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Infection and Immunity, August 2003, p. 4361-4367, Vol. 71, No. 8
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.8.4361-4367.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Kinetics of Cellular Responses to Intraperitoneal Brugia pahangi Infections in Normal and Immunodeficient Mice

Thirumalai Ramalingam, Bhargavi Rajan, James Lee, and T. V. Rajan*

Department of Pathology, University of Connecticut Health Center, Farmington, Connecticut

Received 3 April 2003/ Returned for modification 6 May 2003/ Accepted 24 May 2003

Filarial infections evoke exuberant inflammatory responses in the peritoneal cavities of immunocompetent mice. Clearance of infection appears to be dependent on complex interactions between B1 and B2 B lymphocytes, T cells, eosinophils, macrophages, and the products of these cells. In an earlier communication, we described the course of infection in normal immunocompetent mice. In this study, we utilize mice with well-characterized mutations that disable one or more effector components of adaptive immunity in order to determine their roles in host protection. We characterize peritoneal exudate cells by flow cytometry and determine the kinetics of accumulation of each of the different cell types following infection with Brugia pahangi. We find that (i) four-color flow-cytometric analysis of peritoneal exudate cells using anti-CD3, -CD11b, -CD19, and -Gr1 can distinguish up to six different populations of cells; (ii) an initial influx of neutrophils occurs within 24 h of infection, independent of the adaptive immune status of mice, and these cells disappear by day 3; (iii) an early influx of eosinophils is seen at the site of infection in all strains studied, but a larger, second wave occurs only in mice with T cells; (iv) the presence of T cells and eosinophils is important in causing an increase in macrophage size during the course of infection; and (v) most unexpectedly, T-cell recruitment appears to be optimal only if B cells are present, since JHD mice recruit significantly fewer T cells to the site of infection.

* Corresponding author. Mailing address: Department of Pathology, University of Connecticut Health Center, 263 Farmington Ave., Farmington, CT 06030-3105. Phone: (860) 679-3221. Fax: (860) 679-2936. E-mail: rajan{at}neuron.uchc.edu.

Editor: W. A. Petri, Jr.

Infection and Immunity, August 2003, p. 4361-4367, Vol. 71, No. 8
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.8.4361-4367.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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