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jejuni 81-176 infection. Our results suggest that pre-treatment of the HT-29 cells with EcN induced the anti-inflammatory cytokines and activated the anti-apoptotic Akt signaling which likely to protect the cells against the proinflammatory and apoptosis responses induced by C. jejuni. EcN also positively affected the expression of genes involved in cellular maintenance, growth, development, and proliferation. Further, EcN modulated the expression of genes involved in protective innate immunity, such as TLRs, ERK1/2, p38 MAPK, Ap1, JNK,
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