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Protease allergens induce the expression of IL-25 via Erk and p38 MAPK pathway.

Yu HS, Angkasekwinai P, Chang SH, Chung Y, Dong C - J. Korean Med. Sci. (2010)

Bottom Line: The IL-25 cytokine level in bronchial alveolar lavage (BAL) was also profoundly and significantly increased after treatment with papain.Additionally, the levels of Th2 cytokines were significantly increased, as compared to those in the OVA-only treatment group.The various protease allergens triggered the expression of IL-25 and TSLP mRNA in mouse lung epithelial cells (MLE12) and primary mouse lung epithelial cells; these effects were inhibited by the deactivation of the protease activity of papain.

View Article: PubMed Central - PubMed

Affiliation: Department of Parasitology, Pusan National University Hospital Medical Research Institute, School of Medicine, Pusan National University, Busan, Korea.

ABSTRACT
Allergic diseases, including asthma, are characterized by T helper type 2 (Th2) cell-mediated inflammations, coupled with tissue infiltration by eosinophils. In this study, we demonstrate that multiple protease allergens, including papain and DerP1, efficiently induce interleukin (IL)-25 and thymic stromal lymphopoietin (TSLP) gene expression, and this phenomenon is dependent on the protease activities of these allergens. The IL-25 cytokine level in bronchial alveolar lavage (BAL) was also profoundly and significantly increased after treatment with papain. Additionally, the levels of Th2 cytokines were significantly increased, as compared to those in the OVA-only treatment group. The various protease allergens triggered the expression of IL-25 and TSLP mRNA in mouse lung epithelial cells (MLE12) and primary mouse lung epithelial cells; these effects were inhibited by the deactivation of the protease activity of papain. The allergen papain activates the ErK and p38 MAP pathways; the inhibition of these pathways, but not the NFkappaB or PI-3 kinase pathways, impairs the induction of IL-25 and TSLP expression by proteases. In this study, we demonstrate that the protease allergens induce IL-25 and TSLP via the MAP kinase signal pathways, and their protease activities are essential to this pathway.

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Related in: MedlinePlus

Papain induced allergic inflammation with significant induction of IL-25. Mice were intranasally treated with papain and OVA (Papain) or OVA only (OVA) for 6 repetitions. (A) Total cell number of bronchoalveolar lavage fluid (BALF). (B) Differential cell counts of BALF. (C) Concentration of cytokines in BALF. (D) Chemokine and cytokine mRNA expression of lung cells (*P<0.05; n=5 mice per group; 3 independent experiments).
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Figure 1: Papain induced allergic inflammation with significant induction of IL-25. Mice were intranasally treated with papain and OVA (Papain) or OVA only (OVA) for 6 repetitions. (A) Total cell number of bronchoalveolar lavage fluid (BALF). (B) Differential cell counts of BALF. (C) Concentration of cytokines in BALF. (D) Chemokine and cytokine mRNA expression of lung cells (*P<0.05; n=5 mice per group; 3 independent experiments).

Mentions: Following 6 intranasal administrations of papain, immune cell infiltrations, particularly eosinophils, were evident in the airway (Figs. 1A, B). The IL-25 cytokine level in BAL was also profoundly increased after papain treatment (Fig. 1C). Additionally, the levels of Th2 cytokines (IL-4, -5, and -13) were significantly increased as compared to those in the OVA-only treatment group. However, the levels of the Th17 cytokines, IL-17 and IL-17F, in the papain treatment group did not differ significantly from those of the control group (Fig. 1C). We also that the lung cells of the papain-treated mice much higher expressed IL-25, IL-5, Gro-alpha, and eotaxin genes at much higher levels than those of the control group (Fig. 1D). Therefore, the intranasal administration of papain specifically induces Th2-type chemokines and cytokines in vivo.


Protease allergens induce the expression of IL-25 via Erk and p38 MAPK pathway.

Yu HS, Angkasekwinai P, Chang SH, Chung Y, Dong C - J. Korean Med. Sci. (2010)

Papain induced allergic inflammation with significant induction of IL-25. Mice were intranasally treated with papain and OVA (Papain) or OVA only (OVA) for 6 repetitions. (A) Total cell number of bronchoalveolar lavage fluid (BALF). (B) Differential cell counts of BALF. (C) Concentration of cytokines in BALF. (D) Chemokine and cytokine mRNA expression of lung cells (*P<0.05; n=5 mice per group; 3 independent experiments).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2877219&req=5

Figure 1: Papain induced allergic inflammation with significant induction of IL-25. Mice were intranasally treated with papain and OVA (Papain) or OVA only (OVA) for 6 repetitions. (A) Total cell number of bronchoalveolar lavage fluid (BALF). (B) Differential cell counts of BALF. (C) Concentration of cytokines in BALF. (D) Chemokine and cytokine mRNA expression of lung cells (*P<0.05; n=5 mice per group; 3 independent experiments).
Mentions: Following 6 intranasal administrations of papain, immune cell infiltrations, particularly eosinophils, were evident in the airway (Figs. 1A, B). The IL-25 cytokine level in BAL was also profoundly increased after papain treatment (Fig. 1C). Additionally, the levels of Th2 cytokines (IL-4, -5, and -13) were significantly increased as compared to those in the OVA-only treatment group. However, the levels of the Th17 cytokines, IL-17 and IL-17F, in the papain treatment group did not differ significantly from those of the control group (Fig. 1C). We also that the lung cells of the papain-treated mice much higher expressed IL-25, IL-5, Gro-alpha, and eotaxin genes at much higher levels than those of the control group (Fig. 1D). Therefore, the intranasal administration of papain specifically induces Th2-type chemokines and cytokines in vivo.

Bottom Line: The IL-25 cytokine level in bronchial alveolar lavage (BAL) was also profoundly and significantly increased after treatment with papain.Additionally, the levels of Th2 cytokines were significantly increased, as compared to those in the OVA-only treatment group.The various protease allergens triggered the expression of IL-25 and TSLP mRNA in mouse lung epithelial cells (MLE12) and primary mouse lung epithelial cells; these effects were inhibited by the deactivation of the protease activity of papain.

View Article: PubMed Central - PubMed

Affiliation: Department of Parasitology, Pusan National University Hospital Medical Research Institute, School of Medicine, Pusan National University, Busan, Korea.

ABSTRACT
Allergic diseases, including asthma, are characterized by T helper type 2 (Th2) cell-mediated inflammations, coupled with tissue infiltration by eosinophils. In this study, we demonstrate that multiple protease allergens, including papain and DerP1, efficiently induce interleukin (IL)-25 and thymic stromal lymphopoietin (TSLP) gene expression, and this phenomenon is dependent on the protease activities of these allergens. The IL-25 cytokine level in bronchial alveolar lavage (BAL) was also profoundly and significantly increased after treatment with papain. Additionally, the levels of Th2 cytokines were significantly increased, as compared to those in the OVA-only treatment group. The various protease allergens triggered the expression of IL-25 and TSLP mRNA in mouse lung epithelial cells (MLE12) and primary mouse lung epithelial cells; these effects were inhibited by the deactivation of the protease activity of papain. The allergen papain activates the ErK and p38 MAP pathways; the inhibition of these pathways, but not the NFkappaB or PI-3 kinase pathways, impairs the induction of IL-25 and TSLP expression by proteases. In this study, we demonstrate that the protease allergens induce IL-25 and TSLP via the MAP kinase signal pathways, and their protease activities are essential to this pathway.

Show MeSH
Related in: MedlinePlus