Abstract
Background: Pulmonary infections are a significant concern for HIV/AIDS patients, and the role of macrophage polarization is critical in this context. Shenqinlong Qingfei Peiyuan Granules (QFPY) have been reported to alleviate symptoms of these infections. This study aims to explore the mechanisms through which QFPY reduces lung infections by regulating macrophage polarization.
Methods: We developed an immunocompromised mouse model using Balb/c mice, simulating HIV infection by inoculating them with Friend Leukemia Virus (FLV, VR-245). Pulmonary infection was induced by nasal administration of Streptococcus pneumoniae Type III (ATCC 49619). The mice received QFPY treatment for 14 days. Post-treatment, we collected thymus, spleen, and lung tissue samples. T lymphocyte counts (CD3+, CD4+, and CD8+) were measured, and CD86 and CD163 expressions in bronchoalveolar lavage fluid (BALF) from lung tissue were assessed using flow cytometry. Cytokine levels, including IL-1β, TNF-α, TGF-β1, and IL-10, were evaluated using enzyme-linked immunosorbent assay (ELISA). Additionally, HMGB1 mRNA and protein levels were measured using quantitative PCR (qPCR) and Western blot techniques.
Results: QFPY treatment showed efficacy comparable to the current standard treatment for lung infections, levofloxacin tablets (LEV). In our immunocompromised mouse model, QFPY treatment reversed thymus shrinkage, reduced spleen swelling, increased T cell counts, and inhibited M1 macrophage polarization. These effects were achieved by suppressing the expression of HMGB1.
Conclusions: QFPY effectively restored immune homeostasis and reduced inflammation in HIV/AIDS-related pulmonary infections by modulating HMGB1 expression.
Methods: We developed an immunocompromised mouse model using Balb/c mice, simulating HIV infection by inoculating them with Friend Leukemia Virus (FLV, VR-245). Pulmonary infection was induced by nasal administration of Streptococcus pneumoniae Type III (ATCC 49619). The mice received QFPY treatment for 14 days. Post-treatment, we collected thymus, spleen, and lung tissue samples. T lymphocyte counts (CD3+, CD4+, and CD8+) were measured, and CD86 and CD163 expressions in bronchoalveolar lavage fluid (BALF) from lung tissue were assessed using flow cytometry. Cytokine levels, including IL-1β, TNF-α, TGF-β1, and IL-10, were evaluated using enzyme-linked immunosorbent assay (ELISA). Additionally, HMGB1 mRNA and protein levels were measured using quantitative PCR (qPCR) and Western blot techniques.
Results: QFPY treatment showed efficacy comparable to the current standard treatment for lung infections, levofloxacin tablets (LEV). In our immunocompromised mouse model, QFPY treatment reversed thymus shrinkage, reduced spleen swelling, increased T cell counts, and inhibited M1 macrophage polarization. These effects were achieved by suppressing the expression of HMGB1.
Conclusions: QFPY effectively restored immune homeostasis and reduced inflammation in HIV/AIDS-related pulmonary infections by modulating HMGB1 expression.
Original language | English |
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Article number | 100826 |
Number of pages | 11 |
Journal | Phytomedicine Plus |
Volume | 5 |
Issue number | 3 |
Early online date | 13 Jun 2025 |
DOIs | |
Publication status | E-pub ahead of print - 13 Jun 2025 |
User-Defined Keywords
- Acquired immunodeficiency syndrome (AIDS)
- CD4+ T cell
- Human immunodeficiency virus (HIV)
- Macrophage polarization
- Pulmonary infection
- Traditional Chinese medicine