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Infection and Immunity, October 2003, p. 5986-5993, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.5986-5993.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Host Resistance of CD18 Knockout Mice against Systemic Infection with Listeria monocytogenes

Huaizhu Wu,¹ Joseph E. Prince,² Cory F. Brayton,³ Chirayu Shah,¹ Daniel Zeve,¹ Stephen H. Gregory,⁴ C. Wayne Smith,⁵ and Christie M. Ballantyne^1,5*

Section of Atherosclerosis,¹ Section of Pulmonary and Critical Care Medicine, Department of Medicine ,² Center for Comparative Medicine,³ Section of Leukocyte Biology, Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030,⁵ Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence, Rhode Island 02903⁴

Received 13 May 2003/ Returned for modification 3 June 2003/ Accepted 27 June 2003

Mice with targeted mutations of CD18, the common ß2 subunit of CD11/CD18 integrins, have leukocytosis, impaired transendothelial neutrophil emigration, and reduced host defense to Streptococcus pneumoniae, a gram-positive extracellular bacterium. Previous studies using blocking monoclonal antibodies suggested roles for CD18 and CD11b in hepatic neutrophil recruitment and host innate response to Listeria monocytogenes, a gram-positive intracellular bacterium. We induced systemic listeriosis in CD18 knockout (CD18-ko) and wild-type (WT) mice by tail vein injection with Listeria. By 14 days postinjection (dpi), 8 of 10 WT mice died, compared with 2 of 10 CD18-ko mice (P < 0.01). Quantitative organ culture showed that numbers of Listeria organisms in livers and spleens were similar in both groups at 20 min postinfection. By 3, 5, and 7 dpi, however, numbers of Listeria organisms were significantly lower in livers and spleens of CD18-ko mice than in WT mice. Histopathology showed that following Listeria infection, CD18-ko mice had milder inflammatory and necrotizing lesions in both spleens and livers than did WT mice. Cytokine assays indicated that baseline interleukin-1ß and granulocyte colony-stimulating factor (G-CSF) levels were higher in CD18-ko mice than in WT mice and that CD18-ko splenocytes produced higher levels of interleukin-1ß and G-CSF than WT splenocytes under the same amount of Listeria stimulation. These findings show that CD18 is not an absolute requirement for antilisterial innate immunity or hepatic neutrophil recruitment. We propose that the absence of CD18 in the mice results in the priming of innate immunity, as evidenced by elevated cytokine expression, and neutrophilic leukocytosis, which augments antilisterial defense.

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* Corresponding author. Mailing address: Baylor College of Medicine, 6565 Fannin, MS A-601, Houston, TX 77030. Phone: (713) 798-5034. Fax: (713) 798-3057. E-mail: cmb{at}bcm.tmc.edu.

Editor: F. C. Fang

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Infection and Immunity, October 2003, p. 5986-5993, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.5986-5993.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

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