{'fraction_non_alphanumeric': 0.03235082674335011, 'fraction_numerical': 0.007189072609633357, 'mean_word_length': 4.416342412451362, '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}}
Complement activating property of the protein-rich endotoxin (OEP) of Pseudomonas aeruginosa. II. Complement activating property of the lipopolysaccharide portion and the inhibition by polymyxin B.

In order to elucidate the active principle and the mechanism of complement activation of protein-rich endotoxin (OEP) of P. aeruginosa, the complement consumption of the LPS from OEP was studied either in guinea pig serum (GPS) or in factor D-depleted GPS (D-dpl-GPS) in the presence or absence of polymyxin B. Polymyxin B is an inhibitor of the classical pathway (CP) activation due to the lipid A of LPS. The LPS from OEP had about 5 times higher the activity than OEP in GPS. This value corresponds to the LPS content (about 20%) in OEP. It was not likely that the protein portion (about 80%) of the OEP participates to activate complement. In GPS, the ability of the LPS from OEP was only partially inhibited by polymyxin B. In D-dpl-GPS in which the alternative pathway (AP) may be abrogated, the consumption by the LPS from OEP markedly decreased, and was furthermore diminished in the presence of polymyxin B. These results suggest that the LPS from OEP is the active principle of OEP and activates both the CP and the AP. It was noteworthy that two fold or less polymyxin B in weights did not inhibit the ability of E. coli 0111:B4 LPS to activate only the AP, but rather enhanced it.