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Trichophyton

The Innate Immune Response

Immunity to Trichophyton is acquired by active infection. Since Trichophyton infects the epidermal layer of the skin, the constant turnover of the layers is one way to protect against further spread of infection. Thus the turnover is constantly pushing the infected cells to the surface, which is one reason why the only the layers beyond the stratum corneum are rarely breached and infected. Other non-specific factors that could inhibit the fungal growth are hydration of skin and the specific location and condition of the location where the infection occurred in the stratum corneum (Dahl & Carpenter 1985). Another innate response is unsaturated transferring named “serum inhibitory factor” that binds free iron and thus removes the pathogen’s nutrients (Dahl and Grando 1994).

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Figure 3. Microscope image of Trichophyton rubrum. In attempt to counter the long fibrils of the Trichophyton organism, shown here in the image above, the human body uses several non-specific methods. One such method is how the epidermis continually has a high turnover rate to control fungal penetration into the dermis, where infection would have more devastating consequences. (Permission pending http://www.scientificpsychic.com/health/hygiene.html)

To engulf the Trichophyton, the macrophage interacts with its conidia and once infected produces TNF-alpha and IL-10. IL-10 is an anti-inflammatory cytokine in the body, which will be discussed later (Campos et al). Mannan is made of complex glycoproteins in the Trichophyton cell wall, which is made up of peptides and repeating saccharides (Dahl 1994 and Dahl and Grando 1994). The section of “Evasionof Immune Response Detection” will elaborate on how Trichophyton uses its mannan to evade the immune response.

If roaming macrophages engulfs the pathogen, it activates the alternative complement pathway, which does not kill the pathogen, but merely inhibits its growth. Research has shown that neutrophils are activated in response to infection and activation by C3b of the complement pathway (Dahl 1994). It is believed that C3b acted as an opsonic link between the Trichophyton hyphae and the neutrophil C3b receptors. It is possible for the neutrophil and hyphae to directly interact, but the complementa appraoch seems to show better results for a response. Opsonized fungi were better activators than direct interaction (Dahl). Once activated, the neutrophils or other polymorphonuclear leukocytes move towards the follicle’s crack/break and can generate pustules (Dahl).

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Life cycle

IH vs. DTH

Evasion of Immune System Detection

Prevention & Treatment and Future Research

References

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