This study investigated the respiratory burst responses of rat resident per
itoneal macrophages and of peritoneal macrophages stimulated 5 days previou
sly with viable spores of the fish infecting microsporidian Microgemma caul
leryi. Nitric oxide production by resident macrophages and prestimulated ma
crophages in response to viable microsporidian spores was significantly low
er than in response to Escherichia coli lipopolysaccharide (LPS) (nitrite c
oncentration in medium 57 +/- 1 muM for resident macrophages stimulated wit
h LPS versus 31 +/- 1 muM for resident macrophages stimulated with microspo
ridian spores and 36 +/- 4 muM for M. caulleryi prestimulated macrophages;
P < 0.05). Extracellular release of reactive oxygen species (ROS) by reside
nt macrophages in response to microsporidian spores was similar to that in
response to Kluyveromyces lactis yeast cells and to that in response to pho
rbol myristate (a stimulator of protein C kinase). Intracellular ROS produc
tion by resident macrophages in response to microsporidian spores was simil
ar to that produced in response to yeast cells. Both extracellular ROS prod
uction and intracellular ROS production (in response to all stimuli) were s
ignificantly lower after in vivo prestimulation of macrophages with microsp
oridian spores. These results demonstrate that microsporidian spores of spe
cies other than those that habitually infect mammals are capable of modulat
ing the respiratory burst of rat peritoneal macrophages. Such modulation ma
y contribute to avoidance by the microsporidian of cytotoxic responses asso
ciated with the respiratory burst. (C) 2001 Academic Press.