Inflammatory processes during acute respiratory distress syndrome: a complex system

Reiss, Lucy Kathleen; Schuppert, Andreas; Uhlig, Stefan

doi:10.1097/mcc.0000000000000472

Cited by 60 publications

(41 citation statements)

References 72 publications

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“…Acute respiratory distress syndrome (ARDS) is characterized by increased lung permeability, pulmonary oedema and diffuse inflammation, which lead to disruption of alveolar capillary membranes [1]. Many studies have indicated that excessive activation of multiple inflammatory cell types and release of inflammatory mediators play vital roles in the development of ARDS [2,3]. Among these cell types, CD4+ T cells play an important role in the pathogenesis of ARDS [4].…”

Section: Introductionmentioning

confidence: 99%

Mesenchymal stem cells regulate the Th17/Treg cell balance partly through hepatocyte growth factor in vitro

Chen

Liu

et al. 2020

Stem Cell Res Ther

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Introduction: Mesenchymal stem cells (MSCs) exert immunomodulatory functions by inducing the development and differentiation of naive T cells into T cells with an anti-inflammatory regulatory T cell (Treg) phenotype. Our previous study showed that hepatocyte growth factor (HGF) secreted by MSCs had immunomodulatory effects in the context of lipopolysaccharide (LPS) stimulation. We hypothesized that HGF is a key factor in the MSC-mediated regulation of the T helper 17 (Th17) cell/regulatory T (Treg) cell balance. Methods: We investigated the effects of MSCs on the differentiation of CD4+ T cells and the functions of Th17/ Treg cells in response to LPS stimulation by performing in vitro coculture experiments. MSCs were added to the upper chambers of cell culture inserts, and CD4+ T cells were plated in the lower chambers, followed by treatment with LPS or an anti-HGF antibody. Th17 (CD4+CD3+RORrt+) and Treg (CD4+CD25+Foxp3+) cell frequencies were analysed by flow cytometry, and the expression of Th17 cell-and Treg cell-related cytokines in the CD4+ T cells or culture medium was measured by quantitative PCR (qPCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Neutrophil functions were determined by flow cytometry after a coculture with Th17/Treg cells.Results: The percentage of CD4+CD25+Foxp3+ cells was significantly increased in the CD4+ T cell population, while the percentage of CD4+CD3+RORrt+ cells was significantly decreased after MSC coculture. However, the MSC-induced effect was significantly inhibited by the anti-HGF antibody (p < 0.05). Furthermore, MSCs significantly inhibited the CD4+ T cell expression of IL-17 and IL-6 but increased the expression of IL-10 (p < 0.05 or p < 0.01); these effects were inhibited by the anti-HGF antibody (p < 0.05). In addition, CD4+ T cells cocultured with MSCs significantly inhibited neutrophil phagocytic and oxidative burst activities (p < 0.05 or p < 0.01); however, these MSCinduced effects were inhibited by the anti-HGF antibody (p < 0.05).Conclusion: These data suggested that MSCs induced the conversion of fully differentiated Th17 cells into functional Treg cells and thereby modulated the Th17/Treg cell balance in the CD4+ T cell population, which was partly attributed to HGF secreted by the MSCs.

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Section: Introductionmentioning

confidence: 99%

Mesenchymal stem cells regulate the Th17/Treg cell balance partly through hepatocyte growth factor in vitro

Chen

Liu

et al. 2020

Stem Cell Res Ther

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“…Stimulated Alveolar Epithelial Cells. Excessive lung inflammation is a proverbial feature of sepsis-related ALI/ARDS [6,18]. Therefore, we elucidated the roles of NEAT1 in LPS-induced inflammation in AECs.…”

Section: Neat1 Knockdown Suppressed Inflammation In Lps-mentioning

confidence: 98%

“…For example, AEC lesions disrupt cellular integrity and the ability to clear fluid from the alveolar space, clinically translating into lung edema. Intriguingly, recent studies also have defined ALI/ARDS as a syndrome of diffuse inflammatory lung injury [5,6]. During ALI/ARDS, AECs participate in the inflammatory response by acting as major sources of inflammatory cytokines (e.g., IL-1β, IL-6) and chemokines (e.g., MCP-1, IL-8).…”

Section: Introductionmentioning

confidence: 99%

Depression of lncRNA NEAT1 Antagonizes LPS-Evoked Acute Injury and Inflammatory Response in Alveolar Epithelial Cells via HMGB1-RAGE Signaling

Zhou

Wang

Zhang

2020

Mediators of Inflammation

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Sepsis-evoked acute lung injury (ALI) and its extreme manifestation, acute respiratory distress syndrome (ARDS), constitute a major cause of mortality in intensive care units. High levels of the long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) have been positively correlated with increased severity and unfavorable prognoses in patients with sepsis. Nevertheless, the function and molecular mechanism of NEAT1 in ALI remain elusive. In the current study, high levels of NEAT1 were confirmed in lipopolysaccharide- (LPS-) induced ALI mice models and in LPS-stimulated cells from the alveolar epithelial A549 cell line. Intriguingly, cessation of NEAT1 led to increased cell viability and decreased lactate dehydrogenase release, apoptosis, and caspase-3/9 activity, which conferred protection against LPS-induced injury in these cells. NEAT1 inhibition also restrained LPS-evoked transcripts and production of inflammatory cytokines IL-6, IL-1β, and TNF-α. A mechanism analysis corroborated the activation of high-mobility group box1 (HMGB1)/receptors for advanced glycation end products (RAGE) and NF-κB signaling in LPS-treated A549 cells. NEAT1 suppression reversed the activation of this pathway. Notably, reactivating HMGB1/RAGE signaling via HMGB1 overexpression blunted the anti-injury and anti-inflammation effects of NEAT1 knockdown. These findings suggest that NEAT1 may aggravate the progression of ALI and ARDS by inducing alveolar epithelial cell injury and inflammation via HMGB1/RAGE signaling, implying a promising treatment target for these conditions.

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“…In response to the invading pathogens, immunological mechanisms are activated. Some scholars have described the inflammation induced by the immune response as disease-related network, in which several pathogen-derived components of innate immunity interact nonlinearly [26]. The activation of antigen-presenting cells (APCs) includes the up-regulation of monocytes, macrophages, dendritic cells and endothelial cells.…”

Section: At the Cellular Level Sepsis-induced Inflammatory Cells Dammentioning

confidence: 99%

From sepsis to acute respiratory distress syndrome (ARDS): emerging preventive strategies based on molecular and genetic researches

Hao

Tang

2020

Bioscience Reports

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A healthy body activates the immune response to target invading pathogens (i.e. viruses, bacteria, fungi, and parasites) and avoid further systemic infection. The activation of immunological mechanisms includes several components of the immune system, such as innate and acquired immunity. Once any component of the immune response to infections is aberrantly altered or dysregulated, resulting in a failure to clear infection, sepsis will develop through a pro-inflammatory immunological mechanism. Furthermore, the severe inflammatory responses induced by sepsis also increase vascular permeability, leading to acute pulmonary edema and resulting in acute respiratory distress syndrome (ARDS). Apparently, potential for improvement exists in the management of the transition from sepsis to ARDS; thus, this article presents an exhaustive review that highlights the previously unrecognized relationship between sepsis and ARDS and suggests a direction for future therapeutic developments, including plasma and genetic pre-diagnostic strategies and interference with proinflammatory signaling.

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Inflammatory processes during acute respiratory distress syndrome: a complex system

Abstract: We suggest that therapeutic interventions in ARDS should be based on a systems approach to inflammation.

Cited by 60 publications

References 72 publications

Mesenchymal stem cells regulate the Th17/Treg cell balance partly through hepatocyte growth factor in vitro

Mesenchymal stem cells regulate the Th17/Treg cell balance partly through hepatocyte growth factor in vitro

Depression of lncRNA NEAT1 Antagonizes LPS-Evoked Acute Injury and Inflammatory Response in Alveolar Epithelial Cells via HMGB1-RAGE Signaling

From sepsis to acute respiratory distress syndrome (ARDS): emerging preventive strategies based on molecular and genetic researches

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