Microbial-Driven Immunological Memory and Its Potential Role in Microbiome Editing for the Prevention of Colorectal Cancer - PubMed (original) (raw)
Review
Microbial-Driven Immunological Memory and Its Potential Role in Microbiome Editing for the Prevention of Colorectal Cancer
Laure Campillo-Gimenez et al. Front Cell Infect Microbiol. 2021.
Abstract
Over the last several years, many advances have been made in understanding the role of bacteria in the pathogenesis of gastrointestinal cancers. Beginning with Helicobacter pylori being recognized as the first bacterial carcinogen and the causative agent of most gastric cancers, more recent studies have examined the role of enteric microbes in colorectal cancer. In the digestive tract, these communities are numerous and have a complex interrelationship with local immune/inflammatory responses that impact the health of the host. As modifying the microbiome in the stomach has decreased the risk of gastric cancer, modifying the distal microbiome may decrease the risk of colorectal cancers. To date, very few studies have considered the notion that mucosal lymphocyte-dependent immune memory may confound attempts to change the microbial components in these communities. The goal of this review is to consider some of the factors impacting host-microbial interactions that affect colorectal cancer and raise questions about how immune memory responses to the local microbial consortium affect any attempt to modify the composition of the intestinal microbiome.
Keywords: CRC; IBD; T/B cell repertoire; immune memory; microbiome; microbiome-editing.
Copyright © 2021 Campillo-Gimenez, Rios-Covian, Rivera-Nieves, Kiyono, Chu and Ernst.
Conflict of interest statement
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Figures
Figure 1
Immunological memory selects for familiar microbiota and limits attempt to modify microbiome. (A) The host can have a balanced homeostatic relationship that inhibits (through any innate or adaptive mechanism) the growth of deleterious bacteria (in particular, those that cause acute disease, red dots) while co-existing with symbiotic species (green dot) or even species that pose no immediate risk but may contribute in the future to chronic disease such as IBD or CRC (e.g. a pathobiont, red dots). Antigen-specific activation of T and B cells imparts the immunological memory to the existing microbiome. (B) In dysbiosis, microbes favoring inflammatory responses and carcinogenesis exist in the presence of host responses that are also antigen-specific. These responses have adapted to favor the persistence of the dysbiotic microbial population. (C) When attempts are made to modulate the microbiota – without altering the immunological memory - existing host responses from the dysbiotic state persist and (D) favor the re-selection of the same community, provided through the therapeutic inoculum (such as a fecal transplant) or additional encounters in the host’s normal environment, e.g. microbes shared from family members, dietary ingredients and so on. DCs, dendritic cells; Tfh, follicular T cells; Th, helper T cells; TRM, tissue-resident memory T cells; Treg, regulatory T cells; B, B cells; IgA, immunoglobulin A; IgG, immunoglobulin G; Ag-spe activation, antigen-specific activation; PPs, Peyer’s patches; MLNs, mesenteric lymph nodes.