ArticleInfection and immunity2010
Role of excessive inflammatory response to Stenotrophomonas maltophilia lung infection in DBA/2 mice and implications for cystic fibrosis.
Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
37 citing papers in PubMed, 56 citations in OpenAlex.
- Integrated immunoinformatics for the design of novel multi-epitope vaccine and identification of new drug targets against Stenotrophomonas maltophilia, a multidrug-resistant superbug.Journal, genetic engineering & biotechnology · 2026Article
- From nature to clinic: tracking genetic and environmental drivers of Stenotrophomonas maltophilia pathogenicity.Archives of microbiology · 2026Review
- Dietary Administration of Postbiotics fromAnimals : an open access journal from MDPI · 2025Article
- Lung microbiota: a new hope for treating acute respiratory distress syndrome?Frontiers in microbiology · 2025Review
- A novel pathogenic species of genusFrontiers in cellular and infection microbiology · 2024Article
- Time-course transcriptome analysis of lungs from mice infected with inhaled aerosolizedJournal of thoracic disease · 2023Article
- A guide toFrontiers in cellular and infection microbiology · 2023Review
- Multilocus Sequence Typing for Molecular Epidemiology of Stenotrophomonas maltophilia Clinical and Environmental Isolates from a Tertiary Hospital in West of IranIranian biomedical journal · 2022Article
- Acute Pneumonia Caused by Clinically IsolatedMicroorganisms · 2022Article
- Advances in the Microbiology of Stenotrophomonas maltophilia.Clinical microbiology reviews · 2021Article
- Biological Activity and Antibiofilm Molecular Profile ofMolecules (Basel, Switzerland) · 2020Article
- Cooperativity between Stenotrophomonas maltophilia and Pseudomonas aeruginosa during Polymicrobial Airway Infections.Infection and immunity · 2020Article
- The opportunistic pathogen Stenotrophomonas maltophilia utilizes a type IV secretion system for interbacterial killing.PLoS pathogens · 2019Article
- Stenotrophomonas maltophilia Encodes a VirB/VirD4 Type IV Secretion System That Modulates Apoptosis in Human Cells and Promotes Competition against Heterologous Bacteria, Including Pseudomonas aeruginosa.Infection and immunity · 2019Article
- Article
- Characterization of Phenotypic and Genotypic Diversity ofFrontiers in microbiology · 2019Article
- Draft Genome Sequences of Two Cystic Fibrosis Strains of Stenotrophomonas maltophilia, AU30115 and AU32848.Microbiology resource announcements · 2018Article
- Stenotrophomonas maltophilia produces an EntC-dependent catecholate siderophore that is distinct from enterobactin.Microbiology (Reading, England) · 2017Article
- Genetic susceptibility to toxicologic lung responses among inbred mouse strains following exposure to carbon nanotubes and profiling of underlying gene networks.Toxicology and applied pharmacology · 2017Article
- Evolution ofFrontiers in microbiology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stenotrophomonas maltophilia is a pathogen that causes infections mainly in immunocompromised patients. Despite increased S. maltophilia isolation from respiratory specimens of patients with cystic fibrosis (CF), the real contribution of the microorganism to CF pathogenesis still needs to be clarified. The aim of the present study was to evaluate the pathogenic role of S. maltophilia in CF patients by using a model of acute respiratory infection in DBA/2 mice following a single exposure to aerosolized bacteria. The pulmonary bacterial load was stable until day 3 and then decreased significantly from day 3 through day 14, when the bacterial load became undetectable in all infected mice. Infection disseminated in most mice, although at a very low level. Severe effects (swollen lungs, large atelectasis, pleural adhesion, and hemorrhages) of lung pathology were observed on days 3, 7, and 14. The clearance of S. maltophilia observed in DBA/2 mouse lungs was clearly associated with an early and intense bronchial and alveolar inflammatory response, which is mediated primarily by neutrophils. Significantly higher levels of interleukin-1beta (IL-1beta), IL-6, IL-12, gamma interferon (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), GROalpha/KC, MCP-1/JE, MCP-5, macrophage inflammatory protein 1alpha (MIP-1alpha), MIP-2, and TARC were observed in infected mice on day 1 with respect to controls. Excessive pulmonary infection and inflammation caused systemic effects, manifested by weight loss, and finally caused a high mortality rate. Taken together, our results show that S. maltophilia is not just a bystander in CF patients but has the potential to contribute to the inflammatory process that compromises respiratory function.
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