Bifidobacterium infantis may be able to stimulate inflammatory response, induce the accumulation of immune cells, and promote the secretion of antitumor factors by macrophage.
The possible mechanisms of TLR overexpressions are as follows: (1) various microbial pathogens considered as etiologic agents of IIMs contribute to overexpressions; (2) endogenous molecules and cytokines that are generated during muscle damage or immune response induce the overexpressions.
Substitutable pathways, considered permissive for a given biological response, induce a cascade of biochemical events that converge towards and mobilise key activator(s) of this response, compatible with a positive outcome.
Pleiotropic drug resistance genes (ABC transporter family), which are involved in jasmonic acid pathway response, induce the secretion of secondary metabolites such as diterpenes that inhibit the growth of invading organisms [ 35- 37].
They are capable of bioactivating mutagens and carcinogens, and carry no p53 mutations enabling them to activate DNA damage response, induce growth arrest, and initiate apoptosis (Hsu et al., 1993b; Knasmuller et al., 1998; Wilkening et al., 2003).
