Eosinophil and neutrophil granulocyte exudation in the Chediak-Higashi (beige) mouse

Humans with Chediak-Higashi syndrome (CHS) and mice carrying the beige mutation have a heritable defect which results in the presence of giant inclusion granules in the cytoplasm in a wide variety of cells and a markedly increased susceptibility to infections. To test whether this increased susceptibility to infection might be a consequence of impaired accumulation of granulocytes at sites of inflammatory-immune stimulation, we quantitated the exudation of granulocytes into the peritoneum in response to secondary tetanus toxoid challenge in normal mice and in two inbred mouse strains with the beige mutation. Neutrophil and eosinophil granulocyte responses in the peritoneal cavity were not diminished in the beige mice as compared to normal mice when previously sensitized animals were challenged intraperitoneally with tetanus toxoid. Since accumulation of cells at the in vivo site of inflammatory immune stimulation did not seem impaired in the mutant beige mice, it would appear that their increased susceptibility to infections is not due to impairment of cellular exudative responses, including the immune components of the eosinophil response.