Document Detail


CD8(+)-T-cell depletion ameliorates circulatory shock in Plasmodium berghei-infected mice.
MedLine Citation:
PMID:  11705906     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 HCO(3)(-) 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.
Authors:
W L Chang; S P Jones; D J Lefer; T Welbourne; G Sun; L Yin; H Suzuki; J Huang; D N Granger; H C van der Heyde
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Infection and immunity     Volume:  69     ISSN:  0019-9567     ISO Abbreviation:  Infect. Immun.     Publication Date:  2001 Dec 
Date Detail:
Created Date:  2001-11-13     Completed Date:  2001-12-12     Revised Date:  2013-04-17    
Medline Journal Info:
Nlm Unique ID:  0246127     Medline TA:  Infect Immun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  7341-8     Citation Subset:  IM    
Affiliation:
Department of Medicine, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130, USA. wchang@lsumc.edu
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MeSH Terms
Descriptor/Qualifier:
Acidosis, Lactic
Adenosine Triphosphatases / blood
Animals
Anion Transport Proteins
CD8-Positive T-Lymphocytes / immunology*
Capillary Permeability
Cardiac Output
Edema
Glutamic Acid / blood
Lactic Acid / blood
Lymphocyte Depletion*
Malaria / complications,  immunology*
Models, Immunological
Plasmodium berghei / immunology*
Shock / etiology,  immunology*,  therapy
Grant Support
ID/Acronym/Agency:
KO8 AI01438/AI/NIAID NIH HHS; P01 DK43785/DK/NIDDK NIH HHS; R01 AI 40667/AI/NIAID NIH HHS; R01 HL60849/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Anion Transport Proteins; 50-21-5/Lactic Acid; 56-86-0/Glutamic Acid; EC 3.6.1.-/Adenosine Triphosphatases; EC 3.6.1.-/anion-sensitive ATPases
Comments/Corrections

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