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107. CCR2 signaling regulates anti-chlamydia T cell immune responses in the airway.

Author

Yang, Shuaini, Yu, Jinxi, Dong, Xue, Zeng, Jiajia, Tan, Lu, Zhang, Hong, Sun, Ruoyuan, Tuo, Yuqing, Yang, Jing, Wan, Chunxiao, and Bai, Hong

Subjects
G protein coupled receptors, CHLAMYDIA infections, TH1 cells, SEXUALLY transmitted diseases, MYELOID cells, T cells, WEIGHT loss, MONOCYTES, CHEMOKINE receptors
Abstract

CCR2, a member of the G protein-coupled receptor (GPCR) superfamily, is widely expressed on monocytes, macrophages, activated T cells, and other cell types, and plays a critical role in coordinating the immune response to various infections. Here we demonstrate that CCR2 expression is significantly elevated during Chlamydia muridarum (C. muridarum) respiratory infection, and its absence leads to exacerbated susceptibility, as evidenced by significant weight loss, higher bacterial loads, severe lung pathology, and elevated levels of inflammatory cytokines (il-1β, tnfα, and il-6). The absence of ccr2 impairs both myeloid cell infiltration and T cell responses, which are crucial for effective immune defense. Specifically, ccr2 deficiency disrupts the differentiation and response of Th1 cells, which are the primary effector lineage responsible for clearing chlamydia through secretion of interferon-gamma (IFN-γ). As a result, there is a significant decrease in CD3+CD4+IFN-γ+ T cells in the lung and spleen, accompanied by reduced levels of IFN-γ protein and mRNA, as well as downregulated mRNA expression of Th1-promoting cytokines (il-12p35, il-12p40) and transcription factors (stat4, T-bet), which play crucial roles in Th1 differentiation. Moreover, ccr2 deficiency greatly diminishes STAT1 phosphorylation, a key regulator of IFN-γ secretion by Th1 cells. Meanwhile, we also observed a significant reduction in IFN-γ secretion by CD8+ T cells following ccr2 deficiency. Conversely, ccr2-/- mice exhibit an exaggerated Th2-type immune response, with elevated levels of Th2-promoting cytokines (IL-4), transcription factors (STAT6 and gata3), and il-5, which together lead to more severe lung tissue damage and increased susceptibility to infection. Furthermore, these mice show higher levels of IL-17 along with an enhanced Th17-type immune response, characterized by increased Th17-promoting cytokines TGFB, transcription factors stat3 and RORγt, and il-21, suggesting a compensatory mechanism that drives neutrophil infiltration to exacerbate lung inflammation. These findings underscore the pivotal role of CCR2, a chemokine receptor, in orchestrating the immune response to Chlamydia infection by facilitating Th1 cells differentiation while restraining Th2-type and Th17-type immune responses, thereby alleviating pulmonary inflammation. Author summary: Chlamydia species are obligate intracellular bacterial pathogens responsible for a wide array of infections, including sexually transmitted diseases and respiratory illnesses. Due to their unique life cycle, Chlamydia infections are challenging to eradicate, and current treatments do not ensure complete clearance, often resulting in chronic or recurrent infections. The mechanisms that regulate host protective immunity against Chlamydia remain poorly understood. In this study, we employed ccr2-/- mice to investigate the role of CCR2 in a Chlamydia muridarum respiratory infection model. Our findings indicate that CCR2 plays an important role in regulating the immune response during infection. Mice deficient in CCR2 exhibited exacerbated outcomes, including significant weight loss, increased bacterial burdens, and severe pulmonary damage. This was attributed to impaired immune responses, particularly in CD4+ T cells, which are critical for combating infections. In the absence of CCR2, mice exhibited impaired Th1 cell differentiation and diminished IFN-γ secretion, both of which are essential for effective pathogen clearance. In contrast, they developed an exaggerated Th2 and Th17 immune response, resulting in heightened inflammation and tissue damage. These findings underscore the role of CCR2 in balancing immune responses, thereby promoting a more effective defense while preventing excessive inflammation, and provide valuable insights into potential therapeutic targets for Chlamydia infections. [ABSTRACT FROM AUTHOR]

Published
2025
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109. Identification and Validation of Aging Related Genes Signature in Chronic Obstructive Pulmonary Disease.

Author

Li, Tian-Tian, Bai, Hong-Yan, Zhang, Jing-Hong, Kang, Xiu-He, and Qu, Yi-Qing

Subjects
*REVERSE transcriptase polymerase chain reaction, *GENE expression, *CHRONIC obstructive pulmonary disease, *GENE regulatory networks, *SUPPORT vector machines
Abstract

Purpose: Chronic Obstructive Pulmonary Disease (COPD) is regarded as an accelerated aging disease. Aging-related genes in COPD are still poorly understood. Method: Data set GSE76925 was obtained from the Gene Expression Omnibus (GEO) database. The "limma" package identified the differentially expressed genes. The weighted gene co-expression network analysis (WGCNA) constructes co-expression modules and detect COPD-related modules. The least absolute shrinkage and selection operator (LASSO) and the support vector machine recursive feature elimination (SVM-RFE) algorithms were chosen to identify the hub genes and the diagnostic ability. Three external datasets were used to identify differences in the expression of hub genes. Real-time reverse transcription polymerase chain reaction (RT-qPCR) was used to verify the expression of hub genes. Result: We identified 15 differentially expressed genes associated with aging (ARDEGs). The SVM-RFE and LASSO algorithms pinpointed four potential diagnostic biomarkers. Analysis of external datasets confirmed significant differences in PIK3R1 expression. RT-qPCR results indicated decreased expression of hub genes. The ROC curve demonstrated that PIK3R1 exhibited strong diagnostic capability for COPD. Conclusion: We identified 15 differentially expressed genes associated with aging. Among them, PIK3R1 showed differences in external data sets and RT-qPCR results. Therefore, PIK3R1 may play an essential role in regulating aging involved in COPD. [ABSTRACT FROM AUTHOR]

Published
2024
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128. Rezvilutamide (REZ) plus docetaxel (DOC) in patients (pts) with chemo-naïve metastatic castration-resistant prostate cancer (mCRPC) after progression on abiraterone (ABI).

Author

Liu, Zhenhua, primary, Wei, Qiang, additional, Feng, Ping, additional, Jiang, Shusuan, additional, Luo, Hong, additional, Liao, Hong, additional, Yu, Dexin, additional, Chen, Zhiwen, additional, Zhang, Dahong, additional, Dai, Tao, additional, Li, Zeng, additional, Zhang, Zhiqiang, additional, Bai, Hong, additional, Liu, Feng, additional, Wang, Wenliang, additional, Lin, Jiaqin, additional, and Wang, Yike, additional

Published
2024
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