{'fraction_non_alphanumeric': 0.02086677367576244, 'fraction_numerical': 0.0, 'mean_word_length': 5.362244897959184, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Abrogation of BCG-contact induced tumour inhibition by silica: implications for the mechanism of action.

The outgrowth of tumours from inocula of syngeneic rat tumour cells injected in admixture with BCG (Glaxo strain) is suppressed, the tumour cells apparently being destroyed in the milieu of the granulomatous reaction to the mycobacteria. The possible candidacy of macrophages as the major "effector cell" component was examined in experiments conducted in vivo using silica, a selective macrophage toxin. Intraperitoneal (i.p.) administration of this agent abolished contact-induced inhibition of BCG against three transplanted rat sarcomas, although for two of them the abrogatory effect could not be achieved without prior in vitro cultivation of the tumours. It is suggested that i.p. silica not only destroys macrophages within the cavity but accomplishes systemic depletion to the extent that granulomata contain insufficient macrophages for tumour rejection. This deficit may be compensated to a variable extent by the presence of host macrophages within the initial bacterial: tumour cell inoculum, but in the absence of these cells, total abrogation of the inhibitory effect of BCG is the invariable outcome in silica-treated hosts.