Comparative analysis of lysophospholipid metabolism profiles and clinical characteristics in patients with high vs. low C-reactive protein levels in acute exacerbations of chronic obstructive pulmonary disease.

BACKGROUND: The precise role of lysophospholipids (LysoPLs) in the pathogenesis of acute exacerbations of Chronic Obstructive Pulmonary Disease (AECOPD) remains unclear. In this study, we sought to elucidate the differences in serum LysoPL metabolite profiles and their correlation with clinical features between patients with low versus high CRP levels. METHODS: A total of 58 patients with AECOPD were enrolled in the study. Patients were classified into two groups: low CRP group (CRP < 20 mg/L, n = 34) and high CRP group (CRP ≥ 20 mg/L, n = 24). Clinical data were collected, and the LysoPL metabolite profiles were analyzed using Liquid Chromatography-Mass Spectrometry (LC-MS) and identified by matching with the LipidBlast library. RESULTS: Nineteen differential LysoPLs were initially identified through Student's t-test (p < 0.05 and VIP > 1). Subsequently, four LysoPLs, LPC(16:0), LPE(18:2), LPC(22:0), and LPC(24:0), were identified by FDR adjustment (adjusted p < 0.05). These four lysoPLs had a significant negative correlation with CRP. Integrative analysis revealed that LPC (16:0) and LPC (22:0) correlated with less hypercapnic respiratory failure and ICU admission. CONCLUSION: AECOPD patients with high CRP levels demonstrated a distinctive LysoPL metabolism profile, with LPC (16:0), LPE(18:2), LPC(22:0), and LPC(24:0) being the most significantly altered lipid molecules. These alterations were associated with poorer clinical outcomes.

The Role of Lysophospholipid Metabolites LPC and LPA in the Pathogenesis of Chronic Obstructive Pulmonary Disease.

Chronic obstructive pulmonary disease (COPD) is a heterogeneous lung condition characterized by persistent respiratory symptoms and airflow limitation. While there are some available treatment options, the effectiveness of treatment varies depending on individual differences and the phenotypes of the disease. Therefore, exploring or identifying potential therapeutic targets for COPD is urgently needed. In recent years, there has been growing evidence showing that lysophospholipids, namely lysophosphatidylcholine (LPC) and lysophosphatidic acid (LPA), can play a significant role in the pathogenesis of COPD. Exploring the metabolism of lysophospholipids holds promise for understanding the underlying mechanism of COPD development and developing novel strategies for COPD treatment. This review primarily concentrates on the involvement and signaling pathways of LPC and LPA in the development and progression of COPD. Furthermore, we reviewed their associations with clinical manifestations, phenotypes, and prognosis within the COPD context and discussed the potential of the pivotal signaling molecules as viable therapeutic targets for COPD treatment.

Differences in the lipid metabolism profile and clinical characteristics between eosinophilic and non-eosinophilic acute exacerbation of chronic obstructive pulmonary disease.

Objective: In this study, we aimed to investigate the differences in serum lipid metabolite profiles and their relationship with clinical characteristics between patients with eosinophilic and non-eosinophilic AECOPD. Methods: A total of 71 AECOPD patients were enrolled. Eosinophilic AECOPD was defined as blood EOS% ≥ 2% (n = 23), while non-eosinophilic AECOPD, as blood EOS< 2% (n = 48). Clinical data were collected, and serum lipid metabolism profiles were detected by liquid chromatography-mass spectrometry (LC-MS). The XCMS software package was used to pre-process the raw data, and then, lipid metabolite identification was achieved through a spectral match using LipidBlast library. Differences in lipid profiles and clinical features between eosinophilic and non-eosinophilic groups were analyzed by generalized linear regression. The least absolute shrinkage and selection operator (LASSO) was applied to screen the most characteristic lipid markers for the eosinophilic phenotype. Results: Eosinophilic AECOPD patients had less hypercapnic respiratory failures, less ICU admissions, a shorter length of stay in the hospital, and a lower fibrinogen level. In the lipid metabolism profiles, 32 significantly different lipid metabolites were screened through a t-test adjusted by using FDR (FDR-adjusted p < 0.05 and VIP> 1). Nine differential lipid metabolites were found to be associated with the three clinical features, namely, hypercapnia respiratory failure, ICU admission, and fibrinogen in further integration analysis. The species of triacylglycerol (TAG), phosphatidylcholine (PC), lysophosphatidylcholine (LPC), and diacylglyceryl trimethylhomoserine (DGTS) were high in these eosinophilic AECOPD. The LASSO was applied, and three lipid metabolites were retained, namely, LPC (16:0), TAG (17:0/17:2/17:2), and LPC (20:2). The logistic regression model was fitted using these three markers, and the area under the ROC curve of the model was 0.834 (95% CI: 0.740-0.929). Conclusion: Patients with eosinophilic AECOPD had a unique lipid metabolism status. Species of TAGs and LPCs were significantly increased in this phenotype and were associated with better clinical outcomes.

Malignancies in people living with HIV.

Almost 40 years have passed since the first case of what is known as AIDS was documented. In these 40 years, AIDS has always been a research challenge and hot spot. Researchers and scientists have made tremendous progress in basic and clinical research on HIV. In particular, the widespread use of antiretroviral therapy (ART) has made it less of a deadly disease today and more of a manageable one. In the post- ART era when ART can significantly improve the immunity of people living with HIV (PLWH) and extend their life, the incidence of non-AIDS-defined cancers is greatly increased. Factors related to immunosuppression do not seem to explain this problem sufficiently. This suggests that besides immunosuppression, there are other mechanisms that may also contribute to the increased incidence of cancer in PLWH. Here, we summarized and discussed four possible mechanisms for the increased incidence of cancers in PLWH: immunosuppression, oncogenic viral infection, chronic infection, inflammatory damage, and the direct impact of HIV.

Cellular and Immune Therapy for Treating HIV-1 Infection.

HIV-1 infection has caused a number of deaths worldwide and remains a global health concern. Combined antiretroviral therapy (cART) inhibits viral replication, prevents CD4+ T cell loss, and thus slows HIV disease progression. However, cART does not eradicate HIV-1. Infected individuals must remain on treatment for their entire lives and treatment interruption will result in viral rebound.