Mechanisms of AllergyTNF-α contributes to the development of allergic rhinitis in mice☆
Section snippets
Mice
The C57BL/6 strain of TNF-α–/– mice were generated in our laboratory, as described previously.13 BALB/c mice were obtained from Japan SLC Inc (Hamamatsu, Japan). TNF-α–/– male mice (20-25 g) and wild-type (TNF-α+/+) male mice (20-25 g) were obtained from homozygous inbreeding in the F2 generation (C57BL/6 x BALB/c) because BALB/c mice are thought to be high responders with respect to ovalbumin (OVA), whereas C57BL/6 mice are low responders.14
Sensitization of mice
TNF-α+/+ and TNF-α–/– mice, hereafter referred to as
Appearance of nasal symptoms
Sneezes and nasal rubs were observed for 10 minutes after the last intranasal challenge. As shown in Fig 1, the frequency of sneezes and nasal rubs was significantly lower in TNF-α–/– (OVA) mice than in TNF-α+/+ (OVA) mice (P < .05).
Serum total IgE and OVA-specific IgE
Discussion
The present study clarifies the relationship between TNF-α and antigen-specific IgE production and the necessity of TNF-α for the induction of TH2-type cytokines and chemokines in allergic rhinitis.
It is widely accepted that IL-4 is involved in both IgE production and antigen-specific IgE production,16, 17 and IL-10 has a positive role in the induction of the antigen-specific IgE response.18 It has been recently reported that TNF-α enhances allergic sensitization. Pretreatment with TNF-α before
Acknowledgements
We appreciate the technical assistance of S. Fujigaki, N. Furuta, and H. Ohashi.
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