IL-23, rather than IL-17, is crucial for the development of ovalbumin-induced allergic rhinitis

Guo, Chaobin; Chen, Gui‐E; Ge, Ruifeng

doi:10.1016/j.molimm.2015.07.009

Cited by 11 publications

(11 citation statements)

References 33 publications

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“…We found that in OVA-induced mice IL-1β, IL-23 and IL-6 were increased which is consistent with previous study [ 13 , 14 , 26 ]. After anti-IL-17 administration, the level of IL-1β, IL-23 and IL-6 decreased(Figure 4F-4H ).…”

Section: Discussionsupporting

confidence: 93%

Neutralization of interleukin-17 suppresses allergic rhinitis symptoms by downregulating Th2 and Th17 responses and upregulating the Treg response

Wang

Cao

2017

Oncotarget

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Allergic rhinitis (AR) has long been considered to predominantly involve the actions of Th2 cells, with relatively small contributions from Th1 cells. In recent years, the discovery of Th17 and regulatory T (Treg) cells has rendered the Th1/Th2 balance paradigm more complex and expanded our understanding of the pathogenesis of AR. IL-17, a key cytokine produced by Th17 cells, is known to induce allergen-specific Th2 cell activation, eosinophil and neutrophil accumulation, and serum IgE production in asthma; all of these features may play important roles in AR. To the best of our knowledge, only a few studies have assessed the feasibility of using IL-17 antagonists to treat AR. Thus, the principal objectives of the present study were, first, to determine the status of Th17 and Treg cells in the nasal mucosa of a mouse model of AR, and, second, to investigate the effects of IL-17 on such cells and the therapeutic efficacy of anti-IL-17 antibodies (Abs) in the context of AR. Anti-IL-17 Abs were given intranasally during the re-challenge of BALB/c mice with ovalbumin (OVA)-induced AR. We measured the numbers of nasal rubbing motions and sneezes, eosinophil and neutrophil levels, Th1, Th2, Th17, and Treg parameters in the nasal mucosa. Anti-IL-17 Abs markedly reduced the number of nasal rubbing motions and sneezes, decreased eosinophil and neutrophil infiltration, reduced Th2 and Th17 responses, and increased the Treg response. Anti-IL-17 Ab treatment protects against AR. These results will improve our understanding of AR pathogenesis and may lead to the development of novel therapeutic approaches for management of the condition.

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Section: Discussionsupporting

confidence: 93%

Neutralization of interleukin-17 suppresses allergic rhinitis symptoms by downregulating Th2 and Th17 responses and upregulating the Treg response

Wang

Cao

2017

Oncotarget

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“…Moreover, the expression of IL-17A mRNA level is also increased [22, 23]. These findings are consistent with our results that IL-17A mRNA level was markedly higher in the WT-OVA group than in the IL-17A KO-OVA group.…”

Section: Discussionsupporting

confidence: 90%

“…Thus, IL-17A deficiency may play an important role in the development of allergic rhinitis by reducing Th2 cytokine levels. Results of a 2015 report on an IL-17A-KO ovalbumin-induced allergic rhinitis model were inconsistent with our current findings [23]. In our present experiment, we used BALB/c mice, which are known as the best model for allergic rhinitis induced with ovalbumin, whereas in the 2015 report, the authors used C57BL/6J mice.…”

Section: Discussioncontrasting

confidence: 81%

Role of Interleukin-17A on the Chemotactic Responses to CCL7 in a Murine Allergic Rhinitis Model

et al. 2017

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BackgroundThe proinflammatory cytokine interleukin (IL)-17A is associated with eosinophil infiltration into the nasal mucosa in a mouse model of ovalbumin-induced allergic rhinitis. Chemotaxis of eosinophils is mediated primarily through C-C chemokine receptor type 3 (CCR3). However, the mechanism underlying the IL-17A-mediated enhancement of eosinophil recruitment via chemoattractants/chemokines remains unknown.ObjectivesIn this study, we assessed the contribution of IL-17A to eosinophil-related inflammation via the CCL7/CCR3 pathway in experimental allergic rhinitis.MethodsIL-17A knockout (KO) and wild-type (WT) BALB/c mice were injected intraperitoneally and challenged intranasally with OVA to induce allergic rhinitis. Various parameters of the allergic response were evaluated, and mRNA and protein levels of CCL7 and CCR3 in nasal tissue and serum were compared between the two groups. The chemotactic response to CCL7 with or without IL-17A in bone marrow-derived eosinophils (bmEos) from BALB/c mice was measured.ResultsIn the allergic rhinitis model, IL-17A deficiency significantly decreased nasal symptoms, serum IgE levels, and eosinophil recruitment to the nasal mucosa. CCL7 and CCR3 mRNA and protein levels were decreased in the nasal mucosa of IL-17A KO mice compared with the WT mice. BmEos showed a significantly increased chemotactic response to -low concentration of CCL7 in the presence of IL-17A compared with its absence.ConclusionThe suppression of nasal inflammation due of IL-17A deficiency in allergic rhinitis is partly responsible for the regulation of CCL7 secretion and eosinophil infiltration, which may be regulated via the CCL7/CCR3 pathway.

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“…116 However, another study showed that IL-23 but not IL-17 was essential for OVA-induced allergic rhinitis. 117 In contrast to IL-17E, IL-17 contributes to pulmonary inflammation by promoting type 1 immunity related to neutrophilia rather than eosinophilia, which is mainly mediated by type 2 immunity. Indeed, IL-17 can induce the expression of chemoattractants such as CXCL1, CXCL2, CCL20 or β-defensin two in human airway epithelial cells to favour chronic inflammation in lung diseases.…”

Section: Il-17dmentioning

confidence: 99%

The roles and functional mechanisms of interleukin-17 family cytokines in mucosal immunity

et al. 2016

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The mucosal immune system serves as our front-line defense against pathogens. It also tightly maintains immune tolerance to self-symbiotic bacteria, which are usually called commensals. Sensing both types of microorganisms is modulated by signalling primarily through various pattern-recognition receptors (PRRs) on barrier epithelial cells or immune cells. After sensing, proinflammatory molecules such as cytokines are released by these cells to mediate either defensive or tolerant responses. The interleukin-17 (IL-17) family members belong to a newly characterized cytokine subset that is critical for the maintenance of mucosal homeostasis. In this review, we will summarize recent progress on the diverse functions and signals of this family of cytokines at different mucosal edges.

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IL-23, rather than IL-17, is crucial for the development of ovalbumin-induced allergic rhinitis

Cited by 11 publications

References 33 publications

Neutralization of interleukin-17 suppresses allergic rhinitis symptoms by downregulating Th2 and Th17 responses and upregulating the Treg response

Neutralization of interleukin-17 suppresses allergic rhinitis symptoms by downregulating Th2 and Th17 responses and upregulating the Treg response

Role of Interleukin-17A on the Chemotactic Responses to CCL7 in a Murine Allergic Rhinitis Model

The roles and functional mechanisms of interleukin-17 family cytokines in mucosal immunity

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