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Conclusion & Future Perspective
Recently, significant progress in the understanding of the cellular and molecular pathogeneses of IBD has been achieved using murine models for ulcerative colitis, highlighting the critical role of commensal microbiota and their gene products in the immunopathology of IBD. Data show that deregulation of immune interactions that promote intestinal homeostasis leads to cellular immune dysfunctions, which may result in undesired intestinal inflammation and IBD progression. The precise cellular and molecular mechanisms of IBD remain poorly understood. Questions remain as to how intestinal inflammatory immune components become proinflammatory, and how they can be reprogrammed. In this regard, we have recently demonstrated a pivotal role for gut microflora (i.e., L. acidophilus NCFM) in controlling inflammation of the intestine.
Collectively, our data indicate that the LTA-deficient strain, NCK2025, activates DC and macrophage regulation, which in turn directly elicits CD4 Treg activation. Furthermore, we demonstrate that stimulatory bacterial gene products (i.e., LTA) modify innate and adaptive immune responses in vivo. Such an activation of CD4 effector T cells may result in the promotion of chronic inflammation in IBD. Studies are currently underway to further modify the gene products of L. acidophilus in order to investigate whether dysregulated immune functions can be restored using gene targeting to mitigate colonic diseases, including IBD and colon cancer.
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