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Infection and Immunity, December 2005, p. 8009-8016, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.8009-8016.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Essential Role for Humoral Immunity during Ehrlichia Infection in Immunocompetent Mice

Eric Yager,1 Constantine Bitsaktsis,2 Bisweswar Nandi,2 Jere W. McBride,3 and Gary Winslow1,2*

The Department of Biomedical Sciences, School of Public Health, University at Albany, Albany, New York 12201-0509,1 Department of Pathology, Center for Biodefense and Emerging Infectious Diseases and Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas 77555,3 Wadsworth Center, New York State Department of Health, P.O. Box 22002, Albany, New York 12201-20022

Received 4 May 2005/ Returned for modification 25 May 2005/ Accepted 22 September 2005

Although cellular immunity is essential for host defense during intracellular bacterial infections, humoral immunity can also play a significant role in host defense during infection by some intracellular bacteria, including the ehrlichiae. Antibodies can protect susceptible SCID mice from fatal Ehrlichia chaffeensis infection, an observation that has been hypothesized to involve the opsonization of bacteria released from host cells. To determine whether humoral immunity plays an essential role during ehrlichia infection in immunocompetent mice, we utilized a murine model of fatal monocytotropic ehrlichiosis caused by Ixodes ovatus ehrlichia. Mice lacking either B cells or Fc{gamma}RI were unable to resolve a low-dose (sublethal) I. ovatus ehrlichia infection, which suggested that humoral immunity is essential for resistance. Polyclonal sera generated in I. ovatus ehrlichia-infected mice recognized a conserved ehrlichia outer membrane protein and, when administered to infected mice, caused a significant decrease in bacterial infection. Mice experimentally depleted of complement, or deficient for complement receptors 1 and 2, were also susceptible to sublethal I. ovatus ehrlichia infection, as were mice that lacked the phox91 subunit of NADPH oxidase. The data are consistent with a mechanism whereby bacteria released from infected cells are lysed directly by complement or undergo antibody-mediated Fc{gamma}R-dependent phagocytosis and subsequent exposure to reactive oxygen intermediates. The findings suggest mechanisms whereby antibodies contribute to immunity against intracellular bacteria in immunocompetent mice.

* Corresponding author. Mailing address: Wadsworth Center, 120 New Scotland Avenue, Albany, NY 12208. Phone: (518) 473-2795. Fax: (518) 486-9858. E-mail: gary.winslow{at}wadsworth.org.

Editor: T. R. Kozel

Infection and Immunity, December 2005, p. 8009-8016, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.8009-8016.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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