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Infection and Immunity, December 2005, p. 7914-7921, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.7914-7921.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Syndecan 1 Shedding Contributes to Pseudomonas aeruginosa Sepsis

Allan Haynes III,1,{dagger} Frank Ruda,1 Jeffrey Oliver,2 Abdul N. Hamood,3 John A. Griswold,1 Pyong Woo Park,4 and Kendra P. Rumbaugh1*

Departments of Surgery,1 Pathology,2 Microbiology and Immunology, Texas Tech University Health Sciences Center, 3601 4th St., Lubbock, Texas 79430,3 Department of Medicine, Baylor College of Medicine, Houston, Texas 770304

Received 20 July 2005/ Returned for modification 27 August 2005/ Accepted 1 September 2005

The innate immune system is comprised of many components that function coordinately to prevent bacterial sepsis. However, thermal injury suppresses many of these factors, and the opportunistic pathogen Pseudomonas aeruginosa takes advantage of this condition, making it one of the leading causes of morbidity and mortality in the setting of thermal injury. P. aeruginosa is extremely efficient at colonizing burn wounds, spreading systemically, and causing sepsis, which often results in a systemic inflammatory response, multiple-organ failure, and death. The pathogenicity of P. aeruginosa is due to the arsenal of virulence factors produced by the pathogen and the immunocompromised state of the host. Syndecan 1 is a major heparan sulfate proteoglycan present on many host cells involved in thermal injury. Syndecan 1 anchored to the cell surface can be cleaved in a process termed ectodomain shedding. Syndecan 1 shedding results in the release of intact, soluble proteoglycan ectodomains that have diverse roles in innate immunity. Here we show for the first time that thermal injury results in shedding of syndecan 1 from host tissue. Our data show that syndecan 1 null mice are significantly less susceptible to P. aeruginosa infection than their wild-type counterparts, as demonstrated by (i) significantly lower mortality; (ii) absence of systemic spread of P. aeruginosa; and (iii) significant reductions in some proinflammatory cytokines. These results suggest that shed syndecan 1 plays an important role in the pathogenesis of P. aeruginosa infection of thermal injury and that syndecan 1-neutralizing agents may be effective supplements to current P. aeruginosa treatments.

* Corresponding author. Mailing address: Texas Tech University Health Sciences Center, Department of Surgery, 3601 4th Street, Lubbock, TX 79430. Phone: (806) 743-2460 ext. 264. Fax: (806) 743-2370. E-mail: kendra.rumbaugh{at}ttuhsc.edu.

Editor: J. T. Barbieri

{dagger} Present address: University of Washington Health Sciences Center, Seattle, WA 98195.

Infection and Immunity, December 2005, p. 7914-7921, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.7914-7921.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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