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Infection and Immunity, March 1999, p. 1455-1460, Vol. 67, No. 3
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Involvement of Tumor Necrosis Factor Alpha and Interleukin-1beta in Enhancement of Pentylenetetrazole-Induced Seizures Caused by Shigella dysenteriae

Yael Yuhas,1 Lester Shulman,2 Abraham Weizman,1 Elizabeth Kaminsky,1 Alexey Vanichkin,1 and Shai Ashkenazi1,3,*

The Basil and Gerald Felsenstein Medical Research Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv,1 Central Virology Laboratory, Sheba Medical Center, Tel Hashomer,2 and Schneider Children's Medical Center of Israel, Petah Tikva,3 Israel

Received 5 August 1998/Accepted 3 December 1998

Neurologic manifestations, mainly convulsions, are the most frequent extraintestinal complications of shigellosis. We used an animal model to study the roles of tumor necrosis factor alpha (TNF-alpha ) and interleukin-1 beta  (IL-1beta ) in Shigella-related seizures. Administration of Shigella dysenteriae 60R sonicate enhanced the sensitivity of mice to the proconvulsant pentylenetetrazole (PTZ) within 7 h. This was indicated by a significantly higher mean convulsion score and an increased number of mice responding with clonic-tonic seizures in the Shigella-pretreated group. Preinjection of mice with anti-murine TNF-alpha (anti-mTNF-alpha ) or anti-murine IL-1beta (anti-mIL-1beta ) 30 min prior to administration of Shigella sonicate abolished their enhanced response to PTZ at 7 h. Mean convulsion scores were reduced by anti-mTNF-alpha from 1.2 to 0.8 (P = 0.017) and by anti-mIL-1beta from 1.3 to 0.7 (P = 0.008). Preinjection of anti-mTNF-alpha also reduced the percentage of mice responding with clonic-tonic seizures, from 48 to 29% (P = 0.002), and preinjection of anti-mIL-1beta reduced it from 53 to 21% (P = 0.012). Neutralization of TNF-alpha or IL-1beta did not protect the mice from death due to S. dysenteriae 60R. These findings indicate that TNF-alpha and IL-1beta play a role in the very early sensitization of the central nervous system to convulsive activity after S. dysenteriae administration. Similar mechanisms may trigger neurologic disturbances in other infectious diseases.

* Corresponding author. Mailing address: P.O.B. 8145, Petah Tikva 49181, Israel. Phone: 972-3-9253680/1. Fax: 972-3-9253056/3899. E-mail: shkenazi{at}post.tau.ac.il.

Infection and Immunity, March 1999, p. 1455-1460, Vol. 67, No. 3
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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