“…The rapid spreading of Encephalitozoon has been reported in murine models, where systemic infection was reported within several days. 32 , 39 , 41 However, spores of E. cuniculi are not motile, short distance dispersal in the host is limited to a unique mechanism of invasion of host cells that involves a highly specialized structure, the 10–50 μm long polar tube, which is responsible for the delivery of this organism to the host cell. Nevertheless, Encephalitozoon organisms may replicate to produce mature spores in a variety of immune cells including resident and trafficking macrophages and other phagocytic cells such as neutrophils, monocytes, dendritic cells, and eosinophils which may contribute to the spread of E. cuniculi throughout the host organism, 46 , 47 suggesting that induction of chemokines for inducing innate immune inflammation may also promote recruitment of host cells for continued infection and dissemination 48 – 50 On the other hand, there may be a situation in which microsporidia occurring in the area of induced inflammation are eliminated due to the increased occurrence of IFNγ-, LPS-, and TNFα-activated macrophages 10 ,– 50 – 54 by the means of cytotoxic cytokines, cationic proteins, lipid mediators, metalloproteinases, and components of the oxygen burst.…”