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Published on: February 18, 2015
Expression of interleukin-2 in Candidal balanoposthitis and its clinical significance
Jun Chen1, Yun-xiao Zhou, Xiao-dong Jin
1Department of Urology, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310003, China.
Insights
Candidal balanoposthitis (CB) is linked to lower Interleukin-2 (IL-2) levels, suggesting autoimmune factors in its development. Low IL-2, other STDs, and partner VVC increase CB risk.
Area of Science:
- Immunology
- Dermatology
- Urology
Background:
- Candidal balanoposthitis (CB) is a prevalent male genital infection.
- Autoimmune mechanisms are implicated in CB pathogenesis.
- Interleukin-2 (IL-2) plays a crucial role in cell-mediated immunity.
Purpose of the Study:
- To investigate serum Interleukin-2 (IL-2) levels in patients with candidal balanoposthitis (CB).
- To explore the correlation between serum IL-2 levels and clinical data in CB patients.
Main Methods:
- Serum IL-2 levels were measured in 101 CB patients and 94 healthy controls using ELISA.
- Clinical data, including comorbidities and partner history, were analyzed alongside IL-2 levels.
Main Results:
- CB patients exhibited significantly lower serum IL-2 concentrations compared to controls (p < 0.05).
- A higher incidence of CB was observed in individuals with low serum IL-2 levels (70%) versus high levels (36%) (p < 0.05).
- Low serum IL-2, co-infection with sexually transmitted diseases (STDs), and partners with vulvovaginal candidiasis (VVC) were identified as risk factors for CB.
Conclusions:
- The pathogenesis of candidal balanoposthitis (CB) is multifactorial, involving internal autoimmune factors.
- Reduced Interleukin-2 (IL-2) levels may contribute to the susceptibility and development of CB.
Background:
Candidal balanoposthitis (CB) is a common male genital infection. Autoimmune mechanisms may play an important role in the pathogenesis of CB. Interleukin-2 (IL-2) is an important molecule in cell-mediated immunity.
Methods:
One hundred and one patients were diagnosed with CB using mycology culture in the dermatology and urology clinics in our hospital. Ninety-four healthy males were randomly selected as controls. We studied serum levels of IL-2 of patients with CB using ELISA and analyzed the correlations between serum IL-2 and clinical data.
Results:
Serum IL-2 concentrations in CB patients were significantly lower than that in the control group ((7.80 ± 4.78) vs. (15.44 ± 7.90) ng/L; t = 2.27, P < 0.05). The incidence of CB in the low-level group was significantly higher than that in the high-level group (70% (71/101) vs. 36% (30/84), P < 0.05). Low levels of serum IL-2, comorbidity with other sexually transmitted diseases (STDs), and sexual partners with vulvovaginal candidiasis (VVC) increased the risk of CB.
Conclusion:
The pathogenesis of CB is a complex procedure that includes internal autoimmune factors.
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