title: Signaling pathways bridging microbial-triggered inflammation and cancer.
abstract: Microbial-triggered inflammation protects against pathogens and yet can paradoxically cause considerable secondary damage to host tissues that can result in tissue fibrosis and carcinogenesis, if persistent. In addition to classical pathogens, gut microbiota bacteria, i.e. a group of mutualistic microorganisms permanently inhabiting the gastrointestinal tract and which plays a key role in digestion, immunity, and cancer prevention, can induce inflammation-associated cancer following the alterations of their microenvironment. Emerging experimental evidence indicates that microbiota members like Escherichia coli and several other genotoxic and mutagenic pathogens can cause DNA damage in various cell types. In addition, the inflammatory response induced by chronic infections with pathogens like the microbiota members Helicobacter spp., which have been associated with liver, colorectal, cervical cancers and lymphoma, for instance, can also trigger carcinogenic processes. A microenvironment including active immune cells releasing high amounts of inflammatory signaling molecules can favor the carcinogenic transformation of host cells. Pivotal molecules released during immune response such as the macrophage migration inhibitory factor (MMIF) and the reactive oxygen and nitrogen species' products superoxide and peroxynitrite, can further damage DNA and cause the accumulation of oncogenic mutations, whereas pro-inflammatory cytokines, adhesion molecules, and growth factors may create a microenvironment promoting neoplastic cell survival and proliferation. Recent findings on the implication of inflammatory signaling pathways in microbial-triggered carcinogenesis as well as the possible role of microbiota modulation in cancer prevention are herein summarized and discussed.
authors.affiliation: Department of Veterinary Anatomy, Sokoine University of Agriculture, P.O. Box 3016, Chuo Kikuu, Morogoro, Tanzania.
authors.forename: Maulilio John
authors.initials: MJ
authors.lastname: Kipanyula
authors.forename: Paul Faustin
authors.initials: PF
authors.lastname: Seke Etet
authors.forename: Lorella
authors.initials: L
authors.lastname: Vecchio
authors.forename: Mohammed
authors.initials: M
authors.lastname: Farahna
authors.forename: Elias Nchiwan
authors.initials: EN
authors.lastname: Nukenine
authors.forename: Armel Hervé
authors.initials: AH
authors.lastname: Nwabo Kamdje
mesh_terms: D001424:Bacterial Infections / Q000150:complications / Q000382:microbiology; D051546:Cyclooxygenase 2 / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000378:metabolism*; D054892:Metagenome / Q000502:physiology; D016328:NF-kappa B / Q000378:metabolism; D009369:Neoplasms / Q000378:metabolism* / Q000473:pathology; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000378:metabolism
chemical_list: D016207:Cytokines; D016328:NF-kappa B; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D051193:Toll-Like Receptors; D051546:Cyclooxygenase 2