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Infection and Immunity, December 2001, p. 7341-7348, Vol. 69, No. 12
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.12.7341-7348.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

CD8+-T-Cell Depletion Ameliorates Circulatory Shock in Plasmodium berghei-Infected Mice

Wun-Ling Chang,1,* Steven P. Jones,2 David J. Lefer,2 Tomas Welbourne,2 Guang Sun,3 Lijia Yin,1 Hodaka Suzuki,3 Jian Huang,1 D. Neil Granger,2,4 and Henri C. van der Heyde3,4,5

Departments of Medicine,1 Molecular and Cellular Physiology,2 and Microbiology and Immunology,3 Inflammation and Immunology Research Group,4 and Center of Excellence in Arthritis and Rheumatism,5 Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130

Received 3 March 2001/Returned for modification 14 May 2001/Accepted 18 July 2001

The Plasmodium berghei-infected mouse model is a well-recognized model for human cerebral malaria. Mice infected with P. berghei exhibit (i) metabolic acidosis (pH < 7.3) associated with elevated plasma lactate concentrations, (ii) significant (P < 0.05) vascular leakage in their lungs, hearts, kidneys, and brains, (ii) significantly (P < 0.05) higher cell and serum glutamate concentrations, and (iv) significantly (P < 0.05) lower mean arterial blood pressures. Because these complications are similar to those of septic shock, the simplest interpretation of these findings is that the mice develop shock brought on by the P. berghei infection. To determine whether the immune system and specifically CD8+ T cells mediate the key features of shock during P. berghei malaria, we depleted CD8+ T cells by monoclonal antibody (mAb) treatment and assessed the complications of malarial shock. P. berghei-infected mice depleted of CD8+ T cells by mAb treatment had significantly reduced vascular leakage in their hearts, brains, lungs, and kidneys compared with infected controls treated with rat immunoglobulin G. CD8-depleted mice were significantly (P < 0.05) protected from lactic acidosis, glutamate buildup, and diminished HCO3- levels. Although the blood pressure decreased in anti-CD8 mAb-treated mice infected with P. berghei, the cardiac output, as assessed by echocardiography, was similar to that of uninfected control mice. Collectively, our results indicate that (i) pathogenesis similar to septic shock occurs during experimental P. berghei malaria, (ii) respiratory distress with lactic acidosis occurs during P. berghei malaria, and (iii) most components of circulatory shock are ameliorated by depletion of CD8+ T cells.

* Corresponding author. Mailing address: Department of Medicine, LSU Health Sciences Center-Shreveport, P.O. Box 33932, Shreveport, LA 71130. Phone: (318) 675-5990. Fax: (318) 675-5764. E-mail: wchang{at}lsumc.edu.

Infection and Immunity, December 2001, p. 7341-7348, Vol. 69, No. 12
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.12.7341-7348.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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