ArticleClinical and experimental immunology2008
Tumour necrosis factor-alpha blockade suppresses murine allergic airways inflammation.
Article in Clinical and experimental immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 49 citations in OpenAlex.
- Article
- Zinc and iron complexes of oleanolic acid, (OA) attenuate allergic airway inflammation in rats.Inflammopharmacology · 2019Article
- Protective Role of Eosinophils and TNFa after Ozone Inhalation.Research report (Health Effects Institute) · 2017Article
- Human eosinophil activin A synthesis and mRNA stabilization are induced by the combination of IL-3 plus TNF.Immunology and cell biology · 2016Article
- Hypereosinophilia and seroconversion of rheumatoid arthritis.Clinical rheumatology · 2014Review
- The effect of rhinovirus on airway inflammation in a murine asthma model.Korean journal of pediatrics · 2013Article
- Aging predisposes to acute inflammatory induced pathology after tumor immunotherapy.The Journal of experimental medicine · 2013Article
- IgE cross-linking critically impairs human monocyte function by blocking phagocytosis.The Journal of allergy and clinical immunology · 2013Article
- Minocycline blocks asthma-associated inflammation in part by interfering with the T cell receptor-nuclear factor κB-GATA-3-IL-4 axis without a prominent effect on poly(ADP-ribose) polymerase.The Journal of biological chemistry · 2013Article
- TNF-α-induces airway hyperresponsiveness to cholinergic stimulation in guinea pig airways.British journal of pharmacology · 2012Article
- Anti-inflammatory effects of the neurotransmitter agonist Honokiol in a mouse model of allergic asthma.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Deficiency in the serum-derived hyaluronan-associated protein-hyaluronan complex enhances airway hyperresponsiveness in a murine model of asthma.International archives of allergy and immunology · 2010Article
- Decrease in airway mucous gene expression caused by treatment with anti-tumor necrosis factor alpha in a murine model of allergic asthma.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2009Article
- An investigation of the impact of the location and timing of antigen-specific T cell division on airways inflammation.Clinical and experimental immunology · 2009Article
- Etanercept prevents airway hyperresponsiveness by protecting neuronal M2 muscarinic receptors in antigen-challenged guinea pigs.British journal of pharmacology · 2009Article
- Allergy and the nose.Clinical and experimental immunology · 2008Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Asthma is a heterogeneous disease that has been increasing in incidence throughout western societies and cytokines, including proinflammatory tumour necrosis factor alpha (TNF-alpha), have been implicated in the pathogenesis of asthma. Anti-TNF-alpha therapies have been established successfully in the clinic for diseases such as rheumatoid arthritis and Crohn's disease. TNF-alpha-blocking strategies are now being trialled in asthma; however, their mode of action is poorly understood. Based on the observation that TNF-alpha induces lymph node hypertrophy we have attempted to investigate this as a mechanism of action of TNF-alpha in airway inflammation by employing two models of murine airway inflammation, that we have termed short and long models, representing severe and mild/moderate asthma, respectively. The models differ by their immunization schedules. In the short model, characterized by eosinophilic and neutrophilic airway inflammation the effect of TNF-alpha blockade was a reduction in draining lymph node (DLN) hypertrophy, eosinophilia, interleukin (IL)-5 production and immunoglobulin E (IgE) production. In the long model, characterized by eosinophilic inflammation, TNF-alpha blockade produced a reduction in DLN hypertrophy and IL-5 production but had limited effects on eosinophilia and IgE production. These results indicate that anti-TNF-alpha can suppress DLN hypertrophy and decrease airway inflammation. Further investigations showed that anti-TNF-alpha-induced inhibition of DLN hypertrophy cannot be explained by preventing l-selectin-dependent capture of lymphocytes into the DLN. Given that overall TNF blockade was able to suppress the short model (severe) more effectively than the long model (mild/moderate), the results suggest that TNF-alpha blocking therapies may be more effective in the treatment of severe asthma.
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