RESUMO
Background: Protein is crucial for the rehabilitation of patients with chronic obstructive pulmonary disease (COPD), and appropriate daily protein intake is essential for COPD patients. However, the specific role of protein intake in COPD and its impact on mortality remain uncertain. This study aims to ascertain the relationship between protein intake and mortality in COPD patients. Methods: This investigation included 522 adult COPD patients from the National Health and Nutrition Examination Survey (NHANES) between 2013 and 2018, with a focus on evaluating protein intake. Multivariate Cox proportional hazard models were constructed to analyze the correlation between protein intake and the prognosis of COPD patients. Additionally, the restricted cubic spline (RCS) was employed to investigate the potential non-linear association between protein intake and mortality. Results: A total of 522 patients with COPD were categorized into 4 groups based on the quartiles of protein intake: Q1 (< 25th percentile, 11.7-48.5 gm), Q2 (25-50th percentile, 48.5-67.7 gm), Q3 (50-75th percentile, 67.7-94.3 gm), and Q4 (≥ 75th percentile, 94.3-266.6 gm). Cox regression analysis revealed a significant trend in the p value of the Q3 group compared to the Q1 group when adjusting for other variables. The RCS-fitted Cox regression model indicated no non-linear relationship between protein intake levels and COPD mortality. Conclusion: There is no evidence of a non-linear relationship between protein intake and all-cause mortality in COPD patients. Further investigation is warranted to comprehend the intricate relationship between protein intake and COPD outcomes.
RESUMO
The goal of the present study was to investigate the role of M1 macrophages in acute lung injury (ALI). To address this, we used lipopolysaccharide (LPS)-treated wild-type and CD11b-DTR mice, and examined their M1 macrophage levels, and the extent of their inflammation and pulmonary injuries. In addition, we evaluated pulmonary function by measuring the expressions of SP-A and SP-B in infiltrated M1 macrophages. Finally, we co-cultured the mouse type II-like alveolar epithelial cells (AT-II) and mouse pulmonary microvascular endothelial cells (PMECs) with M1 macrophages in the presence of TNF-α or H2O2 and assessed them for viability and apoptosis. After LPS treatment, we observed that the number of pulmonary M1/M2 macrophages and the serum levels of interleukin-1ß (IL-1ß), tumor necrosis factor α (TNF-α), and reactive oxygen species (ROS) significantly increased. Furthermore, the increase in cytokines was accompanied with the initiation of lung injury indicated by the decreased levels of SP-A and SP-B. In macrophage-depleted CD11b-DTR mice, ALI was attenuated, serum levels of IL-1ß, TNF-α and ROS were reduced, and lung levels of monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-2 (MIP-2) were decreased. After administering TNF-α and H2O2, the proapoptotic effect of M1 macrophages on AT-II or PMECs significantly increased, the cell viabilities significantly decreased, and apoptosis significantly increased. Our results suggest that M1 macrophages are recruited to the lungs where they significantly contribute to an increase in TNF-α and ROS production, thus initiating ALI.