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Infection and Immunity, April 2008, p. 1358-1367, Vol. 76, No. 4
0019-9567/08/$08.00+0     doi:10.1128/IAI.01330-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Bacillus cereus Induces Permeability of an In Vitro Blood-Retina Barrier{triangledown}

A. L. Moyer,1 R. T. Ramadan,2 J. Thurman,3 A. Burroughs,4 and M. C. Callegan1,2,3,5*

Department of Microbiology and Immunology,1 Oklahoma Center for Neuroscience,2 Department of Ophthalmology,3 Oklahoma Christian University,4 Dean McGee Eye Institute, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma5

Received 3 October 2007/ Returned for modification 6 November 2007/ Accepted 28 January 2008

Most Bacillus cereus toxin production is controlled by the quorum-sensing-dependent, pleiotropic global regulator plcR, which contributes to the organism's virulence in the eye. The purpose of this study was to analyze the effects of B. cereus infection and plcR-regulated toxins on the barrier function of retinal pigment epithelium (RPE) cells, the primary cells of the blood-retina barrier. Human ARPE-19 cells were apically inoculated with wild-type or quorum-sensing-deficient B. cereus, and cytotoxicity was analyzed. plcR-regulated toxins were not required for B. cereus-induced RPE cytotoxicity, but these toxins did increase the rate of cell death, primarily by necrosis. B. cereus infection of polarized RPE cell monolayers resulted in increased barrier permeability, independent of plcR-regulated toxins. Loss of both occludin and ZO-1 expression occurred by 8 h postinfection, but alterations in tight junctions appeared to precede cytotoxicity. Of the several proinflammatory cytokines analyzed, only interleukin-6 was produced in response to B. cereus infection. These results demonstrate the deleterious effects of B. cereus infection on RPE barrier function and suggest that plcR-regulated toxins may not contribute significantly to RPE barrier permeability during infection.

* Corresponding author. Mailing address: Department of Ophthalmology, DMEI 418, University of Oklahoma Health Sciences Center, 608 Stanton L. Young Blvd., Oklahoma City, OK 73104. Phone: (405) 271-3674. Fax: (405) 271-8781. E-mail: michelle-callegan{at}ouhsc.edu

{triangledown} Published ahead of print on 11 February 2008.

Editor: B. A. McCormick

Infection and Immunity, April 2008, p. 1358-1367, Vol. 76, No. 4
0019-9567/08/$08.00+0     doi:10.1128/IAI.01330-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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