TNF-α contributes to the development of allergic rhinitis in mice

Masao Iwasaki, Kuniaki Saito, Masao Takemura, Kenji Sekikawa, Hidehiko Fujii, Yasuhiro Yamada, Hisayasu Wada, Keisuke Mizuta, Mitsuru Seishima, Yatsuji Ito

Research output: Contribution to journalArticle

73 Citations (Scopus)

Abstract

Background: Allergic rhinitis is an inflammation involving TH2-type cytokine production, with pathologic eosinophil infiltration in the nasal mucosa. Although TNF-α is thought to be a pro-inflammatory cytokine, the relationship between TNF-α and allergic rhinitis has not been clarified. Objectives: The role of TNF-α in a murine model of ovalbumin (OVA)-sensitized allergic rhinitis was investigated by using mice deficient in the gene encoding TNF-α (TNF-α-/- mice). Methods: Both wild-type (TNF-α+/+) and TNF-α-/- mice were sensitized with OVA by means of intraperitoneal injection. They were then challenged with intranasal OVA, and various allergic responses were assessed. Results: The production of OVA-specific IgE in the serum (P < .05) and the frequency of sneezes (P < .05) and nasal rubs (P < .05) decreased significantly in TNF-α-/- mice after OVA sensitization compared with that in TNF-α+/+ mice (P < .05). The mRNA expression of IL-4, IL-10, and eotaxin in nasal mucosa in TNF-α-/- mice was also significantly suppressed compared with that in TNF-α+/+ mice after OVA sensitization (P < .05). Furthermore, the expression of both endothelial-leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1 mRNA in the nasal mucosa was significantly suppressed (P < .05), although intercellular adhesion molecule 1 mRNA expression did not decrease significantly in TNF-α-/- mice compared with that in TNF-α+/+ mice after OVA sensitization. In addition, the effect of TNF-α on endothelial-leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1 expression by means of Western blot analysis was compatible with the mRNA results. Pathologically, eosinophil infiltration in nasal mucosa was significantly restricted in TNF-α-/- mice compared with in TNF-α+/+ mice after OVA sensitization (P < .05). Conclusion: TNF-α is necessary for antigen-specific IgE production and for the induction of TH2-type cytokines and chemokines. Furthermore, TNF-α might be important for the expression of adhesion molecules to recruit eosinophils to the allergic inflammatory site. We conclude that the lack of TNF-α inhibited the development of allergic rhinitis.

Original languageEnglish
Pages (from-to)134-140
Number of pages7
JournalJournal of Allergy and Clinical Immunology
Volume112
Issue number1
DOIs
Publication statusPublished - 01-07-2003
Externally publishedYes

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Ovalbumin
Nasal Mucosa
Eosinophils
Messenger RNA
E-Selectin
Vascular Cell Adhesion Molecule-1
Cytokines
Immunoglobulin E
Allergic Rhinitis
Intercellular Adhesion Molecule-1
Intraperitoneal Injections
Nose
Chemokines
Interleukin-4
Interleukin-10
Western Blotting
Inflammation
Antigens
Serum
Genes

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cite this

Iwasaki, M., Saito, K., Takemura, M., Sekikawa, K., Fujii, H., Yamada, Y., ... Ito, Y. (2003). TNF-α contributes to the development of allergic rhinitis in mice. Journal of Allergy and Clinical Immunology, 112(1), 134-140. https://doi.org/10.1067/mai.2003.1554
Iwasaki, Masao ; Saito, Kuniaki ; Takemura, Masao ; Sekikawa, Kenji ; Fujii, Hidehiko ; Yamada, Yasuhiro ; Wada, Hisayasu ; Mizuta, Keisuke ; Seishima, Mitsuru ; Ito, Yatsuji. / TNF-α contributes to the development of allergic rhinitis in mice. In: Journal of Allergy and Clinical Immunology. 2003 ; Vol. 112, No. 1. pp. 134-140.
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abstract = "Background: Allergic rhinitis is an inflammation involving TH2-type cytokine production, with pathologic eosinophil infiltration in the nasal mucosa. Although TNF-α is thought to be a pro-inflammatory cytokine, the relationship between TNF-α and allergic rhinitis has not been clarified. Objectives: The role of TNF-α in a murine model of ovalbumin (OVA)-sensitized allergic rhinitis was investigated by using mice deficient in the gene encoding TNF-α (TNF-α-/- mice). Methods: Both wild-type (TNF-α+/+) and TNF-α-/- mice were sensitized with OVA by means of intraperitoneal injection. They were then challenged with intranasal OVA, and various allergic responses were assessed. Results: The production of OVA-specific IgE in the serum (P < .05) and the frequency of sneezes (P < .05) and nasal rubs (P < .05) decreased significantly in TNF-α-/- mice after OVA sensitization compared with that in TNF-α+/+ mice (P < .05). The mRNA expression of IL-4, IL-10, and eotaxin in nasal mucosa in TNF-α-/- mice was also significantly suppressed compared with that in TNF-α+/+ mice after OVA sensitization (P < .05). Furthermore, the expression of both endothelial-leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1 mRNA in the nasal mucosa was significantly suppressed (P < .05), although intercellular adhesion molecule 1 mRNA expression did not decrease significantly in TNF-α-/- mice compared with that in TNF-α+/+ mice after OVA sensitization. In addition, the effect of TNF-α on endothelial-leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1 expression by means of Western blot analysis was compatible with the mRNA results. Pathologically, eosinophil infiltration in nasal mucosa was significantly restricted in TNF-α-/- mice compared with in TNF-α+/+ mice after OVA sensitization (P < .05). Conclusion: TNF-α is necessary for antigen-specific IgE production and for the induction of TH2-type cytokines and chemokines. Furthermore, TNF-α might be important for the expression of adhesion molecules to recruit eosinophils to the allergic inflammatory site. We conclude that the lack of TNF-α inhibited the development of allergic rhinitis.",
author = "Masao Iwasaki and Kuniaki Saito and Masao Takemura and Kenji Sekikawa and Hidehiko Fujii and Yasuhiro Yamada and Hisayasu Wada and Keisuke Mizuta and Mitsuru Seishima and Yatsuji Ito",
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Iwasaki, M, Saito, K, Takemura, M, Sekikawa, K, Fujii, H, Yamada, Y, Wada, H, Mizuta, K, Seishima, M & Ito, Y 2003, 'TNF-α contributes to the development of allergic rhinitis in mice', Journal of Allergy and Clinical Immunology, vol. 112, no. 1, pp. 134-140. https://doi.org/10.1067/mai.2003.1554

TNF-α contributes to the development of allergic rhinitis in mice. / Iwasaki, Masao; Saito, Kuniaki; Takemura, Masao; Sekikawa, Kenji; Fujii, Hidehiko; Yamada, Yasuhiro; Wada, Hisayasu; Mizuta, Keisuke; Seishima, Mitsuru; Ito, Yatsuji.

In: Journal of Allergy and Clinical Immunology, Vol. 112, No. 1, 01.07.2003, p. 134-140.

Research output: Contribution to journalArticle

TY - JOUR

T1 - TNF-α contributes to the development of allergic rhinitis in mice

AU - Iwasaki, Masao

AU - Saito, Kuniaki

AU - Takemura, Masao

AU - Sekikawa, Kenji

AU - Fujii, Hidehiko

AU - Yamada, Yasuhiro

AU - Wada, Hisayasu

AU - Mizuta, Keisuke

AU - Seishima, Mitsuru

AU - Ito, Yatsuji

PY - 2003/7/1

Y1 - 2003/7/1

N2 - Background: Allergic rhinitis is an inflammation involving TH2-type cytokine production, with pathologic eosinophil infiltration in the nasal mucosa. Although TNF-α is thought to be a pro-inflammatory cytokine, the relationship between TNF-α and allergic rhinitis has not been clarified. Objectives: The role of TNF-α in a murine model of ovalbumin (OVA)-sensitized allergic rhinitis was investigated by using mice deficient in the gene encoding TNF-α (TNF-α-/- mice). Methods: Both wild-type (TNF-α+/+) and TNF-α-/- mice were sensitized with OVA by means of intraperitoneal injection. They were then challenged with intranasal OVA, and various allergic responses were assessed. Results: The production of OVA-specific IgE in the serum (P < .05) and the frequency of sneezes (P < .05) and nasal rubs (P < .05) decreased significantly in TNF-α-/- mice after OVA sensitization compared with that in TNF-α+/+ mice (P < .05). The mRNA expression of IL-4, IL-10, and eotaxin in nasal mucosa in TNF-α-/- mice was also significantly suppressed compared with that in TNF-α+/+ mice after OVA sensitization (P < .05). Furthermore, the expression of both endothelial-leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1 mRNA in the nasal mucosa was significantly suppressed (P < .05), although intercellular adhesion molecule 1 mRNA expression did not decrease significantly in TNF-α-/- mice compared with that in TNF-α+/+ mice after OVA sensitization. In addition, the effect of TNF-α on endothelial-leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1 expression by means of Western blot analysis was compatible with the mRNA results. Pathologically, eosinophil infiltration in nasal mucosa was significantly restricted in TNF-α-/- mice compared with in TNF-α+/+ mice after OVA sensitization (P < .05). Conclusion: TNF-α is necessary for antigen-specific IgE production and for the induction of TH2-type cytokines and chemokines. Furthermore, TNF-α might be important for the expression of adhesion molecules to recruit eosinophils to the allergic inflammatory site. We conclude that the lack of TNF-α inhibited the development of allergic rhinitis.

AB - Background: Allergic rhinitis is an inflammation involving TH2-type cytokine production, with pathologic eosinophil infiltration in the nasal mucosa. Although TNF-α is thought to be a pro-inflammatory cytokine, the relationship between TNF-α and allergic rhinitis has not been clarified. Objectives: The role of TNF-α in a murine model of ovalbumin (OVA)-sensitized allergic rhinitis was investigated by using mice deficient in the gene encoding TNF-α (TNF-α-/- mice). Methods: Both wild-type (TNF-α+/+) and TNF-α-/- mice were sensitized with OVA by means of intraperitoneal injection. They were then challenged with intranasal OVA, and various allergic responses were assessed. Results: The production of OVA-specific IgE in the serum (P < .05) and the frequency of sneezes (P < .05) and nasal rubs (P < .05) decreased significantly in TNF-α-/- mice after OVA sensitization compared with that in TNF-α+/+ mice (P < .05). The mRNA expression of IL-4, IL-10, and eotaxin in nasal mucosa in TNF-α-/- mice was also significantly suppressed compared with that in TNF-α+/+ mice after OVA sensitization (P < .05). Furthermore, the expression of both endothelial-leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1 mRNA in the nasal mucosa was significantly suppressed (P < .05), although intercellular adhesion molecule 1 mRNA expression did not decrease significantly in TNF-α-/- mice compared with that in TNF-α+/+ mice after OVA sensitization. In addition, the effect of TNF-α on endothelial-leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1 expression by means of Western blot analysis was compatible with the mRNA results. Pathologically, eosinophil infiltration in nasal mucosa was significantly restricted in TNF-α-/- mice compared with in TNF-α+/+ mice after OVA sensitization (P < .05). Conclusion: TNF-α is necessary for antigen-specific IgE production and for the induction of TH2-type cytokines and chemokines. Furthermore, TNF-α might be important for the expression of adhesion molecules to recruit eosinophils to the allergic inflammatory site. We conclude that the lack of TNF-α inhibited the development of allergic rhinitis.

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