Modifying factors on phagocytosis of polymorphonuclear allergic subjects.

Supernatants from pollen-activated cultures of mononuclear (MN) cells obtained from two subjects allergic to gramineae pollen were tested for their effect on phagocytic activity of human polymorphonuclear leucocytes (PMN). An enhancement of phagocytosis was observed. Similarly prepared supernatants from MN cells of non-allergic control subjects did not affect PMN phagocytic activity. On the basis of these findings it is suggested that in the presence of allergen, cultures of MN cells from pollen-sensitized subjects produce a substance that stimulates PMN phagocytic activity. The direct effect of pollen on PMN was also studied. The allergen caused an inhibition of phagocytosis by PMN from allergic subjects. Pollen had no effect on phagocytosis by PMN from non-allergic control subjects.

Isolation of L-forms from the spleens of Brucella suis-infected, penicillin-treated mice.

Previous attempts to obtain in vitro wall-deficient stable L-forms of various strains of Brucella have failed because the obtained spheroplasts revert quickly to bacterial form. Here, we report the isolation of L-forms from mice infected with a B. suis strain type 1 and treated with penicillin. In defined experimental conditions, L-type microcolonies associated with tissue debris were observed in primary spleen cultures, even on antibiotic free media. After several transfers on penicillin-containing medium. typical, tissue-free L colonies were obtained. At first, when cultivated on antibiotic-free medium, these colonies reverted to the bacterial form (identified as B suis, biotype 1). Later, after approximately fifteen transfers on penicillin-supplemented medium, they no longer reverted even after several subcultures on antibiotic-free medium. The L-forms' ultrastructural features included many giant empty bodies, considerable variation in size, shape and density of the wall-deficient cells, and many multilayered membranes. The stabilized L-forms were propagated in vitro and inoculated into mice, and then recovered from their spleens as tissue associated L-microcolonies. An occasional in vivo revertant was identified as B. suis, biotype 1. These data provide one possible explanation for earlier failures to detect the presence of atypical bacteria in clinical or experimental Brucella infections.