Role of innate and acquired immunity in controlling fungal infections

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In this article, I briefly describe how innate immunity and acquired immunity play an important role in controlling fungal infections.

Fungal infections

Fungi are diverse and ubiquitous, possessing characteristics of both plants and animals. They depend on external sources for nutrients. Fungi have their kingdom and provide many beneficial services for humans. They ferment bread, cheese, wine, and beer. One important use of them is in the production of penicillin. Among the million species of fungi, only 400 are potential agents of human disease.

Exogenous organisms are introduced into the body through injury or inhalation, which leads to infection. Endogenous organisms, like commensals, enter the body through host disruptions. In the case of reduced immune competence in the host, fungal agents may penetrate mucosal barriers and access extracellular spaces deep inside the body.

Types of fungal diseases

Fungal diseases are classified according to the site of infection, the route of acquisition, and the level of virulence. Fungal attacks on skin, hair, and nails include cutaneous infections. Trauma triggers subcutaneous infections and they come with inflammation. Deep mycoses (deep fungal infections) involve the lungs, the central nervous system, bones, and the abdominal viscera. These infections happen through ingestion, inhalation, or inoculation into the bloodstream.

The most common best-studied human fungal pathogens are Cryptococcus neoformans, Aspergillus Fumigatus, Coccidioides immitis, Histoplasms capsulatum, and Blastomyces dermatitidis. The virulence types can be categorized into two types, i.e., primary and opportunistic. Primary types are the rare agents with high pathogenicity, whereas opportunistic types include weakly virulent agents that primarily infect individuals with compromised immunity. Most fungal infections of healthy individuals get resolved rapidly, with few clinical signs.

Role of innate immunity in controlling fungal infections

Innate immunity involves physical barriers and agents, which control most fungal infections. Commensal microorganisms also help control pathogens. Long-term treatment with broad-spectrum antibiotics destroys normal mucosal bacterial flora. This ultimately leads to oral or vulvovaginal infection with Candida albicians, an opportunistic fungus. Neutrophil phagocytosis acts as a strong defense against most fungi. Therefore, people with low neutrophil counts are more susceptible to fungal disease.

The rapid resolution of fungal infection in healthy individuals is agile and begins by recognition of common fungal cell wall PAMPs by pathogen recognition receptors, present in the C-type lectin receptor (CLR) family. The three most immunologically relevant fungal cell wall components include β-glucans, mannans (long chains of mannose), and chitin (a polymer of N-acetylglucosamine). Parasites undergoing intracellular life cycle stages need cell-mediated immune reactions as a defense.

Acquired immunity against fungal pathogens

The presence of memory against any infectious agent signifies acquired immunity.

Acquired immunity does not always work for fungal diseases as primary infection often goes unnoticed. However, positive skin reactivity against fungal antigens indicates a prior infection and the presence of memory. The pathogen M. tuberculosis gives a granulomatous inflammation response, which also controls the spread of C. neoformans and H. capsulatum in most individuals. Thus, this shows the presence of acquired cell-mediated immunity. The infectious organism, however, may remain latent within the granuloma.

The presence of specific antibodies also shows a sign of prior exposure and lasting immunity. The frequency of normally rare fungal diseases in patients with compromised immunity provides the most suitable argument for pre-existing immunity against fungal pathogens. HIV patients suffer an increased incidence of mucosal candidiasis, histoplasmosis, coccidioidomycosis, and cryptococcosis.

Macrophages get activated optimally by strong TH1 responses and the production of IFN-γ, which is associated with protection against fungi. However, TH2-cell and TREG-cell responses are associated with susceptibility to mycoses. This seems in patients displaying distinct T-helper responses to coccidioidomycosis. TH1 immune activity to this fungus is associated with a mild, asymptomatic infection. However, TH2 responses to the fungus result in a severe and mostly relapsing form of the disease.

Conclusion

The fungal diseases are classified based on the site of infection, the route of acquisition, and the level of virulence. Fungal attacks on skin, hair, and nails include cutaneous infections. Innate immunity involves physical barriers and agents, which control most fungal infections. Commensal microorganisms also help control pathogens. Long-term treatment with broad-spectrum antibiotics destroys normal mucosal bacterial flora.

The most common best-studied human fungal pathogens are Cryptococcus neoformans, Aspergillus fumigatus, Coccidioides immitis, Histoplasms capsulatum, and Blastomyces dermatitidis. The virulence types can be categorized into two types, i.e., primary and opportunistic.

Innate immunity involves physical barriers and agents, which control most fungal infections. Commensal microorganisms also help control pathogens. Long-term treatment with broad-spectrum antibiotics destroys normal mucosal bacterial flora. This ultimately leads to oral or vulvovaginal infection with Candida albicians, an opportunistic fungus. Neutrophil phagocytosis acts as a strong defense against most fungi.

Acquired immunity does not always work for fungal diseases as primary infection often goes unnoticed. However, positive skin reactivity against fungal antigens indicates a prior infection and the presence of memory. The presence of specific antibodies also shows a sign of prior exposure and lasting immunity.

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