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Infect Immun, February 1998, p. 839-842, Vol. 66, No. 2
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Role of Tumor Necrosis Factor Alpha in the Host Response of Mice to Bacteremia Caused by Pneumolysin-Deficient Streptococcus pneumoniae

Kimberly A. Benton,1,dagger John L. VanCott,1 and David E. Briles1,2,3,*

Departments of Microbiology,1 Pediatrics,2 and Comparative Medicine,3 The University of Alabama at Birmingham, Birmingham, Alabama 35294

Received 16 May 1997/Returned for modification 2 July 1997/Accepted 18 November 1997

Pneumolysin-deficient mutant strains of Streptococcus pneumoniae are known to cause less-severe sepsis than wild-type pneumococcal strains that produce pneumolysin. This difference is associated with greater host resistance in mice infected with the pneumolysin-deficient strains. These studies show that the host resistance developed during the first 1 to 2 days after infection with a pneumolysin-deficient mutant strain is dependent on tumor necrosis factor alpha but is apparently independent of interleukin 1beta (IL-1beta ) or IL-6. Survival beyond 5 days appeared to depend on the ability of the mice to produce IL-1beta .

* Corresponding author. Mailing address: BBRB 658, Box 10, University of Alabama at Birmingham, Birmingham, AL 35294-2170. Phone: (205) 934-6595. Fax: (205) 934-0605. E-mail: dbriles{at}uab.edu.

dagger Present address: Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261.




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