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)

The influence of bacterial and synthetic peptidoglycans on the toxicity of acellular pertussis preparations (APP) has been studied in the mouse weight gain test and in the endotoxic shock development test on mice treated with Actinomycin D. The data obtained in these tests indicate that the immunomodulators (IM) under study are capable of changing (increasing or decreasing, depending on the dose) the toxic properties of APP. The antitoxic action of IM, established in this study, depends on the combination of the doses of IM and APP and the time elapsed from the time of immunization. The possibility of using these IM in a dose of 0.0001 microgram for reducing the LD50 of APP has been established. The use of IM belonging to the group of bacterial synthetic peptidoglycans for the development of acellular pertussis vaccines with reduced reactogenicity has been shown to hold much promise.
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PMID:[The effect of bacterial and synthetic peptidoglycans on the toxicity of a cell-free pertussis preparation]. 233 Jul 81

Toxigenic bacteria such as Bordetella pertussis and Staphylococcus aureus have been implicated in some cases of sudden infant death syndrome (SIDS). We have previously demonstrated that the Lewis(a) antigen is an epithelial cell receptor for S. aureus, and this study demonstrated that Lewis(a) on human monocytes is also a receptor for staphylococcal enterotoxin B (SEB). Values obtained in assays for production of TNF-alpha and nitric oxide were greater for monocytes treated with SEB compared with those treated with lipopolysaccharide (LPS). Exposure to LPS increased the expression of Lewis(a) on monocytes. These results are discussed with reference to the reported enhancement of endotoxic shock by pyrogenic toxins.
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PMID:Lewis antigen expression on human monocytes and binding of pyrogenic toxins. 791 70

1. Antioxidants can exert protective effects in endotoxic shock by either a reduction of the oxidant damage or attenuation of Tumour Necrosis Factor (TNF-alpha) production. 2. Lazaroids are a family of compounds that inhibit lipid peroxidation. Besides, they can also reduce TNF-alpha. U-83836E is a new lazaroid lacking the glucocorticoid ring. 3. Aim of our study was to investigate the effect of U-83836E on TNF-alpha production either in vivo or in vitro. Endotoxic shock was produced in male rats by a single intravenous (i.v.) injection of 20 mg kg(-1) of S. enteritidis lipopolysaccharide (LPS). LPS administration reduced survival rate (0% survival, 72 h after endotoxin administration), decreased mean arterial blood pressure, increased serum and macrophage TNF-alpha and enhanced plasma malonylaldehyde (MAL) levels. Furthermore aortic rings from shocked rats showed a marked hyporeactivity to phenylephrine (PE 1 nM-10 microM). 4. Treatment with U-83836E (7.5, 15 and 30 mg kg(-1), i.v.) 5 min after endotoxin challenge significantly protected against LPS induced lethality (90% survival rate and 80% survival rate 24 h and 72 h after LPS injection respectively, following the highest dose of the drug), reduced hypotension, blunted plasma MAL, decreased serum and macrophage TNF-alpha and restored the hyporeactivity of aortic rings to control values. In vitro LPS stimulation (50 microg ml(-1) for 4 h) significantly increased cytokine production in macrophages (Mphi) harvested from untreated normal rats. Pretreatment with pertussis toxin (PT; 0.1, 1 and 10 ng ml(-1) 4 h before LPS) significantly increased TNF-alpha production. PT effects on these LPS responses were correlated with a PT mediated ADP ribosylation of a 41 kDa protein. U-83836E (50 microM) reduced, in a dose dependent manner, LPS induced TNF-alpha production and inhibited the PT effects on cytokine production and on ADP ribosylation of the protein. 5. Our data suggest that lazaroids may affect the early events associated with LPS receptor mediated activation of a G protein in LPS induced TNF-alpha production. These molecular events may explain, at least in part, the in vivo inhibition of cytokine production and reversal of endotoxic shock.
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PMID:Inhibition of tumour necrosis factor and reversal of endotoxin-induced shock by U-83836E, a 'second generation' lazaroid in rats. 972 Aug 3

High mobility group box-1 (HMGB1) protein is a nonhistone, DNA-binding protein that plays a critical role in regulating gene transcription. Recently, HMGB1 has also been shown to act as a late mediator of endotoxic shock and to exert a variety of proinflammatory, extracellular activities. Here, we report that HMGB1 simultaneously acts as a chemoattractant and activator of dendritic cells (DCs). HMGB1 induced the migration of monocyte-derived, immature DCs (Mo-iDCs) but not mature DCs. The chemotactic effect of HMGB1 on iDCs was pertussis toxin-inhibitable and also inhibited by antibody against the receptor of advanced glycation end products (RAGE), suggesting that HMGB1 chemoattraction of iDCs is mediated by RAGE in a Gi protein-dependent manner. In addition, HMGB1 treatment of Mo-iDCs up-regulated DC surface markers (CD80, CD83, CD86, and HLA-A,B,C), enhanced DC production of cytokines (IL-6, CXCL8, IL-12p70, and TNF-alpha), switched DC chemokine responsiveness from CCL5-sensitive to CCL21-sensitive, and acquired the capacity to stimulate allogeneic T cell proliferation. Based on its dual DC-attracting and -activating activities as well as its reported capacity to promote an antigen-specific immune response, we consider HMGB1 to have the properties of an immune alarmin.
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PMID:High mobility group box-1 protein induces the migration and activation of human dendritic cells and acts as an alarmin. 1696 86