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Query: UMLS:C0008354 (cholera)
 20,452 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Secretory antibodies in mucosal surfaces are known to play an essential role in protection against various infectious diseases. To enhance the production of such antibodies, influenza HA vaccine was inoculated intranasally into rabbits, together with cholera toxin B subunit (CTB) which is known to augment antibody response to an unrelated antigen. This combination resulted in high levels of serum IgG antibody responses against HA and CTB molecules, 3-4 weeks after inoculation, compared with the inoculation of HA vaccine alone. The adjuvant mechanism for CTB was studied by using Ussing chambers, in which nasal mucosa from rabbits were mounted. CTB was found to enhance the transepithelial flux of HA vaccine, from the mucosal side (lumen) into the serosal side (lamina propria), indicating that the permeability of the membrane was changed by CTB. Moreover, to achieve effective flux of HA vaccines, some interactions between the vaccine and CTB across the membrane were found, which may effect the effectiveness of the vaccine formulation. The results suggest that one of the mechanisms by which CTB enhances the production of mucosal antibody response is to enhance the transepithelial influx of vaccine into the nasal mucosa, where the cells involved in the antibody production are located. CTB may be used as a potent adjuvant to induce antibody response, by nasal vaccination, against pathogens impinging on mucosal surfaces.
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PMID:Stimulation of the transepithelial flux of influenza HA vaccine by cholera toxin B subunit. 153 62

WHO statistics indicated that as of October 1, 1991 there were 418,403 acquired immunodeficiency syndrome (AIDS) patients in the world, and an estimated 5-10 million persons infected with the human immunodeficiency virus (HIV) were at risk of developing AIDS. 50% of AIDS victims have died. It has been reported that after 1 year of clinical use HIV could develop resistance to AZT (azidothymidine), the only effective drug used worlwide and recommended for clinical use by the US government. AIDS has also been treated by acupuncture and moxibustion which recent experiments have associated with improving immune function and enhancing resistance to disease. The American scientists Smith and Naomi Rabinowitz used acupuncture and moxibustion in the clinical treatment of AIDS from 1982 to 1988 when they treated 350 patients with AIDS and AIDS related complex. 1 advanced case with Kaposi's sarcoma and signs of hemorrhage was significantly improved after treatment. Traditional Chinese medicine (TCM) has been used successfully in treating cholera, syphilis, epidemic encephalitis, influenza, and hepatitis with a great variety of clinical treatment measures and experiences. In recent years the treatment of AIDS by TCM using herbs and their extracts has been increasing. Dr. Yu of Santa Barbara, California, Hospital, in cooperation with Dr. Chen of China, successfully treated on AIDS patient with Chinese herbal medicine. The patient was still living and well more than 2 years later when another 24 cases which were not treated with TCM died during the same period. In China there are no special laboratories dealing with the prevention and treatment of AIDS, although scientific HIV research could benefit from such activities. On the other hand, foreign scientists and Chinese abroad have accomplished a significant amount of relevant research.
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PMID:Recent development of studies on traditional Chinese medicine in prophylaxis and treatment of AIDS. 159 94

Cross-protection against influenza virus infection was examined in mice, immunized intranasally with a nasal site-restricted volume of inactivated vaccines together with cholera toxin B subunit (CTB) as an adjuvant. The mice were challenged with either a small or a large volume of mouse-adapted virus suspension, each of which gave virgin mice either a predominant upper or lower respiratory tract infection. A single dose of a monovalent influenza A H3N2 virus vaccine with CTB provided complete cross-protection against the small-volume challenge with a drift virus within the same subtype, but a slight cross-protection against the large-volume challenge. A second dose of another drift virus vaccine increased the efficacy of cross-protection against the large-volume challenge. Similar cross-protection against H1N1, H3N2, or B type drift virus challenge was provided in the mice having received a primary dose of a mixture of H1N1, H3N2, and B virus vaccines with CTB and a second dose of another trivalent vaccine. The degree of cross-protection against the small- and the large-volume infection paralleled mainly the amount of cross-reacting IgA antibodies to challenge virus hemagglutinin in the nasal wash and that of cross-reacting IgG antibodies in the bronchoalveolar wash, respectively. On the other hand, in mice immunized subcutaneously with the trivalent vaccines having no cross-reacting IgA antibodies, the efficacy of cross-protection was not so high as that of nasal vaccination. These results suggest that the nasal inoculation of trivalent vaccines with CTB provides cross-protection against a broader range of viruses than does the current parenteral vaccination.
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PMID:Cross-protection against influenza virus infection afforded by trivalent inactivated vaccines inoculated intranasally with cholera toxin B subunit. 163 80

Mice that were intranasally immunized with different influenza A virus hemagglutinins (HA), derived from PR8 (H1N1), A/Yamagata (H1N1) or A/Fukuoka (H3N2) virus, together with cholera toxin B subunit as an adjuvant, were examined for protection against PR8 infection; PR8 HA and A/Yamagata HA immunization conferred complete protection, while A/Fukuoka HA immunization failed to confer protection. In parallel with protection, PR8 HA-, A/Yamagata HA-, and A/Fukuoka HA-immunized mice produced a high, a moderate and a low level of PR8 HA-reactive IgA in the respiratory tract, respectively. These IgA antibodies were not only higher in content in the nasal secretions, but also more cross-reactive than IgG. The purified IgA antibodies from respiratory tract washings of PR8 HA-immunized mice, which contained the HA-specific IgA corresponding to the amount detected in the nasal wash, were able to protect mice from PR8 challenge when transferred to the respiratory tract of naive mice. The transfer of IgA from A/Yamagata HA-immunized mice also afforded cross-protection against PR8 infection, whereas the IgA from A/Fukuoka HA-immunized mice failed to provide protection. The ability of transferred IgA to prevent viral infection was dependent on the amount of HA-reactive IgA remaining in the respiratory tract of the host at the time of infection. These experiments directly demonstrate that IgA antibodies to influenza A virus HA by themselves play a pivotal role in defence not only against homologous virus infection, but also against heterologous drift virus infection at the respiratory mucosa, the portal of entry for the viruses.
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PMID:Cross-protection against influenza A virus infection by passively transferred respiratory tract IgA antibodies to different hemagglutinin molecules. 164 12

The influence of mono-, di-, and trisialogangliosides on the dynamics of influenza B virus reproduction in human embryo fibroblast (HEF) cell culture and human diploid cells was established. The cells were treated with neuraminidase of non-cholera vibrio for removal of natural receptors followed by treatment with gangliosides. Virus reproduction was assessed by infectious titres for chick embryos and HA test of the culture fluid at certain intervals. Gangliosides restored influenza virus reception and enhanced the infectious process as compared with the controls. Treatment with gangliosides of HEF culture of low sensitivity increased its susceptibility to virus markedly.
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PMID:[The acceleration of experimental influenza B infection under the influence of gangliosides]. 188 18

The relationship between the antibody responses to various influenza B type virus HA vaccines and protection against live B virus infection was investigated in Balb/c mice which had been inoculated intranasally with a combination of the HA vaccines and B subunit of cholera toxin (CTB) 4 weeks previously. The inoculation of HA vaccine, prepared from B/Ibaraki/2/85 (B/Ibaraki), B/Nagasaki/1/87 (B/Nagasaki) or B/Aichi/5/88 (B/Aichi) viruses, combined with CTB induced high levels of both nasal IgA and serum HI antibodies to any of B/Ibaraki, B/Nagasaki and B/Aichi viral antigens. Simultaneous inoculation of each CTB-combined HA vaccine provided complete protection against B/Ibaraki virus infection which is demonstrated by both rapid clearance of pulmonary virus and complete survival. On the other hand, the inoculation of HA vaccine prepared from B/Yamagata/16/88 (B/Yamagata) virus together with CTB induced only a low level of nasal IgA antibodies, cross-reactive to B/Ibaraki, B/Nagasaki and B/Aichi viral antigens and protected only partially against B/Ibaraki virus challenge. The involvement of the B type virus-specific immunity in this protection was suggested by the absence of protection against B/Ibaraki virus infection in mice previously inoculated with both A/PR/8/34 (H1N1) virus HA vaccine and CTB. These results suggest that antibodies to various influenza B viruses are cross-reactive to each B type virus antigens and that cross-protection against B virus infection could be conferred depending on the degree of B type virus cross-reactive immunity including secretory IgA antibodies.
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PMID:Cross-protection against influenza B type virus infection by intranasal inoculation of the HA vaccines combined with cholera toxin B subunit. 196 78

Cholera toxin B subunit (CTB) has been shown to augment the antibody responses to influenza virus haemagglutinin (HA) in BALB/c mice immunized with HA vaccine together with CTB. In this study, mouse strain differences in the adjuvant effect of CTB on anti-HA antibody responses were investigated along with those in the antibody responses to CTB or HA, using various inbred and H-2 congenic strains. The antibody responsiveness to CTB depended on the H-2 haplotype of the strain: strains with the H-2b haplotype were high responders, those with H-2a, H-2k and H-2s were low responders, and those with H-2d were intermediate. The responsiveness to HA was also related to the H-2 haplotype: H-2a and H-2k strains were high responders, H-2b and H-2s strains were low responders, and H-2d strains were intermediate. However, the degree of the adjuvant effect of CTB on anti-HA antibody responses was almost constant, regardless of the H-2 haplotype or other genetic backgrounds of the strain. The lack of genetic restriction of the adjuvant effect would be favourable for application of CTB-combined HA vaccine to humans, who are genetically diverse. Moreover, these results suggest that the immunogenicity and adjuvanticity of CTB differ essentially in their mechanisms.
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PMID:H-2-unrestricted adjuvant effect of cholera toxin B subunit on murine antibody responses to influenza virus haemagglutinin. 202 41

Neutrophil dysfunction consequent to influenza A virus infection has been described in vivo and in vitro and may contribute to the serious bacterial sequelae which occur in influenza-infected hosts. On the premise that such dysfunction may represent a form of "deactivation," we sought to characterize neutrophil activation by the virus in comparison with other agonists. The virus induces a respiratory burst in which H2O2 (but not O2-) are formed. Preceding the respiratory burst, a rise in intracellular calcium (Ca2+i) is noted, but both responses are nearly independent of extracellular Ca2+, unlike those elicited by the other well-characterized Ca2+-dependent agonists, formyl-methyl-leucyl-phenylalanine (FMLP), or Concanavalin-A (Con-A). The Ca2+ increase is paralleled by IP3 generation, implying that it is the result of phospholipase C (PLC) activation. The virus also elicits neutrophil membrane depolarization, which is independently mediated from the Ca2+ increase and respiratory burst and may reflect protein kinase C (PK-C) activation. Virus-induced responses are insensitive to pertussis toxin (PT); cholera toxin does inhibit these responses but in a nonspecific manner. Thus, although influenza virus activates PLC in neutrophils, it does so in a PT-insensitive manner and does not elicit or require a discernible Ca2+ influx to generate a respiratory burst response. In aggregate, the data indicate that influenza A virus activates neutrophils in a manner distinct from that of other well-described neutrophil agonists. These results illustrate the diversity of neutrophil activation mechanisms and support the notion that further characterization of this pathway may facilitate understanding of neutrophil dysfunction induced by the virus.
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PMID:Characterization of influenza A virus activation of the human neutrophil. 215 30

Intranasal inoculation of haemagglutinin (HA) purified from influenza virus A/PR/8/34 (PR8, H1N1) together with cholera toxin B subunit, into Balb/c mice resulted in complete protection against PR8 infection in parallel with the induction of high levels of HA-specific IgA and IgG antibodies on the respiratory tract. The respiratory tract IgA and IgG were purified from nasal and lung washings of the immunized mice using affinity columns, and their HA-specific activities were measured by enzyme-linked immunosolvent, plaque neutralization and haemagglutination inhibition assays. The purified IgA and IgG had the following properties: (1) They were able to neutralize virus in vitro. (2) The purified IgA included major antibodies directed against PR8 virus and minor antibodies cross-reactive with A/Yamagata/120/86 (H1N1) or A/Fukuoka/C29/85 (H3N2) virus, while the purified IgG included major antibodies to the homotypic virus, minor antibodies to the H1N1 virus and only a trace amount of antibodies to the H3N2 virus. (3) When separated on a Sephacryl column, most of the IgA anti-HA activities occurred in the polymeric fractions of purified IgA, whereas the IgG anti-HA activities occurred in the monomeric fractions. (4) When passively administered to normal mouse respiratory tract before infection, the purified IgA protected against PR8 infection. These results suggest that HA-specific, polymeric IgA antibodies on the respiratory tract by themselves provide not only protection against the homotypic virus but also higher levels of heterotypic immunity than IgG.
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PMID:Functional role of respiratory tract haemagglutinin-specific IgA antibodies in protection against influenza. 225 74

In these studies we analyzed the adjuvant effect of cholera holotoxin or cholera toxin (CT) B subunit on the B cell response to mucosal antigens. Purified Peyer's patch B cells obtained from mice at varying periods of time after oral administration of inactivated influenza virus, with or without a CT preparation, were stimulated in vitro in the absence or presence of various lymphokines. Responses were measured by an antigen- and isotype-specific ELISPOT assay. In this system cultures containing a combination of lymphokines [interleukin 5 (IL 5), interferon-gamma (IFN-gamma), IL 4] gave comparable responses to those containing T cells from immunized mice or supernatant of concanavalin A-stimulated T cells and therefore were assumed to express optimum or near optimum B cell responses. Administration of a CT preparation along with influenza virus increased the number of B cells producing anti-influenza antibodies of both the IgM and IgA isotypes, with the effect on the IgA response at least threefold greater than the effect on the IgM response. These results thus indicate that CT preparations enhance the memory B cells response in Peyer's patches and, in addition, suggest that CT enhances isotype switching. In this antigen-specific B cell system IL 4 augmented responses in cultures containing IL 5 but not IFN-gamma; in addition, IL 5 and IFN-gamma acted in an additive fashion. Thus, these findings suggest that the effects of IL 5 and IFN-gamma are at least in part, mediated via different cellular differentiation pathways.
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PMID:Cholera holotoxin and its B subunit enhance Peyer's patch B cell responses induced by orally administered influenza virus: disproportionate cholera toxin enhancement of the IgA B cell response. 231 49


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