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Suppression of in vitro lymphocyte transformation during an experimental dermatophyte infection
Abstract:
During primary Trichophyton mentagrophytes infection of strain 2 guinea pigs, the colony-forming units (CFU) of fungi present within the lesion peaked between days 7 and 14, whereas the severity of the lesion itself peaked between days 11 and 16. Concomitant with the latter peak, a pronounced depression in the in vitro mitogenic activity of spleen cells (SPC) and lymph node cells (LNC) was observed. Only after resolution of the primary infection (day 21) did LNC show increased deoxyribonucleic acid (DNA) synthesis in the presence of fungal antigens. During cutaneous reinfection, there was no distinct peak fungal load and CFU appeared to decrease steadily during the accelerated course of a reinfection disease. LNC from guinea pigs with severe, ulcerated reinfection lesions generally exhibited a heightened response to fungal antigen in vitro. LNC from guinea pigs with mild reinfection dermatophytosis had depressed in vitro reactivity to mitogens and dermatophyte antigen. The suppression of blastogenic activity during dermatophyte infection appeared to be associated with autologous serum components, since increased DNA synthesis resulted when SPC or LNC were cultured with fetal calf serum. The depressed in vitro DNA synthesis of lymphocytes (cultured with dermatophyte antigens) that were harvested during reinfection was not accompanied by an impaired ability of infected guinea pigs to respond with a delayed-type hypersensitivity skin test in vivo. These results support the hypothesis that experimental T. mentagrophytes dermatophytosis is a cell-mediated hypersensitivity disease that can be modified by immunosuppressive control mechanisms elaborated or induced by the fungus.
Insights
During Trichophyton mentagrophytes infection, guinea pig immune cells showed reduced activity. However, during reinfection, immune responses varied, suggesting complex immunosuppressive mechanisms in dermatophytosis.
Area of Science:
- Immunology
- Mycology
- Dermatology
Background:
- Trichophyton mentagrophytes causes dermatophytosis.
- Immune responses to fungal infections are complex.
- Understanding immune modulation is key to treating skin fungal infections.
Purpose of the Study:
- To investigate the immune response during primary and secondary Trichophyton mentagrophytes infections in guinea pigs.
- To explore the role of spleen cells (SPC) and lymph node cells (LNC) in T. mentagrophytes infection.
- To determine the mechanisms of immunosuppression during dermatophytosis.
Main Methods:
- Infection of guinea pigs with T. mentagrophytes.
- Measurement of fungal colony-forming units (CFU) and lesion severity.
- In vitro assessment of SPC and LNC mitogenic activity and DNA synthesis.
- Culture of cells with fungal antigens and fetal calf serum.
- In vivo delayed-type hypersensitivity skin testing.
Main Results:
- Primary infection led to peak fungal load and lesion severity, accompanied by suppressed SPC and LNC activity.
- LNC showed increased DNA synthesis post-primary infection resolution.
- Reinfection resulted in accelerated disease with variable LNC responses.
- Suppressed blastogenic activity was linked to autologous serum components.
- In vitro suppressed lymphocyte DNA synthesis did not correlate with impaired in vivo skin test responses.
Conclusions:
- Experimental T. mentagrophytes dermatophytosis is a cell-mediated hypersensitivity disease.
- The fungus may induce immunosuppressive mechanisms.
- Immune responses are modulated during primary and secondary infections.