Encephalitozoon cuniculi is an opportunist intracellular pathogen of
mammals. The
adaptive immune response is essential to eliminate E. cuniculi, but evidence is mounting that the response initiated by the
innate immune response may ultimately define whether or not the
parasite can survive.
B-1 cells may act as
antigen-presenting cells or differentiate into
phagocytes, playing different
roles in many
infection models. However, the
role of these
cells in the dynamics of
Encephalitozoon sp.
infections is still unknown. To investigate the
role of
B-1 cells in E. cuniculi
infection, BALB/c and BALB/c XID (
B-1 cells deficient)
mice were infected with E. cuniculi
spores. Cytometric analyses of peritoneal
cells showed that
B-1 cells and
macrophages increased significantly in infected BALB/c
mice compared to uninfected controls. Despite the increase in the number of CD4(+) and CD8(+)
lymphocytes in XID
mice, these
animals were more susceptible to
infection as evidenced histologically with more prominent inflammatory lesions and
parasite burden. Pro-inflammatory
cytokines increased in both infected BALB/c and BALB/c XID
mice. To confirm
B-1 cells role in
encephalitozoonosis, we adoptively transferred
B-1 cells to BALB/c XID
mice and this group showed few symptoms and microscopic lesions, associated with an increased in
cytokines. Together, these results suggest that
B-1 cells may increase the resistance of BALB/c
mice to
encephalitozoonosis, evidencing for the first
time the important
role of
B-1 lymphocytes in the control of
microsporidia infection.