Table of Contents
ISRN Parasitology
Volume 2013, Article ID 180652, 8 pages
Research Article

Analysis of Spleen Cells in Susceptible and Resistant Mice with Experimental Lagochilascariosis

1Laboratory of Immunochemistry, Butantan Institute, São Paulo, SP, Brazil
2Laboratory of Immunogenetics, Butantan Institute, São Paulo, SP, Brazil
3Department of Microbiology, Immunology, Parasitology and Pathology, Institute of Tropical Pathology and Public Health, Federal University of Goiás, Goiânia, GO, Brazil

Received 12 June 2012; Accepted 2 August 2012

Academic Editors: A. Jabbar and G. Mkoji

Copyright © 2013 Priscila Guirão Lara et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Lagochilascariosis is an emerging parasitic disease caused by the helminth Lagochilascaris minor. The experimental mouse model has been used to study the immune response against L. minor infection. In the present work, immunohistochemistry analysis of spleen cells populations was evaluated in susceptible (C57BL/6) and resistant (BALB/c) mice experimentally infected with L. minor. The BALB/c mice exhibited increased spleen cell indexes as follows: F4/80+ at 100 days after infection (DPI), CD4+ at 100 and 250 DPI, CD8+ at 35 and 100 DPI, and CD19+ at 100, 150, and 250 DPI. In the spleens of the infected C57BL/6 mice, increased indexes of the following spleen cells were observed: F4/80+ cells at 250 DPI, CD4+ cells at 150 DPI, CD8+ cells at 35, 150, and 250 DPI, and CD19+ cells at 150 to 250 DPI. The index of spleen cells confirmed the differences between the control and infected groups at several time points following the infection. These data demonstrate an association between a preferential increase in the number of CD4+ and CD19+ spleen cells and resistance to experimental lagochilascariosis in BALB/c mice and between a preferential increase in the number of CD8+ spleen cells and susceptibility in C57BL/6 mice.