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Primary role for CD4(+) T lymphocytes in recovery from oropharyngeal candidiasis.

Oral Biology and Pathology, School of Dentistry, University of Queensland, Brisbane, Queensland, Australia.
Infection and Immunity (Impact Factor: 4.16). 03/2002; 70(2):724-31. DOI: 10.1128/IAI.70.2.724-731.2002
Source: PubMed

ABSTRACT Oropharyngeal candidiasis is associated with defects in cell-mediated immunity and is commonly seen in human immunodeficiency virus positive individuals and AIDS patients. A model for oral candidiasis in T-cell-deficient BALB/c and CBA/CaH nu/nu mice was established. After inoculation with 10(8) Candida albicans yeasts, these mice displayed increased levels of oral colonization compared to euthymic control mice and developed a chronic oropharyngeal infection. Histopathological examination of nu/nu oral tissues revealed extensive hyphae penetrating the epithelium, with polymorphonuclear leukocyte microabscess formation. Adoptive transfer of either naive or immune lymphocytes into immunodeficient mice resulted in the recovery of these animals from the oral infection. Reconstitution of immunodeficient mice with naive CD4(+) but not CD8(+) T cells significantly decreased oral colonization compared to controls. Interleukin-12 and gamma interferon were detected in the draining lymph nodes of immunodeficient mice following reconstitution with naive lymphocytes. This study demonstrates the direct requirement for T lymphocytes in recovery from oral candidiasis and suggests that this is associated with the production of cytokines by CD4(+) T helper cells.

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    • "Establishment of infection at mucosal sites generally requires treatment with immunosuppressive agents, oestrogen, or antibiotics prior to infection, or the use of germ-free animals [66] [67] [68]. However, the nude (Foxn1 nu ) mouse model of oral infection allows infection to be established without any immunosuppression or other pretreatment [69]. Greater detail can be found in more extensive reviews of these infection models [67] [68] [70] [71]. "
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    • "AIDS, transplant and steroid therapy) are more susceptible to oropharyngeal candidiasis (Klein et al., 1984). Additionally, CD4 + T cell protection appears to work in combination with certain cytokines, including IL-12, IFNγ , IL-4, TNF-α, and nitric oxide (Elahi et al., 2000, 2001; Farah et al., 2002a, 2002b). "
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    ABSTRACT: Rodent models of oral, vaginal and gastrointestinal Candida infection are described and discussed in terms of their scientific merits. The common feature of all experimental mucosal Candida infections is the need for some level of host immunocompromise or exogenous treatment to ensure quantitatively reproducible disease. A growing literature describes the contributions of such candidiasis models to our understanding of certain aspects of fungal virulence and host response to mucosal Candida albicans challenge. Evidence to date shows that T-lymphocyte responses dominate host immune defences to oral and gastrointestinal challenge, while other, highly compartmentalized responses defend vaginal surfaces. By contrast the study of C. albicans virulence factors in mucosal infection models has only begun to unravel the complex of attributes required to define the difference between strongly and weakly muco-invasive strains.
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    • "Resistance against mucocutaneous candidiasis in mice appears to be determined by both innate and cell-mediated immunity. Nude mice infected orally develop a severe infection that does not heal, and is dependent on CD4 + cells for its resolution (Farah et al. 2002), but gastrointestinal candidiasis was shown to disseminate only in mice with defects in both innate and adaptive immunity. After intragastric or oral inoculation of C. albicans, multiply-immunodeficient (bg/bg, nu/nu) mice, deficient in both T cells and phagocytic cells, developed a persistent gastrointestinal infection (Balish et al. 1990), whereas mice that lacked only phagocytic cells (bg/bg, nu/+) cleared the infection efficiently (Cantorna and Balish 1990). "
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