ArticlePulmonary pharmacology & therapeutics2016
Mitochondrial N-formyl peptides cause airway contraction and lung neutrophil infiltration via formyl peptide receptor activation.
Article in Pulmonary pharmacology & therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 54 citations in OpenAlex.
- Systemic neutrophil activation and N-formyl methionine-formyl peptide receptor-1 signaling define inflammatory endotypes in rheumatoid arthritis-associated lung involvement.Journal of internal medicine · 2025Article
- Mechanisms of mitochondrial damage-associated molecular patterns associated with inflammatory response in cardiovascular diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Astrocyte-microglia crosstalk in subarachnoid hemorrhage: mechanisms and treatments.Frontiers in immunology · 2025Review
- Cycling back to folate metabolism in cancer.Nature cancer · 2024Review
- Mitochondrial Dysfunction: A Key Player in Brain Aging and Diseases.Current issues in molecular biology · 2024Review
- Inflammatory changes in the choroid plexus following subarachnoid hemorrhage: the role of innate immune receptors and inflammatory molecules.Frontiers in cellular neuroscience · 2024Article
- CSF Mitochondrial N-Formyl Methionine Peptide as Complementary Diagnostic Tool in Anti-NMDAR Encephalitis and Anti-LGI1 Encephalitis.Neuropsychiatric disease and treatment · 2024Article
- Mitochondrial damage-associated molecular patterns in chronic obstructive pulmonary disease: Pathogenetic mechanism and therapeutic target.Journal of translational internal medicine · 2023Article
- The role of mtDAMPs in the trauma-induced systemic inflammatory response syndrome.Frontiers in immunology · 2023Review
- Chronic Lung Allograft Dysfunction Is Associated with Increased Levels of Cell-Free Mitochondrial DNA in Bronchoalveolar Lavage Fluid of Lung Transplant Recipients.Journal of clinical medicine · 2022Article
- Systemic inflammatory response syndrome is triggered by mitochondrial damage (Review).Molecular medicine reports · 2022Review
- Role of Mitochondria-Derived Danger Signals Released After Injury in Systemic Inflammation and Sepsis.Antioxidants & redox signaling · 2021Review
- Ethanol: striking the cardiovascular system by harming the gut microbiota.American journal of physiology. Heart and circulatory physiology · 2021Review
- Mitochondrial N-formyl methionine peptides associate with disease activity as well as contribute to neutrophil activation in patients with rheumatoid arthritis.Journal of autoimmunity · 2021Article
- The Role of Formyl Peptide Receptors in Permanent and Low-Grade Inflammation:International journal of molecular sciences · 2021Review
- Mitochondrial DAMPs and altered mitochondrial dynamics in OxLDL burden in atherosclerosis.Molecular and cellular biochemistry · 2021Review
- FPR-1 (Formyl Peptide Receptor-1) Activation Promotes Spontaneous, Premature Hypertension in Dahl Salt-Sensitive Rats.Hypertension (Dallas, Tex. : 1979) · 2021Article
- The Role of Formyl Peptide Receptor 1 in Uterine Contraction During Parturition.Frontiers in pharmacology · 2021Article
- Formyl peptide receptors in the mucosal immune system.Experimental & molecular medicine · 2020Review
- SPECT imaging of lung ischemia-reperfusion injury using [American journal of physiology. Lung cellular and molecular physiology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Respiratory failure is a common characteristic of systemic inflammatory response syndrome (SIRS) and sepsis. Trauma and severe blood loss cause the release of endogenous molecules known as damage-associated molecular patterns (DAMPs). Mitochondrial N-formyl peptides (F-MITs) are DAMPs that share similarities with bacterial N-formylated peptides, and are potent immune system activators. Recently, we observed that hemorrhagic shock-induced increases in plasma levels of F-MITs associated with lung damage, and that antagonism of formyl peptide receptors (FPR) ameliorated hemorrhagic shock-induced lung injury in rats. Corroborating these data, in the present study, it was observed that F-MITs expression is higher in plasma samples from trauma patients with SIRS or sepsis when compared to control trauma group. Therefore, to better understand the role of F-MITs in the regulation of lung and airway function, we studied the hypothesis that F-MITs lead to airway contraction and lung inflammation. We observed that F-MITs induced concentration-dependent contraction in trachea, bronchi and bronchioles. However, pre-treatment with mast cells degranulator or FPR antagonist decreased this response. Finally, intratracheal challenge with F-MITs increased neutrophil elastase expression in lung and inducible nitric oxide synthase and cell division control protein 42 expression in all airway segments. These data suggest that F-MITs could be a putative target to treat respiratory failure in trauma patients.
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