Bibliometric analysis of intestinal microbiota and lung diseases.

Background: Increasing evidence suggests a close association between the intestinal microbiome and the respiratory system, drawing attention to studying the gut-lung axis. This research employs bibliometric methods to conduct a visual analysis of literature in the field of intestinal microbiota and lung diseases over the past two decades. It offers scientific foundations for research directions and critical issues in this field. Methods: We retrieved all articles on intestinal microbiota and lung diseases from the SCI-Expanded of WoSCC on October 25, 2023. The analysis included original articles and reviews published in English from 2011 to 2023. We utilized Python, VOSviewer, and CiteSpace to analyze the retrieved data visually. Results: A total of 794 publications were analyzed. China ranked first in the number of publications, while the United States had the highest citations and H-index. Jian Wang was the most prolific author. Zhejiang University was the institution with the highest number of publications. Frontiers in Microbiology was the journal with the most publications. Author keywords appearing more than 100 times included "intestinal microbiota/microbiome", "microbiota/microbiome", and "gut-lung axis". Conclusion: The correlation and underlying mechanisms between intestinal microbiota and lung diseases, including asthma, COPD, lung cancer, and respiratory infections, remain hot topics in research. However, understanding the mechanisms involving the gut-lung axis is still in its infancy and requires further elucidation.

Fusu mixture alleviates inflammatory reactions in lipopolysaccharide-induced acute respiratory distress syndrome mice via regulation of surfactant-associated protein C, aquaporin 5, and Notch1.

Background: Acute respiratory distress syndrome (ARDS) is a common life-threatening critical illness with high mortality. Fusu mixture (FSM) can improve the mechanical ventilation in ARDS patients. However, the detailed pharmacological mechanisms and active substances of FSM are still unclear. This study aimed to explore the potential pharmacological mechanisms of FSM for treating ARDS and its chemical compositions. Methods: A lipopolysaccharide (LPS)-induced ARDS mouse model was established, and the mice subsequently received FSM (50 mg/kg) orally for 5 days. Then, the blood samples and lung tissues were collected. Enzyme-linked immunosorbent assay (ELISA) was used to determine the levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in serum, and histopathology examinations were applied to analyze the inflammatory response of lung tissues in ARDS mice. In addition, protein expressions of aquaporin 5 (AQP-5), surfactant-associated protein C (SP-C), and Notch1 were detected by western blot assays and immunohistochemical (IHC) examination. In addition, the chemical compositions of FSM were analyzed by high performance liquid chromatography (HPLC), using standard reference agents. Results: After LPS induction, the serum levels of IL-6 and TNF-α in ARDS mice were significantly increased (P<0.01, vs. Control), and FSM significantly reduced these 2 pro-inflammatory cytokines (IL-6 and TNF-α) compared to the model mice (P<0.01). Histopathology examinations showed FSM significantly attenuated the inflammatory responses in lung tissues. Furthermore, after FSM treatment, the SP-C and AQP-5 were significantly increased, compared to the Model mice (P<0.01), and FSM also up-regulated the Notch1 expressions in lung tissues of ARDS mice (P<0.001, vs. Model). Conclusions: Collectively, it is suggested that FSM alleviates inflammatory reactions and promotes the proliferation of alveolar epithelial cells in LPS-induced ARDS mice via regulation of SP-C, AQP-5, and Notch1 in lung tissues.