Gut microbiota-derived acetic acids promoted sepsis-induced acute respiratory distress syndrome by delaying neutrophil apoptosis through FABP4 DOI Creative Commons

Weixia Xuan,

Wu Xu, Zheng Li

et al.

Cellular and Molecular Life Sciences, Journal Year: 2024, Volume and Issue: 81(1)

Published: Oct. 25, 2024

In patients with sepsis, neutrophil apoptosis tends to be inversely proportional the severity of but its mechanism is not yet clear. This study aimed explore fatty acid binding protein 4 (FABP4) regulating through combined analysis gut microbiota and short-chain acids (SCFAs) metabolism. First, neutrophils from bronchoalveolar lavage fluid (BALF) sepsis-induced acute respiratory distress syndrome (ARDS) were purified isolated RNA was applied for sequencing. Then, cecal ligation puncture (CLP) method induce mouse sepsis model. After intervention differential SCFAs sodium acetate, FABP4 expression further analyzed. inhibitor BMS309403 used treat neutrophils. We found CLP group had increased lung injury score, tissue wet/dry ratio, vascular permeability, inflammatory factors IL-1β, TNF-α, IL-6, IFN-γ, CCL3 levels in both tissue. Additionally, lower ARDS mice. Meanwhile, CLP-induced dysbiosis changes observed. Further verification showed that acetic reduced via FFAR2. Besides, affected endoplasmic reticulum (ER) stress, depletion alleviated promotion development by BMS309403. Moreover, regulated RLE-6TN factors. conclusion, microbiota-derived delayed ER leading mediating epithelial cell damage.

Language: Английский

Bibliometric analysis of pyroptosis in pathogenesis and treatment of acute lung injury DOI Creative Commons
Chun Wang, Na Liu

Frontiers in Medicine, Journal Year: 2025, Volume and Issue: 11

Published: Jan. 22, 2025

Objective This study aims to conduct a bibliometric analysis assess the present state, thematic focus, and emerging developments in research literature on involvement of pyroptosis pathogenesis treatment acute lung injury (PFALI), as well other pertinent areas. Methods examined PFALI published from 1 January 2004 24 May 2024, utilizing Web Science database. The was conducted using CiteSpace, VOSviewer, R, GraphPad Prism 8.0, encompassed metadata countries, institutions, authors, journals, keywords represented literature. Results analyzed 1,495 publications, comprising 1,194 articles 301 reviews, publication output PFALI. China exhibited highest with 964 (64.48%) articles. Central South University most prolific institution, contributing 54 (3.61%) publications. Zhou, Yong had greatest individual record, 15 (3.59%) journal International Immunopharmacology PFALI-related at 76 (5.09%). identified frontiers for upcoming years include “iron,” “sirt1,” “repair,” “alveolar macrophage pyroptosis.” Conclusion comprehensively trends advancements related PFALI, including contributions key countries.

Language: Английский

Citations

0
Ficolin A and ficolin B aggravate poly(I:C) secondary LPS stimulation-induced acute lung injury by modulating alveolar and interstitial macrophages DOI
Ziqi Hu, Xu Wu,

Duoduo Yao

et al.

Cytokine, Journal Year: 2025, Volume and Issue: 188, P. 156868 - 156868

Published: Jan. 31, 2025

Language: Английский

Citations

0
Analysis of Stratifin Expression and Proteome Variation in a Rat Model of Acute Lung Injury DOI Creative Commons
Ayaka Yoshida, Yoshiaki Hashimoto,

Hirotoshi Akane

et al.

Journal of Proteome Research, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 28, 2025

Diffuse alveolar damage (DAD) is a pathological hallmark of severe interstitial lung diseases, such as acute respiratory distress syndrome (ARDS), and linked to poor prognosis. Previously, we identified 14–3–3σ/stratifin (SFN) serum biomarker candidate for diagnosing DAD. To clarify the time-dependent relationship between SFN expression DAD, here investigated molecular changes in serum, bronchoalveolar lavage fluid (BALF), tissue an oleic acid (OA)-induced ARDS rat model. Acute edema was observed after OA administration, followed by epithelial cell proliferation increased BALF levels. Proteomic analysis extracts revealed that proteins related "inflammatory response" "HIF-1 signaling," including plasminogen activator inhibitor-1, were markedly 3 h injury, gradual decrease. Conversely, associated with "cell cycle" "p53 pathway," SFN, showed persistent increase starting at peaking 48 h. Western blotting immunohistochemistry confirmed expressed part proliferated type-II cells, accompanied p53 activation, important event differentiation into type-I cells. may be closely remodeling during repair process injury.

Language: Английский

Citations

0
The role of Ficolins in Lung Injury DOI Creative Commons

Meiyun Zhao,

Xiaowu Tan,

Xu Wu

et al.

Journal of Innate Immunity, Journal Year: 2024, Volume and Issue: 16(1), P. 440 - 450

Published: Aug. 19, 2024

Background: Respiratory diseases seriously threaten human health worldwide, and lung injury is an important component of respiratory disease. Complement activation function the innate immune system. helps body defend against invasion by external microorganisms, whereas excessive complement can exacerbate tissue damage or lead to unwanted side effects. Ficolins are a class immune-related proteins in lectin pathway that play roles body’s defense. Although individual ficolins not well understood, current information suggests may regulatory role injury. Summary: Several studies have shown involved response lung, particularly infectious inflammatory processes. Key Messages: This review summarizes influence development repair recognizing binding pathogenic modulating response, promoting clearance cells. In addition, associated with progression (such as pneumonia ARDS) impact on pathophysiological processes diseases.

Language: Английский

Citations

0
Gut microbiota-derived acetic acids promoted sepsis-induced acute respiratory distress syndrome by delaying neutrophil apoptosis through FABP4 DOI Creative Commons

Weixia Xuan,

Wu Xu, Zheng Li

et al.

Cellular and Molecular Life Sciences, Journal Year: 2024, Volume and Issue: 81(1)

Published: Oct. 25, 2024

In patients with sepsis, neutrophil apoptosis tends to be inversely proportional the severity of but its mechanism is not yet clear. This study aimed explore fatty acid binding protein 4 (FABP4) regulating through combined analysis gut microbiota and short-chain acids (SCFAs) metabolism. First, neutrophils from bronchoalveolar lavage fluid (BALF) sepsis-induced acute respiratory distress syndrome (ARDS) were purified isolated RNA was applied for sequencing. Then, cecal ligation puncture (CLP) method induce mouse sepsis model. After intervention differential SCFAs sodium acetate, FABP4 expression further analyzed. inhibitor BMS309403 used treat neutrophils. We found CLP group had increased lung injury score, tissue wet/dry ratio, vascular permeability, inflammatory factors IL-1β, TNF-α, IL-6, IFN-γ, CCL3 levels in both tissue. Additionally, lower ARDS mice. Meanwhile, CLP-induced dysbiosis changes observed. Further verification showed that acetic reduced via FFAR2. Besides, affected endoplasmic reticulum (ER) stress, depletion alleviated promotion development by BMS309403. Moreover, regulated RLE-6TN factors. conclusion, microbiota-derived delayed ER leading mediating epithelial cell damage.

Language: Английский

Citations

0