Actinomycetoma, caused by the intracellular
bacterium Nocardia brasiliensis, is characterized by an
infiltration of several inflammatory cell populations. To
explore aspects of the immune response in the
pathogenesis of these bacteria we injected 106 CFU in
footpads of BALB/c mice. After 1, 2, 3, 4, 7, 30 and 90
days immunohistochemistry was performed to compare
presence and distribution of the inflammatory cytokines
TNF-alpha, IL-1 beta, IL-6, IFN-gamma, IL-4, IL-10,
and TGF-beta. Analysis of serial paraffin tissue sections
showed strong participation and differences in
distribution of cytokine-producing cells during the
course of infection. Several TNF-alpha immunoreactive
lymphocytes of the dermis were present during the
course of the infection, but absent in the site of
inflammation. During the first 4 days, IL-1 beta
immunoreactivity was observed in dendritic epidermal
cells and in cells surrounding the neutrophils around the
grain. In later stages of infection, immunoreactive cells
to this cytokine were mainly in the periphery of the
microabscesses. Strong immunoreactivity was observed
with IL-6 during the course of infection. Some cells in
the epidermis and dermis, as well as muscle cells and several cells at the periphery of the microabscesses,
showed strong IL-6 immunoreactivity. Cells
immunoreactive to IL-4, IL-10, IFN-gamma and TGFbeta
were present at the site of infection and, in later
stages, in cells at the periphery of the microabscesses. In
conclusion a mix of proinflammatory and
antiinflammatory cytokines are produced at the same
time by host cells. According to their distribution,
inflammatory cytokines seems to have different
functions during the course of infection with the
intracellular bacterium N. brasiliensis