This study was designed to evaluate the effects of tetanus toxin (TT) on lysozyme (LZM) activity by the GG2EE macrophage cell line. GG2EE cells spontaneously produced low amounts of LZM, which were mostly secreted into the culture medium. Upon treatment with various cytokines, GG2EE cells exhibited altered LZM activity. In particular, exposure of GG2EE cells to alpha/beta interferon (IFN-a/I) reduced LZM activity, as opposed to treatment with gamma interferon (IFN-y) or colony-stimulating factor 1, which potentiated LZM activity. Spontaneous LZM activity of GG2EE cells was not susceptible to TT action; in contrast, when IFN-'yor colony-stimulating factor 1-susceptible cells were treated with TT, a significant reduction on LZM activity was observed. The TT inhibitory effect was dose dependent and manifested only after a 6-h incubation of GG2EE cells with TT. Treatment of GG2EE cells with heat-inactivated TT as well as Ibcand B-IIb-TT-derived fragments was found to be ineffective, while pretreatment with B-IIbbut not with Ibc-TT-derived fragment abrogated the TT effect. Overall, these data indicate the existence of a specific TT-GG2EE cell interaction, leading to selective inhibition of cytokine-induced LZM activity.
We have established an experimental murine model to gain insight into the pathogenicity and clinical features of type IV group B streptococcus (GBS) infections. Adult CD-1 mice were challenged intravenously with 10(7) type IV GBS cells, inducing systemic invasion. Most of the animals were able to clear the infection from the blood, brain, and lungs within 2 weeks and from the spleen and liver within 1 month. However, the animals were unable to clear the microorganism from the joints and kidneys during the 60-day observation period. About 80% of the mice challenged intravenously with type IV GBS manifested early septic arthritis, which evolved from an acute exudative synovitis to permanent lesions characterized by irreversible joint damage and ankylosis. Induction of persistent septic arthritis was dependent on the number and viability of microorganisms inoculated and was unrelated to the strain of type IV GBS and the growth phase of the inoculum. Type-specific antibodies of both immunoglobulin M and G classes could be detected by agglutination and enzyme-linked immunosorbent assay from days 7 and 14, respectively; immunoglobulin G antibodies persisted for more than 40 days. Complexes of antibodies and group- and type-specific antigens were detected in mouse sera 24 h after infection and persisted up to day 22. These results were obtained an experimental model of type IV GBS chronic infection with early development of septic arthritis, which could be useful in future studies of pathogenicity and immune mechanisms involved in the host resistance to this microorganism.
Clostridioides difficile (C. difficile) is responsible for a high percentage of gastrointestinal infections and its pathological activity is due to toxins A and B. C. difficile infection (CDI) is increasing worldwide due to the unstoppable spread of C. difficile in the anthropized environment and the progressive human colonization. The ability of C. difficile toxin B to induce senescent cells and the direct correlation between CDI, irritable bowel syndrome (IBS), and inflammatory bowel diseases (IBD) could cause an accumulation of senescent cells with important functional consequences. Furthermore, these senescent cells characterized by long survival could push pre-neoplastic cells originating in the colon towards the complete neoplastic transformation in colorectal cancer (CRC) by the senescence-associated secretory phenotype (SASP). Pre-neoplastic cells could appear as a result of various pro-carcinogenic events, among which, are infections with bacteria that produce genotoxins that generate cells with high genetic instability. Therefore, subjects who develop IBS and/or IBD after CDI should be monitored, especially if they then have further CDI relapses, waiting for the availability of senolytic and anti-SASP therapies to resolve the pro-carcinogenic risk due to accumulation of senescent cells after CDI followed by IBS and/or IBD.
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