Immunological activities of a Candida albicans protein which plays an important role in the survival of the microorganism in the host

Tavares, Delfina; Salvador, Antonio; Ferreira, Paula; Arala-Chaves, M.P.

doi:10.1128/iai.61.5.1881-1888.1993

Cited by 25 publications

(32 citation statements)

References 33 publications

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“…Numerous previous investigations on the immune response to infection have established that the increase in antibody production, induced by polyelonal B cell activators, is often accompanied by enhanced suppression ofthe immune response to T cell-dependent antigens such as sheep erythroeytes [30][31][32][33]. Our data are in accordance with this interpretation, since we found direct correlation between the number of anti-BrM erythrocyte autoantibody-producitig cells and the degree of suppression of sheep erythroeytes.…”

Section: Discussionsupporting

confidence: 91%

Mycobacteria-induced autoantibody production is associated with susceptibility to infection but not with host propensity to develop autoimmune disease

Bras

Águas

1995

Clinical and Experimental Immunology

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SUMMARYMycobacteria cause increase in autoantibody production in the host during the first weeks of infection. The level of the autoantibody enhancement varies widely in different hosts, suggesting that it depends on features of the host make-up. We have investigated the participation of two characteristics of the host in the modulation of mycobacteria-induced autoantibody production: (i) the host being genetically determined to later develop spontaneous autoimmune disease; (ii) the host being susceptible/resistant to mycobacterial infection. Mycobacterium avium infection was studied in 3-month-old mice that are prone (NZB and C57Bl/6-lpr/lpr strains) or not (NZW and C.D2 strains) to develop, when older, autoimmune disease; these murine strains are either naturally susceptible (C57Bl/6-lpr/lpr and NZW) or resistant (NZB and C.D2) to mycobacteria. Mycobacterium avium infection was produced by i.p. injection of 3 x 107 viable bacilli. At days 15 and 30 of the infection, we determined the following parameters: (i) number of cells producing natural autoantibodies (splenic cells showing surface antibodies against bromelain-treated mouse (BrM) erythrocytes); (ii) suppression of the primary response to T cell-dependent antigen (i.e. to sheep erythrocytes); (iii) immunoglobulin classes and IgG isotypes; (iv) titres of anti-dsDNA antibodies; and (v) serum concentrations of interferon-gamma (IFN--y). We found that the highest elevations in natural autoantibodies were associated with hosts being naturally susceptible to mycobacteria, but not with the host being genetically determined to later develop autoimmune disease. The rise in autoantibodies was predominantly of the IgM type, being associated with suppression of the T cell response and accompanied by increase in serum IFN-y. Mycobacteria failed to induce any significant enhancement in pathogenic anti-dsDNA antibodies. Our data suggest that the finding of a high level of autoantibodies during the early phase of mycobacterial infection reflects host susceptibility to the infectious agent, and that it is not related with its propensity to later develop autoimmune disorders.

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Section: Discussionsupporting

confidence: 91%

Mycobacteria-induced autoantibody production is associated with susceptibility to infection but not with host propensity to develop autoimmune disease

Bras

Águas

1995

Clinical and Experimental Immunology

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“…A virulence-associated immunomodulation protein secreted by C. albicans was responsible for immunoprotection against candidiasis after the spontaneous healing of mice inoculated with 10 6 blastoconidia (Tavares et al, 2003). This molecule was a B cell mitogen, a feature of L. donovani hsp90, suggesting that it was related to the 47-kDa fragment of candidal hsp90 (Tavares et al, 1993;Kumar et al, 2003). Immunoenhancement potentiated the effect of amphotericin B on L. donovani (Murray et al, 2003) and human sera improved the in vitro activity of caspofungin against A. fumigatus (Chiller et al, 2000).…”

Section: Mycograb Smentioning

confidence: 99%

Fungal heat-shock proteins in human disease

Burnie¹,

Carter²,

Hodgetts³

et al. 2006

FEMS Microbiol Rev

135

108

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Heat-shock proteins (hsps) have been identified as molecular chaperones conserved between microbes and man and grouped by their molecular mass and high degree of amino acid homology. This article reviews the major hsps of Saccharomyces cerevisiae, their interactions with trehalose, the effect of fermentation and the role of the heat-shock factor. Information derived from this model, as well as from Neurospora crassa and Achlya ambisexualis, helps in understanding the importance of hsps in the pathogenic fungi, Candida albicans, Cryptococcus neoformans, Aspergillus spp., Histoplasma capsulatum, Paracoccidioides brasiliensis, Trichophyton rubrum, Phycomyces blakesleeanus, Fusarium oxysporum, Coccidioides immitis and Pneumocystis jiroveci. This has been matched with proteomic and genomic information examining hsp expression in response to noxious stimuli. Fungal hsp90 has been identified as a target for immunotherapy by a genetically recombinant antibody. The concept of combining this antibody fragment with an antifungal drug for treating life-threatening fungal infection and the potential interactions with human and microbial hsp90 and nitric oxide is discussed.

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Section: Introductionmentioning

confidence: 99%

“…We have already described two immunosuppressive/lymphocyte mitogenic (ISM) proteins of microbial origin: p36, isolated from culture supernatants of porcine monocytes infected with African swine fever virus (ASFV) [1] and p43 produced by Candida albicans [2]. In vivo proliferation of splenic B and T cells was observed in mice treated with p36 or p43 [1][2][3][4]. This mitogenic effect correlates to the suppression of specific immune responses to allo or heteroantigens [1,2,4] and seems to play an important role in the survival of the micro-organisms in the host [2,3].…”

Section: Introductionmentioning

confidence: 99%

“…In vivo proliferation of splenic B and T cells was observed in mice treated with p36 or p43 [1][2][3][4]. This mitogenic effect correlates to the suppression of specific immune responses to allo or heteroantigens [1,2,4] and seems to play an important role in the survival of the micro-organisms in the host [2,3]. We have previously hypothesized that these kind of proteins were Bcell mitogens and that T-lymphocyte proliferation was secondary to B-cell activation [4].…”

Section: Introductionmentioning

confidence: 99%

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Role of Monocytes in the Up‐Regulation of the Early Activation Marker CD69 on B and T Murine Lymphocytes Induced by Microbial Mitogens

Vilanova¹,

Tavares

Ferreira³

et al. 1996

Scand J Immunol

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CD69 is an early marker of lymphoid cell activation. The authors report on an up-regulation of CD69 in splenic B and T cells of C57Bl/6 mice after administration of lipopolysaccharide (LPS) or microbial immunosuppressive/mitogenic (ISM) proteins produced by C. albicans (p43) and African Swine Fever Virus (p36). This up-regulation of CD69 was observed 6 and 24 h after mitogenic treatments. The same pattern of increased CD69 expression was observed in the lymph nodes of mice treated with p43 or LPS, whereas p36 treatment failed to induce increased CD69 expression in this organ. Intracellular calcium mobilization was induced in splenic B and T lymphocytes after incubation of total spleen cells with LPS, p43 or p36. This increase was higher in B than in T cells. Increased calcium mobilization was also seen in lymph node B cells after incubation with p43 or p36 and in lymph node T cells after p43 stimulation. Up-regulation of CD69 expression on B and T cells was also observed after in vitro stimulation of spleen cells with the three mitogens used. Similar results were obtained with culture supernatants of macrophage/monocyte (M phi) cells activated with LPS (LPS/M phi CS). Stimulation of M phi cells with LPS or with the ISM proteins is demonstrated by the increased production of nitrites by these cells. The increased in vitro expression of CD69 was, however, not abolished by monoclonal antibodies to M phi cytokines such as IL-6, IL-10 or TNF alpha. No increased expression of CD69 was found in vitro on purified B or T cells, even when mixed upon stimulation with p43, p36, LPS or with LPS/M phi CS. However, an increase in the expression of CD69 was observed on B cells co-cultured with M phi cells after treatment with LPS or p36. All three mitogens failed to induce increased CD69 expression on cultured T cells mixed with M phi cells.

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Immunological activities of a Candida albicans protein which plays an important role in the survival of the microorganism in the host

Cited by 25 publications

References 33 publications

Mycobacteria-induced autoantibody production is associated with susceptibility to infection but not with host propensity to develop autoimmune disease

Mycobacteria-induced autoantibody production is associated with susceptibility to infection but not with host propensity to develop autoimmune disease

Fungal heat-shock proteins in human disease

Role of Monocytes in the Up‐Regulation of the Early Activation Marker CD69 on B and T Murine Lymphocytes Induced by Microbial Mitogens

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