J Med Microbiol Track the topics, authors and articles important to you
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Duarte, R.
Right arrow Articles by Nicoli, J. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Duarte, R.
Right arrow Articles by Nicoli, J. R.
Agricola
Right arrow Articles by Duarte, R.
Right arrow Articles by Nicoli, J. R.
J Med Microbiol 53 (2004), 741-748; DOI: 10.1099/jmm.0.45657-0
© 2004 Society for General Microbiology
ISSN 0022-2615

Influence of normal microbiota on some aspects of the immune response during experimental infection with Trypanosoma cruzi in mice

Rinaldo Duarte1, Andréia M. Silva1, Leda Q. Vieira2, Luiz Carlos C. Afonso3 and Jacques R. Nicoli1

1,2Departamento de Microbiologia1 and Departamento de Bioquímica-Imunologia2, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil 3Departamento de Ciências Biológicas, ICEB/NUPEB, Universidade Federal de Ouro Preto, Ouro Preto, MG, Brazil

Correspondence Jacques R. Nicoli, jnicoli{at}icb.ufmg.br

Received March 2, 2004
Accepted April 27, 2004

To study the influence of normal associated microbiota on systemic immunological responses during experimental Chagas’ disease, germ-free and conventional NIH Swiss mice were infected with Y strain of Trypanosoma cruzi. Although no statistical differences in mortality and parasitaemia were found, conventional mice showed IFN-{gamma}, TNF-{alpha} and NO production (P < 0.05) by spleen cell cultures and higher blood levels of immunoglobulins of the IgG2a isotype (P < 0.05) when compared to their germ-free counterparts. Moreover, higher levels of IgG1 were also found in conventional animals. On the other hand, no differences in IL10 production were found between germ-free and conventional mice after infection (P < 0.05). Interestingly, spleen cell cultures from non-infected germ-free mice spontaneously produced higher levels of IL10 than cultures from conventional mice. Moreover, cultures from non-infected germ-free mice responded to T. cruzi antigens with IFN-{gamma} production, contrary to cultures from conventional animals. In conclusion, the presence of the normal microbiota skews the immune response towards production of inflammatory cytokines during experimental infection with T. cruzi in mice. However, the increase in production of cytokines that is linked to resistance to this parasite did not alter the outcome of infection significantly, probably due to high virulence of the Y strain.


Abbreviations: LPS, lipopolysaccharide; tGPI mucin, T. cruzi glycophosphatidylinositol-anchored mucin-like glycoconjugates.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL J MED MICROBIOL MICROBIOLOGY J GEN VIROL ALL SGM JOURNALS
Copyright © 2004 Society for General Microbiology.