The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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Published online 30 June 2003 doi:10.1084/jem.20022129
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© Rockefeller University Press, 0022-1007/2003/7/145 $5.00
The Journal of Experimental Medicine, Volume 198, Number 1, 145-151

Platelet-activating Factor–mediated NF-{kappa}B Dependency of a Late Anaphylactic Reaction

Il-Whan Choi1, Young-Suk Kim1, Dae-Ki Kim1, Jung-Hwa Choi3, Kook-Heon Seo3, Shun-Young Im3, Keun-Sang Kwon2, Myung-Shik Lee4, Tai-You Ha1 and Hern-Ku Lee1

1 Department of Immunology, Chonbuk National University Medical School, Chonju 561-180, South Korea
2 Department of Preventive Medicine, Chonbuk National University Medical School, Chonju 561-180, South Korea
3 Department of Biological Sciences, College of Natural Sciences, Chonnam National University, Kwangju 500-757, South Korea
4 Department of Medicine, Samsung Medical Center, Sungkyunkwan University College of Medicine, Seoul 135-710, South Korea

Address correspondence to Hern-Ku Lee, Dept. of Immunology, University National Medical School, Chonju, Chonbuk, 561-182, South Korea. Phone: 82-63-270-3069; Fax: 82-63-250-4215; E-mail: leeh-k{at}chonbuk.ac.kr

Anaphylaxis is a life-threatening systemic allergic reaction with the potential for a recurrent or biphasic pattern. Despite an incidence of biphasic reaction between 5 and 20%, the molecular mechanism for the reaction is unknown. Using a murine model of penicillin V–induced systemic anaphylaxis, we show an autoregulatory cascade of biphasic anaphylactic reactions. Induction of anaphylaxis caused a rapid increase in circulating platelet-activating factor (PAF) levels. In turn, the elevated PAF contributes to the early phase of anaphylaxis as well as the subsequent activation of the nuclear factor (NF)-{kappa}B, a crucial transcription factor regulating the expression of many proinflammatory cytokines and immunoregulatory molecules. The induction of NF-{kappa}B activity is accompanied by TNF-{alpha} production, which, in turn, promotes late phase PAF synthesis. This secondary wave of PAF production leads eventually to the late phase of anaphylactic reactions. Mast cells do not appear to be required for development of the late phase anaphylaxis. Together, this work reveals the first mechanistic basis for biphasic anaphylactic reactions and provides possible therapeutic strategies for human anaphylaxis.

Key Words: early anaphylaxis • biphasic anaphylaxis • mast cell • penicillin V • TNF-{alpha}


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