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Infection and Immunity, September 2005, p. 6157-6164, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.6157-6164.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Role of Toll-Like Receptor 4 in the Proinflammatory Response to Vibrio cholerae O1 El Tor Strains Deficient in Production of Cholera Toxin and Accessory Toxins

G. Kenneth Haines III,1 Blayne Amir Sayed,2 Melissa S. Rohrer,2 Verena Olivier,2 and Karla J. Fullner Satchell2*

Departments of Pathology,1 Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois2

Received 5 November 2004/ Returned for modification 3 March 2005/ Accepted 16 May 2005

Following intranasal inoculation, Vibrio cholerae KFV101 ({Delta}ctxAB {Delta}hapA {Delta}hlyA {Delta}rtxA) colonizes and stimulates tumor necrosis factor alpha and interleukin 1ß (IL-1ß) in mice, similar to what occurs with isogenic strain P4 ({Delta}ctxAB), but is less virulent and stimulates reduced levels of IL-6, demonstrating a role for accessory toxins in pathogenesis. Morbidity is enhanced in C3H/HeJ mice, indicating that Toll-like receptor 4 is important for infection containment.


* Corresponding author. Mailing address: Northwestern University, Dept. of Microbiology-Immunology, 303 E. Chicago Avenue, Tarry 3-713, Chicago, IL 60611. Phone: (312) 503-2162. Fax: (312) 503-1339. E-mail: k-satchell{at}northwestern.edu.

Editor: V. J. DiRita


Infection and Immunity, September 2005, p. 6157-6164, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.6157-6164.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




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