. Alternatively, isolated atria from untreated mice were suspended in Krebs-Henseleit solution, incubated for 16 h with pertussis toxin (1.0 and 4.0 micrograms/ml) or vehicle and subsequently incubated with [3H]-noradrenaline. The effectiveness of pertussis toxin pretreatment was assessed indirectly using carbachol. Carbachol caused a dose dependent fall in both the rate and force of contraction of isolated, spontaneously beating atria from mice pretreated with vehicle in vivo or in vitro. This effect of carbachol was not seen in atria from mice pretreated with pertussis toxin in vivo or in vitro, suggesting that active toxin penetrated the myocardium. 3. Pertussis toxin pretreatment, either in vivo or in vitro did not alter the inhibitory effect of clonidine (0.03 and 0.1 mumol/l), or the facilitatory effect of the alpha-adrenoceptor antagonist phentolamine (1.0 mumol/l), on the stimulation-induced overflow of radioactivity. These results suggest that alpha 2-adrenoceptor modulation of noradrenaline release from sympathetic nerve terminals is not dependent on an inhibitory guanine-nucleotide-binding protein.
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PMID:Pertussis toxin does not attenuate alpha 2-adrenoceptor mediated inhibition of noradrenaline release in mouse atria. 289 Oct 42

Effects of pertussis toxin (PT) and betamethasone on delayed-type hypersensitivity (DTH) in mice were studied. When mice received PT (1 microgram/mouse) at the time of immunization or elicitation, a depression of DTH responses was observed. In addition, when mice received PT five days before and at the time of immunization, the DTH responses were suppressed. The administration of betamethasone along with PT at the time of immunization and elicitation caused an inhibition of DTH responses. These results suggest that PT depressed the DTH responses and that betamethasone suppressed such responses. Based on these findings, possible mechanisms by which PT and betamethasone affect DTH are discussed.
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PMID:Delayed-type hypersensitivity responses in mice treated with pertussis toxin and betamethasone. 322 95

Male BALB/c mice at 8 to 14 weeks of age were divided into three groups: group 1 was immunized with an emulsion of testicular cells (TCs) (10(7)/mouse), complete Freund's adjuvant (CFA), and extract of Bordetella pertussis (BP); group 2 was given CFA and BP injections; and group 3 was given sterile saline injections. Suspensions of TCs and spleen cells (SCs) from each mouse were prepared 4 weeks after the first immunization for a cytotoxic T lymphocyte (CTL) assay. For the antibody-dependent cell-mediated cytotoxicity (ADCC) and antibody-dependent complement-mediated cytotoxicity (ACC) assays, TCs and SCs were prepared from normal male and female mice, respectively. Targets were labeled with Na251 Cr0(4). The interactions of targets (TCs) and effectors (SCs) were conducted at 32.5 degrees C (for CTL, ADCC, and ACC assays) or 37 degrees C (for ACC assay). In the CTL assay, SCs from group 1 and group 2 caused significantly more killing than those from group 3. Specific cytotoxicity in the ADCC assay was only detected in the serum (maximum specific lysis 47.65%) of one mouse. No other cytotoxicity was detectable in 61 serum samples from group 1 (n = 25), group 2 (n = 17), and group 3 (n = 19). In the ACC assay, no significant specific cytolysis was found at different incubation temperatures (32.5 and 37.0 degrees C) in 44 serum samples from the three groups. These results suggest that CTLs are important in the pathogenesis of experimental allergic orchitis (EAO). Adjuvant alone, probably because of breakdown of the blood-testis barrier, causes significant T lymphocyte cytotoxicity to TCs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vitro cell-mediated and complement-mediated cytotoxicity to murine testicular cells. 349 47


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