ArticleAmerican journal of respiratory cell and molecular biology2009
Defective acid sphingomyelinase pathway with Pseudomonas aeruginosa infection in cystic fibrosis.
Article in American journal of respiratory cell and molecular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- Furin inhibition protects against acute lung injury in a mouse model of Pseudomonas aeruginosa infection.American journal of respiratory cell and molecular biology · 2026Article
- Podocyte-specific silencing of acid sphingomyelinase gene to abrogate hyperhomocysteinemia-induced NLRP3 inflammasome activation and glomerular inflammation.American journal of physiology. Renal physiology · 2024Article
- The impact of sphingomyelin on the pathophysiology and treatment response to olipudase alfa in acid sphingomyelinase deficiency.Genetics in medicine open · 2024Review
- Functional roles of sphingolipids in immunity and their implication in disease.Experimental & molecular medicine · 2023Review
- The Air-Liquid Interface Reorganizes Membrane Lipids and Enhances the Recruitment of Slc26a3 to Lipid-Rich Domains in Human Colonoid Monolayers.International journal of molecular sciences · 2023Article
- Functions of Sphingolipids in Pathogenesis During Host-Pathogen Interactions.Frontiers in microbiology · 2021Review
- Neisseria meningitidis Type IV Pili Trigger CaInfection and immunity · 2019Article
- Neutrophil elastase correlates with increased sphingolipid content in cystic fibrosis sputum.Pediatric pulmonology · 2018Article
- The Role of Sphingolipids on Innate Immunity to Intestinal Salmonella Infection.International journal of molecular sciences · 2017Review
- Acid sphingomyelinase mediates human CD4Cell death & disease · 2017Review
- Sphingolipids Are Dual Specific Drug Targets for the Management of Pulmonary Infections: Perspective.Frontiers in immunology · 2017Review
- Evidence for the Involvement of Lipid Rafts and Plasma Membrane Sphingolipid Hydrolases inMediators of inflammation · 2017Article
- ClEuropean biophysics journal : EBJ · 2016Article
- Ion channels in regulated cell death.Cellular and molecular life sciences : CMLS · 2016Review
- Development of rAAV2-CFTR: History of the First rAAV Vector Product to be Used in Humans.Human gene therapy methods · 2016Review
- Role of acid sphingomyelinase bioactivity in human CD4+ T-cell activation and immune responses.Cell death & disease · 2015Article
- Pseudomonas aeruginosa pyocyanin induces neutrophil death via mitochondrial reactive oxygen species and mitochondrial acid sphingomyelinase.Antioxidants & redox signaling · 2015Article
- Administration of antenatal glucocorticoids and postnatal surfactant ameliorates respiratory distress syndrome-associated neonatal lethality in Erk3(-/-) mouse pups.Pediatric research · 2014Article
- Article
- GBA2-encoded β-glucosidase activity is involved in the inflammatory response to Pseudomonas aeruginosa.PloS one · 2014Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Acid sphingomyelinase (ASMase) is a key enzyme in sphingolipid metabolism, which can be activated by various cellular stress mechanisms including bacterial pathogens. Activation of ASMase generates ceramide, which is important for innate immune response to eliminate infected pathogens. The current study reveals a defective ASMase pathway after Pseudomonas aeruginosa infection in both a cystic fibrosis (CF) bronchial epithelial cell line (IB3-1 cell) and in the lungs of CF transmembrane conductance regulator (CFTR) knockout (KO) mice as compared with S9 cells and wild-type C57BL/6 mice. ASMase activity and total ceramide levels significantly increased in S9 cells and C57BL/6 mice with P. aeruginosa infection, but not in IB3-1 cells and CFTR KO mice. The silencing of CFTR by CFTR RNAi in S9 cells significantly decreased ASMase activity after bacterial infection as compared with controls. This study also demonstrates that induction of ASMase is responsible for modulating the immune response to bacterial infection. Blocking ASMase activity with specific ASMase RNAi, an ASMase inhibitor, or an ASMase antibody in S9 cells significantly increased IL-8 levels with P. aeruginosa infection compared with controls. Reciprocally, adding exogenous bacterial sphingomyelinase to IB3-1 cells significantly decreased IL-8 levels compared with untreated cells. In addition, silencing of ASMase in S9 cells also significantly decreased bacterial internalization. Adding exogenous bacterial sphingomyelinase to IB3-1 cells reconstituted the cell death response to P. aeruginosa infection. This study demonstrates that the defective ASMase pathway in CF is a key contributor to the unabated IL-8 response with P. aeruginosa infection and to the compromised host response failing to eradicate bacteria.
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