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Infection and Immunity, June 2004, p. 3315-3324, Vol. 72, No. 6
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.6.3315-3324.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Clearance of Citrobacter rodentium Requires B Cells but Not Secretory Immunoglobulin A (IgA) or IgM Antibodies

Christian Maaser,1,{dagger} Michael P. Housley,1 Mitsutoshi Iimura,1 Jennifer R. Smith,1 Bruce A. Vallance,2 B. Brett Finlay,2 John R. Schreiber,3 Nissi M. Varki,1 Martin F. Kagnoff,1 and Lars Eckmann1*

Department of Medicine, University of California, San Diego, La Jolla, California 92093,1 Biotechnology Laboratory, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3,2 Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, Ohio 441063

Received 20 October 2003/ Returned for modification 26 January 2004/ Accepted 10 February 2004

Citrobacter rodentium, a murine model pathogen for human enteropathogenic Escherichia coli, predominantly colonizes the lumen and mucosal surface of the colon and cecum and causes crypt hyperplasia and mucosal inflammation. Mice infected with C. rodentium develop a secretory immunoglobulin A (IgA) response, but the role of B cells or secretory antibodies in host defense is unknown. To address this question, we conducted oral C. rodentium infections in mice lacking B cells, IgA, secreted IgM, polymeric Ig receptor (pIgR), or J chain. Normal mice showed peak bacterial numbers in colon and feces at 1 week and bacterial eradication after 3 to 4 weeks. B-cell-deficient mice were equally susceptible initially but could not control infection subsequently. Tissue responses showed marked differences, as infection of normal mice was accompanied by transient crypt hyperplasia and mucosal inflammation in the colon and cecum at 2 but not 6 weeks, whereas B-cell-deficient mice had few mucosal changes at 2 weeks but severe epithelial hyperplasia with ulcerations and mucosal inflammation at 6 weeks. The functions of B cells were not mediated by secretory antibodies, since mice lacking IgA or secreted IgM or proteins required for their transport into the lumen, pIgR or J chain, cleared C. rodentium normally. Nonetheless, systemic administration of immune sera reduced bacterial numbers significantly in normal and pIgR-deficient mice, and depletion of IgG abrogated this effect. These results indicate that host defense against C. rodentium depends on B cells and IgG antibodies but does not require production or transepithelial transport of IgA or secreted IgM.

* Corresponding author. Mailing address: Department of Medicine 0623D, University of California, San Diego, 9500 Gilman Dr., La Jolla, CA 92093-0623. Phone: (858) 534-0683. Fax: (858) 534-5691. E-mail: leckmann{at}ucsd.edu.

Editor: A. D. O'Brien

{dagger} Present address: Department of Medicine B, University of Muenster, 48149 Muenster, Germany.

Infection and Immunity, June 2004, p. 3315-3324, Vol. 72, No. 6
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.6.3315-3324.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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