How BCG-Urocidin works. For those who are scientifically curious. Here is a good link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746687/
"Bacille Calmette–Guerin induces a massive influx of inflammatory cells and production of cytokines in the bladder mucosa and lumen that leads to an immune response against tumor cells. An intact immune system is a necessary prerequisite to successful BCG therapy. Studies in human patients receiving BCG, as well as in animal models, have provided further elucidation of the mechanism of BCG therapy. When BCG is instilled in the bladder it binds to urothelial cells via fibronectin attachment to fibronectin attachment protein (FAP) on BCG [27,28]. BCG is internalized by both urothelial cells and inflammatory cells, such as neutrophils, and triggers an inflammatory cascade of cytokine release and immune cell recruitment. Early responding cells include primarily neutrophils (75%) as well as macrophages [29]. Later in the immune response, CD4+ T cells are prevalent [30]. Debate exists over the role of various inflammatory cell subsets and most subsets have been implicated in the cascade of events that lead to a response.
Many studies have examined the cytokines present in the urine of patients treated with BCG and found elevated amounts of IL-1, -2, -6, -8 and -12, TNF, INF-γ and GM-CSF, among others [26,31]. This proinflammatory cytokine profile, especially IL-2, TNF and INF-γ, is a Th1 response. A Th1 cytokine profile, rather than a Th2 profile, is needed for tumor destruction. Studies have been performed looking at specific cytokines found in BCG-induced murine bladder inflammation compared with lipopolysaccharide (LPS)- and TNF-induced inflammation. While levels of many cytokines are altered with BCG, the massive neutrophil infiltration and granuloma formation are two events unique to BCG instillation when compared with the other inflammatory stimuli [32]. is a visual representation of a proposed mechanism for the BCG mechanism of action."
"The rationale behind cellular component therapy is that live BCG may not be needed to induce the bladder inflammatory cascade and, presumably, the antitumoral effects. Live BCG is responsible for the majority of the serious side effects seen with BCG, such as sepsis. Cellular component therapy could theoretically reduce these complications. Several mycobacterial components have been shown to play specific roles in the immune reaction to BCG. The mycobacterial cell wall has been the best characterized activator of immune response in multiple studies. Fractionation of BCG showed that the cell wall component was responsible for the majority of TRAIL released [40]"
All these cascading of cytokines based immune-responses usually need to be triggered by the Ab-Ag complexes like the ignition keys.
Enjoy!