A central aspect of the authors’ conclusions is that neutrophil impairment by lethal and/or edema toxin exacerbates the disease and increases the likelihood of infection of the central nervous system. However, they have not demonstrated a significant role of neutrophils in preventing the disease caused by Bacillus anthracis Sterne; simply a correlation of their reduced presence early in infection with the production of toxins. Indeed, previous publications (Cote et al. Infection and Immunity, Jan. 2006, p. 469–480) have demonstrated that neutrophils play little role in resisting infection by the fully virulent Ames strain in mouse models of infection, thus calling into question the relevance of the data reported by Van Sorge et al. If the authors wish to claim that the cause of increased meningitis is caused by a reduction in neutrophil recruitment, they should determine if depletion of neutrophils increases the frequency of bacteria crossing the barrier. Alternatively, CXCR1 knockout mice could be considered (Cacalano,et al. Science 265:682).
