Open AccessThymocyte depletion during acute Trypanosoma cruzi infection in C57BL/6 mice is partly reverted by lipopolysaccharide pretreatment
Author(s) -
Roggero Eduardo,
Piazzon Isabel,
Nepomnaschy Irene,
Perez Ana,
Velikovsky Alejandro,
Revelli Silvia,
Bottasso Oscar
Publication year - 2004
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1016/j.femsim.2004.02.003
Subject(s) - trypanosoma cruzi , biology , lipopolysaccharide , microbiology and biotechnology , chagas disease , thymocyte , immunology , trypanosomiasis , kinetoplastida , ratón , virology , protozoal disease , parasite hosting , immune system , cd8 , world wide web , computer science , malaria
Infection with Trypanosoma cruzi in C57BL/6 mice leads to a progressive fatal disease accompanied by thymocyte depletion, which is not related with a higher parasite burden but with increased serum levels of tumour necrosis factor alpha (TNF‐α). Because this situation may result from an excessive inflammatory syndrome, mice were now given anti‐TNF‐α mAbs throughout their acute infection, or subjected to a LPS desensitization protocol before parasite challenge. Treatment with anti‐TNF‐α mAbs failed to ameliorate thymocyte depletion but shortened survival time and increased parasite load. Pretreatment with LPS (desensitization followed by a sublethal LPS dose) prolonged survival time with a trend to reduce parasitemias and TNF‐α serum concentrations. Given that pentoxifylline (PTx) interferes with in vitro LPS tolerance, experiments by administering PTx in combination with the tolerance‐inducing LPS doses were also performed. Such schedule significantly reduced mortality, TNF‐α and IL‐6 serum concentrations, and CD4 + CD8 + thymocyte loss. LPS pretreatment allowed a better infection control and protected from the accompanying tissue damage.