Regulation of the NLRP3 inflammasome and macrophage pyroptosis by the p38 MAPK signaling pathway in a mouse model of acute lung injury
Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) is characterized by uncontrolled progressive lung inflammation. Macrophages serve a key role in the pathogenesis of ALI/ARDS. Macrophage pyroptosis is a process of cell death releasing the proinflammatory cytokines interleukin (IL)...
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| Published in | Molecular medicine reports Vol. 18; no. 5; pp. 4399 - 4409 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
Greece
Spandidos Publications
01.11.2018
Spandidos Publications UK Ltd D.A. Spandidos |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1791-2997 1791-3004 1791-3004 |
| DOI | 10.3892/mmr.2018.9427 |
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| Abstract | Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) is characterized by uncontrolled progressive lung inflammation. Macrophages serve a key role in the pathogenesis of ALI/ARDS. Macrophage pyroptosis is a process of cell death releasing the proinflammatory cytokines interleukin (IL)‑1β and IL‑18. It was hypothesized that macrophage pyroptosis may partially account for the uncontrolled lung inflammation of ALI/ARDS. In the present study, greater macrophage pyroptosis in lipopolysaccharide (LPS)‑treated macrophages and the ALI/ARDS mouse model was observed. The expression of nucleotide‑binding domain, leucine‑rich‑containing family, pyrin domain‑containing (NLRP)3 and IL‑1β and cleavage of caspase‑1 were significantly elevated following LPS treatment accompanied by greater activation of p38 mitogen‑activated protein kinase (MAPK) signaling in vitro and in vivo. However, blocking p38 MAPK signaling through the inhibitor SB203580 significantly suppressed the acute lung injury and excessive lung inflammation in vivo, consistent with the reduced expression of the NLRP3 inflammasome and IL‑1β and cleavage of caspase‑1. Pretreatment of the rat NR8383 macrophage cell line with SB203580 significantly decreased the population of caspase‑1+PI+ pyroptotic cells and expression of NLRP3/IL‑1β. However, a larger population of Annexin V+PI‑ apoptotic cells was observed following blocking of the p38 MAPK signaling pathway. The results indicated that blockage of p38 MAPK signaling pathway skewed macrophage cell death from proinflammatory pyroptosis towards non‑inflammatory apoptosis. These effects may contribute to attenuated acute lung injury and excessive inflammation in the SB203580‑treated mice. The results may provide a novel therapeutic strategy for the treatment of uncontrolled lung inflammation in patients with ALI/ARDS. |
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| AbstractList | Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) is characterized by uncontrolled progressive lung inflammation. Macrophages serve a key role in the pathogenesis of ALI/ARDS. Macrophage pyroptosis is a process of cell death releasing the proinflammatory cytokines interleukin (IL)-1[beta] and IL-18. It was hypothesized that macrophage pyroptosis may partially account for the uncontrolled lung inflammation of ALI/ARDS. In the present study, greater macrophage pyroptosis in lipopolysaccharide (LPS)-treated macrophages and the ALI/ARDS mouse model was observed. The expression of nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing (NLRP)3 and IL-1[beta] and cleavage of caspase-1 were significantly elevated following LPS treatment accompanied by greater activation of p38 mitogen-activated protein kinase (MAPK) signaling in vitro and in vivo. However, blocking p38 MAPK signaling through the inhibitor SB203580 significantly suppressed the acute lung injury and excessive lung inflammation in vivo, consistent with the reduced expression of the NLRP3 inflammasome and IL-1[beta] and cleavage of caspase-1. Pretreatment of the rat NR8383 macrophage cell line with SB203580 significantly decreased the population of caspase-1+PI+ pyroptotic cells and expression of NLRP3/IL-1[beta]. However, a larger population of Annexin V+PI- apoptotic cells was observed following blocking of the p38 MAPK signaling pathway. The results indicated that blockage of p38 MAPK signaling pathway skewed macrophage cell death from proinflammatory pyroptosis towards non-inflammatory apoptosis. These effects may contribute to attenuated acute lung injury and excessive inflammation in the SB203580-treated mice. The results may provide a novel therapeutic strategy for the treatment of uncontrolled lung inflammation in patients with ALI/ARDS. Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) is characterized by uncontrolled progressive lung inflammation. Macrophages serve a key role in the pathogenesis of ALI/ARDS. Macrophage pyroptosis is a process of cell death releasing the proinflammatory cytokines interleukin (IL)‑1β and IL‑18. It was hypothesized that macrophage pyroptosis may partially account for the uncontrolled lung inflammation of ALI/ARDS. In the present study, greater macrophage pyroptosis in lipopolysaccharide (LPS)‑treated macrophages and the ALI/ARDS mouse model was observed. The expression of nucleotide‑binding domain, leucine‑rich‑containing family, pyrin domain‑containing (NLRP)3 and IL‑1β and cleavage of caspase‑1 were significantly elevated following LPS treatment accompanied by greater activation of p38 mitogen‑activated protein kinase (MAPK) signaling in vitro and in vivo. However, blocking p38 MAPK signaling through the inhibitor SB203580 significantly suppressed the acute lung injury and excessive lung inflammation in vivo, consistent with the reduced expression of the NLRP3 inflammasome and IL‑1β and cleavage of caspase‑1. Pretreatment of the rat NR8383 macrophage cell line with SB203580 significantly decreased the population of caspase‑1+PI+ pyroptotic cells and expression of NLRP3/IL‑1β. However, a larger population of Annexin V+PI‑ apoptotic cells was observed following blocking of the p38 MAPK signaling pathway. The results indicated that blockage of p38 MAPK signaling pathway skewed macrophage cell death from proinflammatory pyroptosis towards non‑inflammatory apoptosis. These effects may contribute to attenuated acute lung injury and excessive inflammation in the SB203580‑treated mice. The results may provide a novel therapeutic strategy for the treatment of uncontrolled lung inflammation in patients with ALI/ARDS.Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) is characterized by uncontrolled progressive lung inflammation. Macrophages serve a key role in the pathogenesis of ALI/ARDS. Macrophage pyroptosis is a process of cell death releasing the proinflammatory cytokines interleukin (IL)‑1β and IL‑18. It was hypothesized that macrophage pyroptosis may partially account for the uncontrolled lung inflammation of ALI/ARDS. In the present study, greater macrophage pyroptosis in lipopolysaccharide (LPS)‑treated macrophages and the ALI/ARDS mouse model was observed. The expression of nucleotide‑binding domain, leucine‑rich‑containing family, pyrin domain‑containing (NLRP)3 and IL‑1β and cleavage of caspase‑1 were significantly elevated following LPS treatment accompanied by greater activation of p38 mitogen‑activated protein kinase (MAPK) signaling in vitro and in vivo. However, blocking p38 MAPK signaling through the inhibitor SB203580 significantly suppressed the acute lung injury and excessive lung inflammation in vivo, consistent with the reduced expression of the NLRP3 inflammasome and IL‑1β and cleavage of caspase‑1. Pretreatment of the rat NR8383 macrophage cell line with SB203580 significantly decreased the population of caspase‑1+PI+ pyroptotic cells and expression of NLRP3/IL‑1β. However, a larger population of Annexin V+PI‑ apoptotic cells was observed following blocking of the p38 MAPK signaling pathway. The results indicated that blockage of p38 MAPK signaling pathway skewed macrophage cell death from proinflammatory pyroptosis towards non‑inflammatory apoptosis. These effects may contribute to attenuated acute lung injury and excessive inflammation in the SB203580‑treated mice. The results may provide a novel therapeutic strategy for the treatment of uncontrolled lung inflammation in patients with ALI/ARDS. Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) is characterized by uncontrolled progressive lung inflammation. Macrophages serve a key role in the pathogenesis of ALI/ARDS. Macrophage pyroptosis is a process of cell death releasing the proinflammatory cytokines interleukin (IL)-1[beta] and IL-18. It was hypothesized that macrophage pyroptosis may partially account for the uncontrolled lung inflammation of ALI/ARDS. In the present study, greater macrophage pyroptosis in lipopolysaccharide (LPS)-treated macrophages and the ALI/ARDS mouse model was observed. The expression of nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing (NLRP)3 and IL-1[beta] and cleavage of caspase-1 were significantly elevated following LPS treatment accompanied by greater activation of p38 mitogen-activated protein kinase (MAPK) signaling in vitro and in vivo. However, blocking p38 MAPK signaling through the inhibitor SB203580 significantly suppressed the acute lung injury and excessive lung inflammation in vivo, consistent with the reduced expression of the NLRP3 inflammasome and IL-1[beta] and cleavage of caspase-1. Pretreatment of the rat NR8383 macrophage cell line with SB203580 significantly decreased the population of caspase-1+PI+ pyroptotic cells and expression of NLRP3/IL-1[beta]. However, a larger population of Annexin V+PI- apoptotic cells was observed following blocking of the p38 MAPK signaling pathway. The results indicated that blockage of p38 MAPK signaling pathway skewed macrophage cell death from proinflammatory pyroptosis towards non-inflammatory apoptosis. These effects may contribute to attenuated acute lung injury and excessive inflammation in the SB203580-treated mice. The results may provide a novel therapeutic strategy for the treatment of uncontrolled lung inflammation in patients with ALI/ARDS. Key words: acute lung injury and acute respiratory distress syndrome, alveolar macrophages, p38 mitogen-activated protein kinase signaling pathway, pyroptosis, nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 inflammasome Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) is characterized by uncontrolled progressive lung inflammation. Macrophages serve a key role in the pathogenesis of ALI/ARDS. Macrophage pyroptosis is a process of cell death releasing the proinflammatory cytokines interleukin (IL)-1β and IL-18. It was hypothesized that macrophage pyroptosis may partially account for the uncontrolled lung inflammation of ALI/ARDS. In the present study, greater macrophage pyroptosis in lipopolysaccharide (LPS)-treated macrophages and the ALI/ARDS mouse model was observed. The expression of nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing (NLRP)3 and IL-1β and cleavage of caspase-1 were significantly elevated following LPS treatment accompanied by greater activation of p38 mitogen-activated protein kinase (MAPK) signaling in vitro and in vivo . However, blocking p38 MAPK signaling through the inhibitor SB203580 significantly suppressed the acute lung injury and excessive lung inflammation in vivo , consistent with the reduced expression of the NLRP3 inflammasome and IL-1β and cleavage of caspase-1. Pretreatment of the rat NR8383 macrophage cell line with SB203580 significantly decreased the population of caspase-1+PI+ pyroptotic cells and expression of NLRP3/IL-1β. However, a larger population of Annexin V+PI- apoptotic cells was observed following blocking of the p38 MAPK signaling pathway. The results indicated that blockage of p38 MAPK signaling pathway skewed macrophage cell death from proinflammatory pyroptosis towards non-inflammatory apoptosis. These effects may contribute to attenuated acute lung injury and excessive inflammation in the SB203580-treated mice. The results may provide a novel therapeutic strategy for the treatment of uncontrolled lung inflammation in patients with ALI/ARDS. Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) is characterized by uncontrolled progressive lung inflammation. Macrophages serve a key role in the pathogenesis of ALI/ARDS. Macrophage pyroptosis is a process of cell death releasing the proinflammatory cytokines interleukin (IL)‑1β and IL‑18. It was hypothesized that macrophage pyroptosis may partially account for the uncontrolled lung inflammation of ALI/ARDS. In the present study, greater macrophage pyroptosis in lipopolysaccharide (LPS)‑treated macrophages and the ALI/ARDS mouse model was observed. The expression of nucleotide‑binding domain, leucine‑rich‑containing family, pyrin domain‑containing (NLRP)3 and IL‑1β and cleavage of caspase‑1 were significantly elevated following LPS treatment accompanied by greater activation of p38 mitogen‑activated protein kinase (MAPK) signaling in vitro and in vivo. However, blocking p38 MAPK signaling through the inhibitor SB203580 significantly suppressed the acute lung injury and excessive lung inflammation in vivo, consistent with the reduced expression of the NLRP3 inflammasome and IL‑1β and cleavage of caspase‑1. Pretreatment of the rat NR8383 macrophage cell line with SB203580 significantly decreased the population of caspase‑1+PI+ pyroptotic cells and expression of NLRP3/IL‑1β. However, a larger population of Annexin V+PI‑ apoptotic cells was observed following blocking of the p38 MAPK signaling pathway. The results indicated that blockage of p38 MAPK signaling pathway skewed macrophage cell death from proinflammatory pyroptosis towards non‑inflammatory apoptosis. These effects may contribute to attenuated acute lung injury and excessive inflammation in the SB203580‑treated mice. The results may provide a novel therapeutic strategy for the treatment of uncontrolled lung inflammation in patients with ALI/ARDS. Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) is characterized by uncontrolled progressive lung inflammation. Macrophages serve a key role in the pathogenesis of ALI/ARDS. Macrophage pyroptosis is a process of cell death releasing the proinflammatory cytokines interleukin (IL)-1β and IL-18. It was hypothesized that macrophage pyroptosis may partially account for the uncontrolled lung inflammation of ALI/ARDS. In the present study, greater macrophage pyroptosis in lipopolysaccharide (LPS)-treated macrophages and the ALI/ARDS mouse model was observed. The expression of nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing (NLRP)3 and IL-1β and cleavage of caspase-1 were significantly elevated following LPS treatment accompanied by greater activation of p38 mitogen-activated protein kinase (MAPK) signaling in vitro and in vivo. However, blocking p38 MAPK signaling through the inhibitor SB203580 significantly suppressed the acute lung injury and excessive lung inflammation in vivo, consistent with the reduced expression of the NLRP3 inflammasome and IL-1β and cleavage of caspase-1. Pretreatment of the rat NR8383 macrophage cell line with SB203580 significantly decreased the population of caspase-1+PI+ pyroptotic cells and expression of NLRP3/IL-1β. However, a larger population of Annexin V+PI- apoptotic cells was observed following blocking of the p38 MAPK signaling pathway. The results indicated that blockage of p38 MAPK signaling pathway skewed macrophage cell death from proinflammatory pyroptosis towards non-inflammatory apoptosis. These effects may contribute to attenuated acute lung injury and excessive inflammation in the SB203580-treated mice. The results may provide a novel therapeutic strategy for the treatment of uncontrolled lung inflammation in patients with ALI/ARDS. |
| Audience | Academic |
| Author | Zhu, Lei Ren, Weiying Jiang, Zhilong Li, Dandan |
| AuthorAffiliation | 2 Department of Gerontology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China 1 Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China |
| AuthorAffiliation_xml | – name: 2 Department of Gerontology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China – name: 1 Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China |
| Author_xml | – sequence: 1 givenname: Dandan surname: Li fullname: Li, Dandan organization: Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China – sequence: 2 givenname: Weiying surname: Ren fullname: Ren, Weiying organization: Department of Gerontology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China – sequence: 3 givenname: Zhilong surname: Jiang fullname: Jiang, Zhilong organization: Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China – sequence: 4 givenname: Lei surname: Zhu fullname: Zhu, Lei organization: Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30152849$$D View this record in MEDLINE/PubMed |
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| Snippet | Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) is characterized by uncontrolled progressive lung inflammation. Macrophages serve a key... |
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| SubjectTerms | Acute Lung Injury - drug therapy Acute Lung Injury - genetics Acute Lung Injury - pathology Animals Annexin V Apoptosis Care and treatment Caspase Caspase-1 Caspases - genetics Cell culture Cell death Cellular signal transduction Cytokines Diagnosis Disease Models, Animal Edema Gene expression Genetic aspects Health aspects Humans Imidazoles - pharmacology Inflammasomes Inflammasomes - genetics Inflammation Inflammation - drug therapy Inflammation - genetics Inflammation - pathology Interleukin 18 Interleukin-18 - genetics Interleukin-1beta - genetics Kinases Laboratory animals Leucine Lipopolysaccharides Lung - drug effects Lung - metabolism Lung - pathology Lung diseases Lungs Macrophages Macrophages - drug effects Macrophages - pathology MAP kinase Mice Mortality Neutrophils NLR Family, Pyrin Domain-Containing 3 Protein - genetics p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors p38 Mitogen-Activated Protein Kinases - genetics Pathogens Protein kinase Protein kinases Proteins Pyridines - pharmacology Pyrin protein Pyroptosis Pyroptosis - genetics Respiratory distress syndrome Respiratory Distress Syndrome, Adult - drug therapy Respiratory Distress Syndrome, Adult - genetics Rodents Signal Transduction Studies Tumor necrosis factor-TNF |
| Title | Regulation of the NLRP3 inflammasome and macrophage pyroptosis by the p38 MAPK signaling pathway in a mouse model of acute lung injury |
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