Literature DB >> 24464743

A limited CpG-containing oligodeoxynucleotide therapy regimen induces sustained suppression of allergic airway inflammation in mice.

John D Campbell1, Sariah A Kell1, Heather M Kozy1, Jeremy A Lum1, Rosemary Sweetwood1, Mabel Chu1, Cameron R Cunningham1, Hugh Salamon2, Clare M Lloyd3, Robert L Coffman1, Edith M Hessel1.   

Abstract

BACKGROUND: CpG-containing oligodeoxynucleotides (CpG-ODNs) are potent inhibitors of T helper 2 mediated allergic airway disease in sensitised mice challenged with allergen. A single treatment has transient effects but a limited series of treatments has potential to achieve clinically meaningful sustained inhibition of allergic airway disease.
OBJECTIVE: To optimise the treatment regimen for sustained efficacy and to determine the mechanisms of action in mice of an inhaled form of CpG-ODN being developed for human asthma treatment.
METHODS: We set up a chronic allergic-asthma model using ragweed-sensitised mice exposed weekly to intranasal ragweed. Using this model, the effects of a limited series of weekly intranasal 1018 ISS (CpG-ODN; B-class) treatments were evaluated during treatment and for several weeks after treatments had stopped but weekly allergen exposures continued. Treatment efficacy was evaluated by measuring effects on lung T helper 2 cytokines and eosinophilia, and lung dendritic cell function and T-cell responses.
RESULTS: Twelve intranasal 1018 ISS treatments induced significant suppression of bronchoalveolar lavage eosinophilia and interleukin 4, 5 and 13 levels. This suppression of allergic T helper 2 parameters was maintained through 13 weekly ragweed exposures administered after treatment cessation. Subsequent experiments demonstrated that at least five treatments were required for lasting suppression. Although CpG-ODN induced moderate T helper 1 responses, suppression of allergic airway disease did not require interferon γ but was associated with induction of a regulatory T-cell response.
CONCLUSIONS: A short series of CpG-ODN treatments results in sustained suppression of allergic lung inflammation induced by a clinically relevant allergen. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

Entities:  

Keywords:  Allergic Lung Disease; Asthma; Asthma Pharmacology; Innate Immunity

Mesh:

Substances:

Year:  2014        PMID: 24464743      PMCID: PMC4558941          DOI: 10.1136/thoraxjnl-2013-204605

Source DB:  PubMed          Journal:  Thorax        ISSN: 0040-6376            Impact factor:   9.139


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