Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008354 (cholera)
 20,452 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cultured epithelial cells isolated from guinea pig trachea were treated with Vibrio cholerae sialidase. The treatment was not cytotoxic and resulted in membrane desialylation as assessed by measurement of sialic acids released, along with an increased fixation of the galactose-specific lectin peanut agglutinin. After incubation in serum from normal guinea pigs, membrane-bound immunoglobulins were detected using peroxidase-labelled antibodies. Sialidase-treated cells bound significantly more IgM than controls (P < 0.0005), whereas binding of IgG was not significantly different between treated and untreated cells (0.1 < P < 0.375); IgA were never detected. In influenza-infected guinea-pigs, as assessed by reactivity with peanut agglutinin, the tracheal and lung epithelium, as well as alveolar cells were hyposialylated. In these animals, the level of serum IgG autoantibodies capable to bind sialidase treated cultured cells increased, while the level of IgM autoantibodies did not change. These autoantibodies may participate in cellular dysfunctions and modified bronchoreactivity that occur during infection of the respiratory tract by sialidase-producing microorganisms, either through activation of the complement system, or subsequently to their reaction with cells expressing membrane complement and/or Fc receptors.
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PMID:Binding of serum autoantibodies to sialidase-treated tracheal epithelial cells. Determination of autoantibodies isotypes in normal and influenza virus infected guinea pig sera. 782 32

The influenza virus hemagglutinin glycoprotein (HA) induces a vigorous B cell proliferation and Ig-synthesis by an unknown activation mechanism, which is susceptible to the inhibitory effects of anti-Ig and anti-class II mAbs. To gain further insight into the activation mode of this T cell-independent, B cell "superstimulatory" virus, we analyzed the sensitivity of H2-subtype virus-mediated B cell activation to the inhibitory effects of various signal transduction-blocking agents and compared it to the well characterized anti-mu-mediated and the LPS-employed pathway. Cyclic-AMP agonists (cAMP-analogues, pentoxifylline, cholera toxin, and forskolin) blocked HA-mediated activation of B cells only at concentrations at least 50-fold higher than required for blocking of anti-mu-induced activation. However, HA-treatment failed to induce an increase in intracellular cAMP levels in responding B cells. The B cell response to HA was highly resistant to calcineurin-inhibitory cyclosporin-A treatment and did not result in a measurable Ca2+ influx. Similarly, HA failed to induce an increase in tyrosine phosphorylations, including phosphorylation of phospholipase C gamma 2. HA-activated B cells showed an increase in membrane-associated protein kinase C activity, and depletion of protein kinase C by pretreatment of B cells with phorbol esters inhibited a subsequent activation by HA. Collectively, our results provide a new example of B cell stimulation by multivalent type-2 Ags, which seems to be mediated by a phosphatidylinositol- and Ca(2+)-independent signaling pathway.
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PMID:B cell superstimulatory influenza virus (H2-subtype) induces B cell proliferation by a PKC-activating, Ca(2+)-independent mechanism. 786 86

The MHC class I cytotoxic T-lymphocyte (CTL) response in mice given formalin-inactivated influenza whole-virus vaccine (WVV) with or without cholera toxin B subunit (CTB) was studied. Intraperitoneal injection of Balb/c (H-2d) mice with high doses of A/Taiwan/1/86 (H1N1) WVV stimulated influenza A virus-specific CTL response in a dose-dependent manner. A dose of 4.4 or 44 micrograms induced CTL response equal to or greater than live influenza virus infection. Coadministration of vaccine with 5 or 25 micrograms of CTB resulted in a higher level of CTL than with vaccine alone. CTL lysed A/Taiwan and A/Shanghai (H3N2) virus-infected class I-expressing P815 (H-2d) but not virus-infected EL-4 (H-2b) target cells nor B/Yamagata virus-infected target cells. Virus-infected MHC class II- and class I-expressing A20 (H-2d) targets were also lysed. Depletion of Lyt-2+ (CD8+) T cells with monoclonal antibody completely abrogated lysis of P815 target cells and resulted only in a slight reduction of lysis of A20 target cells. Depletion of L3T4+ (CD4+) T cells or NK cells had minimal effect on lysis of either P815 or A20 target cells. Using limiting dilution analysis, the precursor CTL (pCTL) frequency paralleled CTL activity. Significant CTL activity was detected 7 months after immunization. These results demonstrate that adequate doses of influenza WVV with or without CTB can induce long-lasting influenza A cross-reactive MHC class I-restricted CD8+ CTL response in mice. Thus, coadministration of influenza WVV with CTB may lead to an effective vaccine that stimulates both CTL and antibody responses.
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PMID:Induction of CD8+ cytotoxic T cells by immunization with killed influenza virus and effect of cholera toxin B subunit. 790 15

The aim of vaccinology is to improve the available vaccines and to develop new ones in the light of progress in immunology, molecular biology and biotechnologies. But it must go beyond this, and aim to protect all populations and control diseases, even eradicate them where possible. New vaccine strategies must be developed taking into account the epidemiology of diseases and the inherent logistic problems of implementing these strategies under local conditions. There are three major thrusts to the progress of the discipline. The improvement of the vaccines available. One of the drives of vaccinology is not only to deliver vaccines of increasing safety (replacement of the current vaccine for whooping cough with an acellular vaccine for example), but also to improve vaccine efficacy and immunogenicity (in particular for flu, tuberculosis, cholera and rabies vaccines). The optimisation of vaccination programmes and strategies for vaccinations. The ideal is to protect against the greatest possible number of diseases with the smallest number of vaccinations. The development of combinations of vaccines is central to this goal. The objective for the year 2000 is a hexavalent vaccine DTPP Hib HB. The development of new vaccines. Classic techniques continue to be successfully used (inactivated hepatitis A vaccine; attenuated live vaccines for chicken pox and dengue fever; conjugated polyosidic bacterial vaccines for meningococci and Streptococcus pneumoniae). However, it will become possible to prepare vaccines against most transmissible diseases using genetic engineering techniques.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Vaccination perspectives]. 792 96

Cholera toxin B subunit (CTB) and Escherichia coli heat-labile toxin (LTB) (2 micrograms), each supplemented with a trace amount of cholera toxin (CT) (0.02-20 ng), were examined for the adjuvant effect on antibody (Ab) response against influenza inactivated HA (haemagglutinin) vaccine in Balb/c mice. Each mouse received a primary intranasal (i.n.) inoculation of the vaccine (1.5 micrograms) and the CT-containing CTB and in 4 weeks a second i.n. inoculation of the vaccine alone. The primary inoculation of the vaccine with CTB alone did not induce either anti-HA IgA or IgG Ab response, or haemagglutination-inhibition Ab responses in the serum. The vaccine with less than 2 ng of CT also failed to induce Ab response. On the other hand, the vaccine with CT-containing CTB induced a high Ab response, which increased depending on the CT dose. Moreover, the second vaccine induced a response more than ten times higher than the primary one and the response increased depending on the CT dose. Similar enhancement was found in the local anti-HA IgA Ab response in the nasal wash. Such synergistic effects were observed also between LTB and CT. The amount of Ab produced by the synergism was considered to be enough to protect against virus infection. These results suggest that CTB (or LTB) containing a trace amount of CT (about 0.1%) can be used practically as a potent adjuvant for nasal vaccination of humans against influenza.
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PMID:Synergistic action of cholera toxin B subunit (and Escherichia coli heat-labile toxin B subunit) and a trace amount of cholera whole toxin as an adjuvant for nasal influenza vaccine. 802 50

Attempts were made to formulate an inactivated influenza vaccine to provide effective cross-protection by intranasal vaccination in mice. Mice were immunized with a nasal site-restricted volume of various HA vaccines (split-product virus vaccines), prepared from some of the H1N1 subtype viruses which circulated in humans from 1934 to 1986, together with cholera toxin B subunit (CTB) as an adjuvant. Four weeks later, they were challenged intranasally with a lethal dose of the earliest H1N1 virus strain, A/PR/8/34 (PR8) or the latest virus strain, A/Yamagata/120/86 (Yamagata/86). The adjuvant-combined vaccines, prepared from drift H1N1 viruses, A/Kumamoto/37/79 and A/Bangkok/10/83, provided a higher degree of cross-protection against a challenge with Yamagata/86 than with PR8. A booster with another drift virus vaccine given 4 weeks after the primary vaccination increased the protection against Yamagata/86; the effect was higher when mice were vaccinated with a later strain as the second antigen than when boosted with PR8. These results suggest that vaccination with a later virus strain followed by another later strain in a two-dose nasal vaccination regimen gives effective cross-protection against the current epidemic virus strains.
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PMID:Formulation of inactivated influenza vaccines for providing effective cross-protection by intranasal vaccination in mice. 817 52

The inhibition of sialidase activity from influenza viruses A and B, parainfluenza 2 virus, Vibrio cholerae, Arthrobacter ureafaciens, Clostridium perfringens, and sheep liver by a range of 2-deoxy-2,3-didehydro-N-acetylneuraminic acid analogues modified at the C-4 position has been studied. All substitutions tested resulted in a decrease in the degree of inhibition of the bacterial and mammalian sialidases. For sialidases from influenza viruses A and B, on the other hand, most of the substitutions tested either had no significant effect on binding or, in the case of the basic amino and guanidino substituents, resulted in significantly stronger inhibition. The results for parainfluenza 2 virus sialidase were mostly intermediate, in that inhibition was neither significantly increased nor decreased by most of the modifications. We conclude that only the influenza A and B sialidase active sites possess acid groups correctly positioned to participate in charge-charge interactions in the region of C-4 of bound substrate, and that the C-4 binding pockets of the bacterial and mammalian sialidases examined are considerably smaller than is observed for either the influenza virus or parainfluenza virus sialidases.
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PMID:Inhibition of sialidases from viral, bacterial and mammalian sources by analogues of 2-deoxy-2,3-didehydro-N-acetylneuraminic acid modified at the C-4 position. 835 25

Mankind has been stricken with "major" epidemic diseases throughout its history. The most serious among them immediately threaten man's life e.g. plague, cholera, smallpox, typhus, and dysentery, besides, there are others which take a slower course e.g. lues, leprosy, leishmaniasis, tuberculosis, and malaria. Yet, the "lesser" epidemic diseases like diphtheria, scarlet fever, mumps, pneumococcosis, influenza, and most recently AIDS may also turn into "major" ones. Originally, man exclusively depended on his genetic makeup for protection, and being particularly prone to attacks of disease he was subject to natural selection. Thus, only one human species survived, the homo sapiens. Interbreeding achieved biologic adaptation and created a balanced genetic polymorphism. Advancing in his degree of civilization, man formed groups, developed clothing, fire, houses, and tools, and his increasing cultural awareness allowed him to migrate from the tropical climates to more temperate, and less disease-infested zones. Immigration and wars, and the accompanying infections jeopardized and diminished entire populations and eradicated highly developed cultures like that of the American Indians. The plague, coming from Asia, and lues, from America, as well as cholera, influenza, and smallpox spread around the whole globe. Fear and terror led to irrational conclusions and triggered persecutions. The attitude of accepting disease as a God-sent fate (Hiob), or a God-sent punishment suppressed reasonable measures against disease. The necessary official measures have increasingly restricted liberty, and this patronizing treatment needs to be opposed with a higher sense of responsibility. Medical art has developed from more healing towards prophylactic and predictive medicine, which prognosticates the individual susceptibility to particular infections, and other risk factors.
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PMID:[Effect of major epidemics on cultural awareness]. 857 53

The protective roles of influenza viral nucleoprotein (NP), together with the cellular mechanism of the protection in the nasal site, were examined in BALB/c mice immunized intranasally with an adjuvant (cholera toxin B subunit containing 0.2% of the whole toxin)-combined A or B virus recombinant NP. The NP-immune mice, when challenged intranasally with a sublethal dose of the virus 3 wk after immunization, had accelerated virus clearance from the nasal site in both an influenza type-specific and a nonspecific manner, as shown by the protection from high morbidity from the second day after challenge. Both type-specific and nonspecific acceleration of recovery was confirmed by the increased survival rate after challenge with a lethal dose of virus in mice immunized and boosted with adjuvant-combined NP. The acceleration of nasal virus clearance was accompanied with acceleration of type-specific systemic delayed-type hypersensitivity (DTH) and with IFN-gamma production by nasal lymphocytes. The nasal lymphocytes from the immunized and challenged mice generated a significantly high level of DTH when transferred locally, but no class I MHC-restricted CTL response. Moreover, nasal CD4+ T cells, induced by NP immunization and increased in number by the subsequent challenge, were involved in the accelerated IFN-gamma production. These results suggest that nasal Th1 cells, capable of producing IFN-gamma and mediating DTH, are involved in the type-specific acceleration of recovery from influenza after challenge in mice immunized intranasally with adjuvant-combined NP, although the nonspecific mechanism of accelerated recovery remains to be solved.
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PMID:Acceleration of influenza virus clearance by Th1 cells in the nasal site of mice immunized intranasally with adjuvant-combined recombinant nucleoprotein. 862 28

The capacity of adjuvants to stimulate cytokine production by APC is important for the initiation of the immune response. Novel adjuvant formulations based on the iscom technology have been developed using selected triterpenoid components from Quillaja saponaria Molina. Five of these new Quillaja formulations were used to prepare matrix (an antigen-free particle) and tested for their capacity to stimulate IL-1 secretion by murine peritoneal cells in vitro. The formulation denominated QH 7.0.3 was superior to the other matrix formulations, including the original spikoside matrix. The QH 7.0.3 formulation in iscoms containing influenza virus envelope antigens induced IL-1 secretion more efficiently than the antigen-free matrix, or a mixture of matrix and viral antigens, or the free Quillaja components of similar composition. Compared with adjuvants known as IL-1 inducers, QH 7.0.3 flu-iscoms were as efficient as the most prominent IL-1 inducer, i.e. lipopolysaccharide (LPS) and superior to cholera toxin (CT) and muramyl dipeptide (MDP). These results indicate that the composition per se of triterpenoids included in iscoms or matrix has a prominent influence on the level of APC activation which may result in qualitatively different immune responses in vivo.
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PMID:In vitro activation of antigen-presenting cells (APC) by defined composition of Quillaja saponaria Molina triterpenoids. 869 31


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