Topical corticosteroid inhibits interleukin‐4, ‐5 and ‐13 in nasal secretions following allergen challenge

Erin, Edward M.; Zacharasiewicz, Angela; Nicholson, GC; Tan, Andrew J.; Higgins, Lee Ann; Td, Williams; Murdoch, Robert; Durham, Stephen R.; Barnes, Peter J.; Hansel, Trevor T.

doi:10.1111/j.1365-2222.2005.02381.x

Cited by 70 publications

(58 citation statements)

References 42 publications

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“…Cytokines from T-helper (Th)-2 cells play an important role in orchestrating airway inflammation in asthma through the release of specific cytokines, and particularly on the infiltration of eosinophils, which is mediated by interleukin-5. The present author has shown that nasal grass pollen challenge gives a rapid increase in Th2 cytokines, including IL-5, measured by direct nasal sampling, and that this is completely inhibited by pre-treatment for 30 min with an inhaled corticosteroid [62]. This is likely to be due to an inhibitory effect of corticosteroids on the transcription factor GATA-3 in Th2 cells which regulates the synthesis of Th2 cytokines.…”

Section: Rapid Anti-inflammatory Effects In Clinical Studiesmentioning

confidence: 82%

Scientific rationale for using a single inhaler for asthma control

Barnes¹

2007

Eur Respir J

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139

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Clinical trials have recently demonstrated that using a budesonide/formoterol combination inhaler as regular maintenance treatment twice daily but also as a rescue therapy for breakthrough symptoms can provide more effective control of asthma, particularly in reducing exacerbations, than using a short-acting b 2 -agonist or formoterol as rescue therapy. This suggests that the corticosteroid component of the combination therapy plays an important role in rescue therapy.Formoterol as a rescue therapy is effective in relieving symptoms by relaxing airway smooth muscle but is also likely to have important inhibitory effects on mast cells, plasma exudation and neutrophilic inflammation.Inhaled corticosteroids have much more rapid suppressing effects on airway inflammation than previously recognised and the increased dose used as rescue therapy may prevent the increase in airway inflammation that occurs during the evolution of an exacerbation, thus preventing its development.It is likely that the molecular interactions between b 2 -agonists and corticosteroids also enhance the effect of the combination therapy as rescue therapy. There is now a strong scientific rationale for single inhaler therapy in asthma, but more research is now needed to better understand the mechanisms involved.

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Section: Rapid Anti-inflammatory Effects In Clinical Studiesmentioning

confidence: 82%

Scientific rationale for using a single inhaler for asthma control

Barnes¹

2007

Eur Respir J

Self Cite

139

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“…This might partly be related to the applied doses of allergen and LPS, but also to the low number of patients examined. Along with several groups, we have shown that challenge with allergen, but not LPS, can cause local nasal symptoms [23] and that both allergen and LPS have the ability to release an array of cytokines in the nose [23,24,25,26,27,28,29]. …”

Section: Discussionmentioning

confidence: 99%

Systemic Up-Regulation of TLR4 Causes Lipopolysaccharide-Induced Augmentation of Nasal Cytokine Release in Allergic Rhinitis

Ekman¹,

Virtala²,

Fransson³

et al. 2012

Int Arch Allergy Immunol

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Background: Allergic rhinitis is a systemic disorder, and it is clinically well recognized that it can be aggravated by infection. Activation of the innate immune system constitutes a critical element in the process. Toll-like receptors (TLRs) comprise a part of the innate immune system, and lipopolysaccharide (LPS)-induced activation of TLR4 represents bacterial-induced interactions in various model systems. The present study examines how TLR2 and TLR4 expression is affected by symptomatic allergic rhinitis, and if LPS added upon allergen affects nasal cytokine release. Methods: In patients with pollen-induced allergic rhinitis and healthy non-allergic volunteers, nasal lavage (NAL), peripheral blood and bone marrow were sampled before and during the pollen season. TLR2 and TLR4 expression was determined flow cytometrically. Changes in the TLR receptor expression pattern were evaluated by a nasal challenge with allergen followed by LPS, or vice versa. Symptoms along with cells and cytokines in NAL were analyzed. Results: TLR4 expression increased in leukocytes in NAL, peripheral blood and bone marrow during symptomatic allergic rhinitis. A similar increase was seen for TLR2 in neutrophils in blood. Nasal challenge with allergen followed by LPS augmented the release of IL-4, IL-5, IL-10, IL-13, IFN-γ and TNF-α. Conclusion: A systemic up-regulation of TLR4 in symptomatic allergic rhinitis may explain why LPS preceded by allergen increases nasal cytokine release.

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“…It has been demonstrated that inhalative GC reduced Th2 cytokines in nasal fluids (IL-1a, IL-1b, IL-2, IL-3, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12, IL-13, IL-15, CCL-11, CCL-5, CCL-2 (MCP1), CCL-3, CXCL-10, GM-CSF, IFN-c and TNF-a) (169), but increased the relative frequency of Tregs that express the latent form of TGF-b1 (83,170). Also, systemic treatments with herbal drugs reduced nasal levels of IL-8 and leukotriene B4 (171).…”

Section: Biomarker Usage In Treatment Monitoringmentioning

confidence: 99%

Current and future biomarkers in allergic asthma

Zissler

Bieren

Jakwerth

et al. 2016

Allergy

107

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Diagnosis early in life, sensitization, asthma endotypes, monitoring of disease and treatment progression are key motivations for the exploration of biomarkers for allergic rhinitis and allergic asthma. The number of genes related to allergic rhinitis and allergic asthma increases steadily; however, prognostic genes have not yet entered clinical application. We hypothesize that the combination of multiple genes may generate biomarkers with prognostic potential. The current review attempts to group more than 161 different potential biomarkers involved in respiratory inflammation to pave the way for future classifiers. The potential biomarkers are categorized into either epithelial or infiltrate-derived or mixed origin, epithelial biomarkers. Furthermore, surface markers were grouped into cell-typespecific categories. The current literature provides multiple biomarkers for potential asthma endotypes that are related to T-cell phenotypes such as Th1, Th2, Th9, Th17, Th22 and Tregs and their lead cytokines. Eosinophilic and neutrophilic asthma endotypes are also classified by epithelium-derived CCL-26 and osteopontin, respectively. There are currently about 20 epithelium-derived biomarkers exclusively derived from epithelium, which are likely to innovate biomarker panels as they are easy to sample. This article systematically reviews and categorizes genes and collects current evidence that may promote these biomarkers to become part of allergic rhinitis or allergic asthma classifiers with high prognostic value.

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Topical corticosteroid inhibits interleukin‐4, ‐5 and ‐13 in nasal secretions following allergen challenge

Abstract: Fluticasone propionate has selective inhibitory effects on Th2 cytokine synthesis following nasal challenge, while also decreasing release of chemokines, but not affecting levels of Th1 cytokines.

Cited by 70 publications

References 42 publications

Scientific rationale for using a single inhaler for asthma control

Scientific rationale for using a single inhaler for asthma control

Systemic Up-Regulation of TLR4 Causes Lipopolysaccharide-Induced Augmentation of Nasal Cytokine Release in Allergic Rhinitis

Current and future biomarkers in allergic asthma

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