Characterization of the B-cell immune response elicited in BALB/c mice challenged with Neospora caninum tachyzoites.
Activation of B cells occurring in hosts infected with protozoan parasites has been implicated either in protective or parasite-evasion immune-mediated mechanisms. Intraperitoneal inoculation of Neospora caninum tachyzoites into BALB/c mice induces an acute response characterized by a rapid increase in the numbers of CD69-expressing peritoneal and splenic B cells. This early B-cell stimulatory effect preceded an increase in the numbers of total and immunoglobulin-secreting splenic B cells and a rise in serum levels of N. caninum-specific immunoglobulins, predominantly of the immunoglobulin G2a (IgG2a) and IgM isotypes. Increased numbers of B cells expressing the costimulatory molecules CD80 and CD86 were also observed in the N. caninum-infected mice. The B-cell stimulatory effect observed in mice challenged with N. caninum tachyzoites was reduced in mice challenged with gamma-irradiated parasites. Contrasting with the peripheral B-cell expansion, a depletion of B-lineage cells was observed in the bone-marrow of the N. caninum-infected mice. Intradermal immunization of BALB/c mice with diverse N. caninum antigenic preparations although inducing the production of parasite-specific antibodies nevertheless impaired interferon-gamma (IFN-gamma) mRNA expression and caused lethal susceptibility to infection in mice inoculated with a non-lethal parasitic inoculum. This increased susceptibility to N. caninum was not observed in naïve mice passively transferred with anti-N. caninum antibodies. Taken together, these results show that N. caninum induces in BALB/c mice a parasite-specific, non-polyclonal, B-cell response, reinforce previous observations made by others showing that immunization with N. caninum whole structural antigens increases susceptibility to murine neosporosis and further stress the role of IFN-gamma in the host protective immune mechanisms against this parasite.
Teixeira
Luzia
L
ICBAS - Instituto de Ciências Biomédicas de Abel Salazar, Porto, Portugal.
Marques
Andreia
A
Meireles
Carla Sofia
CS
Seabra
Ana Rita
AR
Rodrigues
Diana
D
Madureira
Pedro
P
Faustino
Augusto M R
AM
Silva
Carolina
C
Ribeiro
Adília
A
Ferreira
Paula
P
Correia da Costa
José Manuel
JM
Canada
Nuno
N
Vilanova
Manuel
M
D000818:Animals; D000913:Antibodies, Protozoan / Q000096:biosynthesis*; D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D000953:Antigens, Protozoan / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology*; D001853:Bone Marrow / Q000276:immunology; D001921:Brain / Q000473:pathology; D002478:Cells, Cultured; D003048:Coccidiosis / Q000276:immunology* / Q000473:pathology; D004198:Disease Susceptibility; D005434:Flow Cytometry / Q000379:methods; D007124:Immunoenzyme Techniques; D037181:Lectins, C-Type; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D018688:Neospora / Q000276:immunology*; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D013154:Spleen / Q000276:immunology; D000099192:CD69 Antigens
D000913:Antibodies, Protozoan; D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D000953:Antigens, Protozoan; D037181:Lectins, C-Type; D000099192:CD69 Antigens