IL-22/IL-22R1 signaling regulates the pathophysiology of chronic rhinosinusitis with nasal polyps via alteration of MUC1 expression

Yasuyuki Noyama, Mitsuhiro Okano, Tazuko Fujiwara, Shin Kariya, Takaya Higaki, Takenori Haruna, Sei ichiro Makihara, Kengo Kanai, Takahisa Koyama, Masami Taniguchi, Jun ichi Ishitoya, Akira Kanda, Yoshiki Kobayashi, Mikiya Asako, Koichi Tomoda, Kazunori Nishizaki

Research output: Contribution to journalArticle

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Abstract

Background IL-22 is an IL-10-family cytokine that regulates chronic inflammation. We investigated the role of IL-22 and its receptor, IL-22R1, in the pathophysiology of chronic rhinosinusitis with nasal polyps (CRSwNP). Methods IL-22 and IL-22R1 protein and mRNA expression in NP and in uncinate tissues (UT) from CRS and non-CRS patients was examined using immunohistochemistry and real-time PCR, respectively. Dispersed NP and UT cells were cultured with the Staphylococcus aureus exotoxins, staphylococcal enterotoxin B and alpha-toxin, following which exotoxin-induced IL-22 levels and their association with clinicopathological factors were analyzed. Effects of IL-22 on MUC1 expression and cytokine release in NP cells were also determined. Results IL-22 and IL-22R1 in NP were mainly expressed in infiltrating inflammatory cells and in epithelial cells, respectively. IL-22 mRNA levels in NP were significantly higher than those in UTs from non-CRS patients whereas IL-22R1 levels were conversely lower in NPs. NP cells produced substantial amounts of IL-22 in response to exotoxins. Exotoxin-induced IL-22 production by NP cells significantly and negatively correlated with the degree of local eosinophilia and postoperative computed tomography (CT) score, whereas conversely it positively correlated with the forced expiratory volume in 1s (FEV1)/forced vital capacity (FVC) ratio. IL-22 significantly enhanced MUC1 mRNA expression in NP cells. IL-22-induced MUC1 mRNA levels were significantly and positively correlated with IL-22R1 mRNA levels in NPs. Conclusions These data suggest that imbalance of IL-22/IL-22R1 signaling regulates the pathogenesis of CRSwNP, including local eosinophilia, via alteration of MUC1 expression.

Original languageEnglish
Pages (from-to)42-51
Number of pages10
JournalAllergology International
Volume66
Issue number1
DOIs
Publication statusPublished - Jan 1 2017

Fingerprint

Nasal Polyps
Exotoxins
Messenger RNA
Eosinophilia
interleukin-22 receptor
interleukin-22
Cytokines
Vital Capacity
Forced Expiratory Volume
Interleukin-10
Staphylococcus aureus
Real-Time Polymerase Chain Reaction
Cultured Cells
Epithelial Cells
Immunohistochemistry
Tomography

Keywords

  • Chronic rhinosinusitis with nasal polyps
  • Exotoxins
  • IL-22
  • MUC1
  • Staphylococcus aureus

ASJC Scopus subject areas

  • Immunology and Allergy

Cite this

IL-22/IL-22R1 signaling regulates the pathophysiology of chronic rhinosinusitis with nasal polyps via alteration of MUC1 expression. / Noyama, Yasuyuki; Okano, Mitsuhiro; Fujiwara, Tazuko; Kariya, Shin; Higaki, Takaya; Haruna, Takenori; Makihara, Sei ichiro; Kanai, Kengo; Koyama, Takahisa; Taniguchi, Masami; Ishitoya, Jun ichi; Kanda, Akira; Kobayashi, Yoshiki; Asako, Mikiya; Tomoda, Koichi; Nishizaki, Kazunori.

In: Allergology International, Vol. 66, No. 1, 01.01.2017, p. 42-51.

Research output: Contribution to journalArticle

Noyama, Y, Okano, M, Fujiwara, T, Kariya, S, Higaki, T, Haruna, T, Makihara, SI, Kanai, K, Koyama, T, Taniguchi, M, Ishitoya, JI, Kanda, A, Kobayashi, Y, Asako, M, Tomoda, K & Nishizaki, K 2017, 'IL-22/IL-22R1 signaling regulates the pathophysiology of chronic rhinosinusitis with nasal polyps via alteration of MUC1 expression', Allergology International, vol. 66, no. 1, pp. 42-51. https://doi.org/10.1016/j.alit.2016.04.017
Noyama, Yasuyuki ; Okano, Mitsuhiro ; Fujiwara, Tazuko ; Kariya, Shin ; Higaki, Takaya ; Haruna, Takenori ; Makihara, Sei ichiro ; Kanai, Kengo ; Koyama, Takahisa ; Taniguchi, Masami ; Ishitoya, Jun ichi ; Kanda, Akira ; Kobayashi, Yoshiki ; Asako, Mikiya ; Tomoda, Koichi ; Nishizaki, Kazunori. / IL-22/IL-22R1 signaling regulates the pathophysiology of chronic rhinosinusitis with nasal polyps via alteration of MUC1 expression. In: Allergology International. 2017 ; Vol. 66, No. 1. pp. 42-51.
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abstract = "Background IL-22 is an IL-10-family cytokine that regulates chronic inflammation. We investigated the role of IL-22 and its receptor, IL-22R1, in the pathophysiology of chronic rhinosinusitis with nasal polyps (CRSwNP). Methods IL-22 and IL-22R1 protein and mRNA expression in NP and in uncinate tissues (UT) from CRS and non-CRS patients was examined using immunohistochemistry and real-time PCR, respectively. Dispersed NP and UT cells were cultured with the Staphylococcus aureus exotoxins, staphylococcal enterotoxin B and alpha-toxin, following which exotoxin-induced IL-22 levels and their association with clinicopathological factors were analyzed. Effects of IL-22 on MUC1 expression and cytokine release in NP cells were also determined. Results IL-22 and IL-22R1 in NP were mainly expressed in infiltrating inflammatory cells and in epithelial cells, respectively. IL-22 mRNA levels in NP were significantly higher than those in UTs from non-CRS patients whereas IL-22R1 levels were conversely lower in NPs. NP cells produced substantial amounts of IL-22 in response to exotoxins. Exotoxin-induced IL-22 production by NP cells significantly and negatively correlated with the degree of local eosinophilia and postoperative computed tomography (CT) score, whereas conversely it positively correlated with the forced expiratory volume in 1s (FEV1)/forced vital capacity (FVC) ratio. IL-22 significantly enhanced MUC1 mRNA expression in NP cells. IL-22-induced MUC1 mRNA levels were significantly and positively correlated with IL-22R1 mRNA levels in NPs. Conclusions These data suggest that imbalance of IL-22/IL-22R1 signaling regulates the pathogenesis of CRSwNP, including local eosinophilia, via alteration of MUC1 expression.",
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T1 - IL-22/IL-22R1 signaling regulates the pathophysiology of chronic rhinosinusitis with nasal polyps via alteration of MUC1 expression

AU - Noyama, Yasuyuki

AU - Okano, Mitsuhiro

AU - Fujiwara, Tazuko

AU - Kariya, Shin

AU - Higaki, Takaya

AU - Haruna, Takenori

AU - Makihara, Sei ichiro

AU - Kanai, Kengo

AU - Koyama, Takahisa

AU - Taniguchi, Masami

AU - Ishitoya, Jun ichi

AU - Kanda, Akira

AU - Kobayashi, Yoshiki

AU - Asako, Mikiya

AU - Tomoda, Koichi

AU - Nishizaki, Kazunori

PY - 2017/1/1

Y1 - 2017/1/1

N2 - Background IL-22 is an IL-10-family cytokine that regulates chronic inflammation. We investigated the role of IL-22 and its receptor, IL-22R1, in the pathophysiology of chronic rhinosinusitis with nasal polyps (CRSwNP). Methods IL-22 and IL-22R1 protein and mRNA expression in NP and in uncinate tissues (UT) from CRS and non-CRS patients was examined using immunohistochemistry and real-time PCR, respectively. Dispersed NP and UT cells were cultured with the Staphylococcus aureus exotoxins, staphylococcal enterotoxin B and alpha-toxin, following which exotoxin-induced IL-22 levels and their association with clinicopathological factors were analyzed. Effects of IL-22 on MUC1 expression and cytokine release in NP cells were also determined. Results IL-22 and IL-22R1 in NP were mainly expressed in infiltrating inflammatory cells and in epithelial cells, respectively. IL-22 mRNA levels in NP were significantly higher than those in UTs from non-CRS patients whereas IL-22R1 levels were conversely lower in NPs. NP cells produced substantial amounts of IL-22 in response to exotoxins. Exotoxin-induced IL-22 production by NP cells significantly and negatively correlated with the degree of local eosinophilia and postoperative computed tomography (CT) score, whereas conversely it positively correlated with the forced expiratory volume in 1s (FEV1)/forced vital capacity (FVC) ratio. IL-22 significantly enhanced MUC1 mRNA expression in NP cells. IL-22-induced MUC1 mRNA levels were significantly and positively correlated with IL-22R1 mRNA levels in NPs. Conclusions These data suggest that imbalance of IL-22/IL-22R1 signaling regulates the pathogenesis of CRSwNP, including local eosinophilia, via alteration of MUC1 expression.

AB - Background IL-22 is an IL-10-family cytokine that regulates chronic inflammation. We investigated the role of IL-22 and its receptor, IL-22R1, in the pathophysiology of chronic rhinosinusitis with nasal polyps (CRSwNP). Methods IL-22 and IL-22R1 protein and mRNA expression in NP and in uncinate tissues (UT) from CRS and non-CRS patients was examined using immunohistochemistry and real-time PCR, respectively. Dispersed NP and UT cells were cultured with the Staphylococcus aureus exotoxins, staphylococcal enterotoxin B and alpha-toxin, following which exotoxin-induced IL-22 levels and their association with clinicopathological factors were analyzed. Effects of IL-22 on MUC1 expression and cytokine release in NP cells were also determined. Results IL-22 and IL-22R1 in NP were mainly expressed in infiltrating inflammatory cells and in epithelial cells, respectively. IL-22 mRNA levels in NP were significantly higher than those in UTs from non-CRS patients whereas IL-22R1 levels were conversely lower in NPs. NP cells produced substantial amounts of IL-22 in response to exotoxins. Exotoxin-induced IL-22 production by NP cells significantly and negatively correlated with the degree of local eosinophilia and postoperative computed tomography (CT) score, whereas conversely it positively correlated with the forced expiratory volume in 1s (FEV1)/forced vital capacity (FVC) ratio. IL-22 significantly enhanced MUC1 mRNA expression in NP cells. IL-22-induced MUC1 mRNA levels were significantly and positively correlated with IL-22R1 mRNA levels in NPs. Conclusions These data suggest that imbalance of IL-22/IL-22R1 signaling regulates the pathogenesis of CRSwNP, including local eosinophilia, via alteration of MUC1 expression.

KW - Chronic rhinosinusitis with nasal polyps

KW - Exotoxins

KW - IL-22

KW - MUC1

KW - Staphylococcus aureus

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