ArticlePloS one2012
Intranasal administration of poly(I:C) and LPS in BALB/c mice induces airway hyperresponsiveness and inflammation via different pathways.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 64 citations in OpenAlex.
- Investigation of the Effects of Perfluorooctane Sulfonic Acid (PFOS) and Perfluorooctanoic Acid (PFOA) Exposure on Interleukin-17 Signalling and Poly(I:C)-Induced Lung Inflammation in BALB/c Mice.Basic & clinical pharmacology & toxicology · 2026Article
- Importance of the delivery route for the tolerability and efficacy of immunomodulatory agents for lung cancer.Scientific reports · 2026Article
- Sex-specific impact of early life stress on adult lung inflammatory response after LPS and Poly I:C exposures.Brain, behavior, & immunity - health · 2026Article
- An innovative nasal nanovaccine against SARS-CoV-2 induces systemic and upper airway immunity controlling viral replication.NPJ vaccines · 2026Article
- Lung dysbiosis disrupts an FFAR2-mediated innate immune circuit againstTheranostics · 2026Article
- Integrated metabolomics and network pharmacology to investigate the effects of Yi-Qi-Xuan-Fei-Hua-Tan decoction for treating acute respiratory distress syndrome.Annals of medicine and surgery (2012) · 2025Article
- Toll-like receptor activation induces airway obstruction and hyperresponsiveness in guinea pigs.Respiratory research · 2024Article
- Pig Milk Exosome Packaging ssc-miR-22-3p Alleviates Pig Intestinal Epithelial Cell Injury and Inflammatory Response by TargetingInternational journal of molecular sciences · 2024Article
- Inhibition of Polyinosinic-Polycytidylic Acid-Induced Acute Pulmonary Inflammation and NF-κB Activation in Mice by a Banana Plant Extract.International journal of medical sciences · 2024Article
- Enhancing autophagy in CD11cCell reports · 2023Article
- Inhibition of γ-glutamyl transferase suppresses airway hyperresponsiveness and airway inflammation in a mouse model of steroid resistant asthma exacerbation.Frontiers in immunology · 2023Article
- Recombinant multimeric dog allergen prevents airway hyperresponsiveness in a model of asthma marked by vigorous TAllergy · 2022Article
- Therapeutic stem cell-derived alveolar-like macrophages display bactericidal effects and resolve Pseudomonas aeruginosa-induced lung injury.Journal of cellular and molecular medicine · 2022Article
- Induction of Innate Immune Response by TLR3 Agonist Protects Mice against SARS-CoV-2 Infection.Viruses · 2022Article
- Innate Lymphoid Cells Are Required to Induce Airway Hyperreactivity in a Murine Neutrophilic Asthma Model.Frontiers in immunology · 2022Article
- Article
- Bronchial Vascular Remodeling Is Attenuated by Anti-IL-17 in Asthmatic Responses Exacerbated by LPS.Frontiers in pharmacology · 2020Article
- Apolipoprotein E is a concentration-dependent pulmonary danger signal that activates the NLRP3 inflammasome and IL-1β secretion by bronchoalveolar fluid macrophages from asthmatic subjects.The Journal of allergy and clinical immunology · 2019Article
- Memory deficits in males and females long after subchronic immune challenge.Neurobiology of learning and memory · 2019Article
- Viral Mimetic-Induced Inflammation Abolishes Q-Pathway, but Not S-Pathway, Respiratory Motor Plasticity in Adult Rats.Frontiers in physiology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBacterial and viral infections are known to promote airway hyperresponsiveness (AHR) in asthmatic patients. The mechanism behind this reaction is poorly understood, but pattern recognizing Toll-like receptors (TLRs) have recently been suggested to play a role. MATERIALS AND
methodsTo explore the relation between infection-induced airway inflammation and the development of AHR, poly(I:C) activating TLR3 and LPS triggering TLR4, were chosen to represent viral and bacterial induced interactions, respectively. Female BALB/c or MyD88-deficient C57BL/6 mice were treated intranasally with either poly(I:C), LPS or PBS (vehicle for the control group), once a day, during 4 consecutive days.
resultsWhen methacholine challenge was performed on day 5, BALB/c mice responded with an increase in airway resistance. The maximal resistance was higher in the poly(I:C) and LPS treated groups than among the controls, indicating development of AHR in response to repeated TLR activation. The proportion of lymphocytes in broncheoalveolar lavage fluid (BALF) increased after poly(I:C) treatment whereas LPS enhanced the amount of neutrophils. A similar cellular pattern was seen in lung tissue. Analysis of 21 inflammatory mediators in BALF revealed that the TLR response was receptor-specific. MyD88-deficient C57BL/6 mice responded to poly (I:C) with an influx of lymphocytes, whereas LPS caused no inflammation.
conclusionIn vivo activation of TLR3 and TLR4 in BALB/c mice both caused AHR in conjunction with a local inflammatory reaction. The AHR appeared to be identical regardless of which TLR that was activated, whereas the inflammation exhibited a receptor specific profile in terms of both recruited cells and inflammatory mediators. The inflammatory response caused by LPS appeared to be dependent on MyD88 pathway. Altogether the presented data indicate that the development of AHR and the induction of local inflammation might be the result of two parallel events, rather than one leading to another.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.