2013
DOI: 10.1177/000348941312200405
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Protective Effects of Exogenous Surfactant Protein A in Allergic Rhinitis: A Mouse Model

Abstract: Exogenous SP-A had a significant therapeutic effect in mice with AR, and its mechanisms of action included inhibition of the differentiation of Th2 cells in the nasal mucosa, reduced levels of Th2 cytokines, and increased levels of Th1 cytokines. Together, these effects corrected the Th1/Th2 imbalance, inhibited the increase of specific immunoglobulin E production, effectively reduced the symptoms of AR, and inhibited the development of AR.

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Cited by 12 publications
(6 citation statements)
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“…SP-A is secreted by type II alveolar epithelial cells into pulmonary surfactant, where it is involved in host defense and immune regulation by inhibiting Th2 cell differentiation, reducing Th2 cytokine levels, and increasing Th1 cytokines. It was also identified in nasal mucosa by immunostaining and PCR, and exogenous application resulted in reduced IL-4 and IL-5 levels in ovalbumin-sensitized mice [9]. These protective effects of SP-A may have therapeutic potential in allergic rhinitis.…”
Section: Nasal Mucus Proteomementioning
confidence: 88%
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“…SP-A is secreted by type II alveolar epithelial cells into pulmonary surfactant, where it is involved in host defense and immune regulation by inhibiting Th2 cell differentiation, reducing Th2 cytokine levels, and increasing Th1 cytokines. It was also identified in nasal mucosa by immunostaining and PCR, and exogenous application resulted in reduced IL-4 and IL-5 levels in ovalbumin-sensitized mice [9]. These protective effects of SP-A may have therapeutic potential in allergic rhinitis.…”
Section: Nasal Mucus Proteomementioning
confidence: 88%
“…Particularly, nasal mucus proteins, major constituents and functional units of this body fluid, have not been studied extensively. Potential therapeutic targets like surfactant protein (SP-A) or clara cell protein (CC10) have been addressed in mouse models or in vitro models by analyzing their expression in the epithelium [9,10]. SP-A is secreted by type II alveolar epithelial cells into pulmonary surfactant, where it is involved in host defense and immune regulation by inhibiting Th2 cell differentiation, reducing Th2 cytokine levels, and increasing Th1 cytokines.…”
Section: Nasal Mucus Proteomementioning
confidence: 99%
“…In addition, research groups utilize different sensitization protocols, varying both the dosage and timing of ovalbumin administration. Some protocols administer IP doses of ovalbumin or allergen followed by intranasal challenges whereas others only give intranasal challenges . Last, the experimental techniques used to assess levels of sinonasal inflammation also vary greatly.…”
Section: Discussionmentioning
confidence: 99%
“…The primary application of using the allergic model of sinonasal inflammation is testing of novel topical or systemic drugs to reverse inflammation . In order to determine the most sensitive and reliable measure of drug efficacy, we pilot‐tested a common topical anti‐inflammatory drug used in treating CRS, budesonide, in the allergic mouse model.…”
Section: Discussionmentioning
confidence: 99%
“…L'étude de la sécrétion de SP-A dans des modèles murins a montré que l'absence de sécré-tions de SP-A entraînait en cas d'exposition allergénique une hyperéosinophilie périphérique majeure et une inflammation de type Th2 au niveau des voies aériennes [23]. En corollaire, l'administration de SP-A exogène chez des souris déficientes entraîne l'inhibition de la synthèse d'IgE spécifiques [24]. Chez l'homme, il a été montré que la sécrétion de SP-A au niveau de l'épithélium nasal était plus élevée en cas de rhinite allergique ou de polypes naso-sinusiens par rapport aux sujets sains [25,26].…”
Section: Les Protéines a Et D Du Surfactant (Sp-a Et Sp-d) Sont Des Punclassified