Commensal microbiota that reside primarily in the gut of mammals influence the hosts' health to a great extent. Shaping of host immunity locally, a vital component of this influence, can have pro-inflammatory, anti-inflammatory, or neutral outcomes, presumably depending on the composition of the microbiota in an individual and type of molecules expressed in the individual members of the microbiota. Thus, these microbial species can be thought of as a reservoir of molecules that can be used to improve or worsen the condition of patients suffering from immunity or inflammation-driven pathologies like inflammatory bowel disease. In the current review, we elaborate, based on the literature available from murine models of disease and clinical case studies, the need to identify individual members of commensal microbiota that can precipitate or resolve inflammatory bowel disease. Therapeutic approaches could entail enrichment of members of microbiota (or molecules from these microbes), which induces expansion or enhancement of function of regulatory T cells or tolerogenic dendritic cells and reduce members that cause inflammation either directly or indirectly by influencing metabolic and other host molecules. Efficiency of bacteria-driven therapy would potentially be enhanced as we refine our approaches from the use of complete feces as done in fecal transplantation to utilization of microbiota-derived molecules as exemplified by the capsular polysaccharide A from the human gut commensal Bacteroides fragilis. We also highlight the advantages and disadvantages of each approach, defining a natural alternative to the current chemical-based immunosuppressive regimen for patients with inflammatory bowel disease.