Distinct Protective Host Defenses against oral and vaginal Candidiasis

Abstract

Oral and vaginal candidiasis are the two most common forms of opportunistic fungal infections. However, the prevalence of each can be quite variable depending on the immune status of the host. While vulvovaginal candidiasis (VVC) is equally common in immunocompetent and immunocompromised women, oropharyngeal candidiasis (OPC) is infrequent except under immunocompromised states. Candida albicans, the causative agent in the majority of cases, is a commensal of the gastrointestinal and lower female reproductive tracts. Thus, most healthy individuals have protective Candida-specific immunity that normally prevents infection. Studies from animal models, women with recurrent VVC (RVVC) and HIV-infected individuals, however, suggest that distinct protective host defense mechanisms may function against OPC and VVC. While local and systemic cell-mediated immunity (CMI) appear important for protection against OPC, there is little evidence to indicate that either local or systemic CMI plays a role against VVC. Innate resistance is also considered distinct at both sites with considerably less activity at the vaginal mucosa, including the newfound anti-Candida activity by epithelial cells. Finally, the protective role of humoral immunity has been and remains uncertain. Taken together, the differential prevalence of VVC and OPC is directly proportional to the levels of demonstrable innate and adaptive host defenses at each site.

Vaginal Heparan Sulfate Linked to Neutrophil Dysfunction in the Acute Inflammatory Response Associated with Experimental Vulvovaginal Candidiasis

“…Previously, RVVC was thought to be attributable to defects in systemic and local cell-mediated immunity, similarly to other forms of candidiasis, in which protection against infection is T-cell dependent (reviewed in reference 4). However, numerous studies using a mouse model and cross-sectional clinical studies have shown that local or systemic adaptive immunity and associated cytokine/chemokines have no role in protection against vaginitis (5–10).…”

A Human-Curated Annotation of the Candida albicans Genome

“…Topics of particular interest are the organism's capacity to shift into several different phenotypic states, some with distinct roles in infection, and its recently discovered capacity to mate, providing at least part of a sexual cycle, although population genetic studies indicate that it is still largely a clonal diploid population. Other special adaptations for infection include a battery of externally displayed proteins and secreted digestive enzymes; complex interactions with the host immune system normally keep C. albicans at bay as a minor part of the mucosal flora [1,4,5]. …”

Citronellal-induced disruption of membrane homeostasis in Candida albicans and attenuation of its virulence attributes

“…It also causes systemic infections in immunocompromised individuals or patients undergoing long-term treatment with antibiotics (1) (2) . Side effects of the present treatment regimens for C. albicans and the advent of multidrug resistance (MDR) are problems affecting effi cient therapy against infections caused by C. albicans (3) (4).…”