IRF4-mediated Treg phenotype switching can aggravate hyperoxia-induced alveolar epithelial cell injury.

Bronchopulmonary dysplasia (BPD) is characterized by alveolar dysplasia, and evidence indicates that interferon regulatory factor 4 (IRF4) is involved in the pathogenesis of various inflammatory lung diseases. Nonetheless, the significance and mechanism of IRF4 in BPD remain unelucidated. Consequently, we established a mouse model of BPD through hyperoxia exposure, and ELISA was employed to measure interleukin-17 A (IL-17 A) and interleukin-6 (IL-6) expression levels in lung tissues. Western blotting was adopted to determine the expression of IRF4, surfactant protein C (SP-C), and podoplanin (T1α) in lung tissues. Flow cytometry was utilized for analyzing the percentages of FOXP3+ regulatory T cells (Tregs) and FOXP3+RORγt+ Tregs in CD4+ T cells in lung tissues to clarify the underlying mechanism. Our findings revealed that BPD mice exhibited disordered lung tissue structure, elevated IRF4 expression, decreased SP-C and T1α expression, increased IL-17 A and IL-6 levels, reduced proportion of FOXP3+ Tregs, and increased proportion of FOXP3+RORγt+ Tregs. For the purpose of further elucidating the effect of IRF4 on Treg phenotype switching induced by hyperoxia in lung tissues, we exposed neonatal mice with IRF4 knockout to hyperoxia. These mice exhibited regular lung tissue structure, increased proportion of FOXP3+ Tregs, reduced proportion of FOXP3+RORγt+ Tregs, elevated SP-C and T1α expression, and decreased IL-17 A and IL-6 levels. In conclusion, our findings demonstrate that IRF4-mediated Treg phenotype switching in lung tissues exacerbates alveolar epithelial cell injury under hyperoxia exposure.

We don't dare to tell her we don't know where to begin: Disclosure experiences and challenges among adolescents living with HIV and their caregivers in China.

BACKGROUND AND OBJECTIVES: With increasing access to antiretroviral therapy, HIV-infected youth are living longer, but are vulnerable as they navigate the transition to adulthood while managing a highly stigmatized condition. Knowing one's HIV status is critical to assuming responsibility for one's health. The process of disclosure to adolescents living with HIV is not well understood globally, even less so in China. To help address this gap, we explored practices for disclosure to adolescents living with HIV (ALHIV) among Chinese caregivers and clinicians, and the disclosure experiences of the adolescents themselves using qualitative methods. DESIGN AND SETTING: The study was conducted in 2014 at the Guangxi Center for Disease Control and Prevention ART (CDC-ART) clinic in Nanning, China. We used a qualitative design, incorporating in-depth interviews (IDIs) and focus group discussions (FGDs). PATIENTS AND METHODS: We conducted IDIs with 19 adolescent/caregiver dyads and five FGDs with adolescents and clinicians. Adolescent participants were aged 10-15 years, and had contracted HIV perinatally. Using NVivoTM software, we summarized major themes. RESULTS: Only 6/19 caregivers reported disclosing to their child; matched adolescents' statements indicate that 9/19 children knew their HIV status. Caregivers planned to disclose when children were 14 years or older. Concerns about stigma toward children and families were associated with reluctance to disclose. CONCLUSION: Disclosure to adolescents living with HIV in China was delayed compared with recommended guidelines. Culturally appropriate disclosure strategies should be developed, focused on supporting caregivers and de-stigmatizing HIV.