Page 71 - Read Online
P. 71

Page 8 of 13                 Martin et al. Microbiome Res Rep 2023;2:17  https://dx.doi.org/10.20517/mrr.2023.10

               Excessive antibiotic use appears to be a risk factor for certain chronic diseases [127,128] . Antibiotics are known
               to cause significant perturbations in the gut microbiota [112,129]  and promote dysbiotic states. The extent to
               which an antibiotic alters the microbiota depends on the spectrum of the antibiotic, dose, and duration of
                            [112]
               administration . Antibiotic use for extended periods opens a window of opportunity to acquire ARB
               through the loss of colonization resistance [Figure 1] . Resistant bacteria are generally present in the gut
                                                             [74]
                                                                                             [112]
               microbiota but at very low levels [74,115] , and antimicrobial therapy increases ARB selection . Moreover,
               hospitalization results in significant exposure to ARB . Similarly, germ-free or antibiotic-treated animals
                                                             [112]
               develop severe infections compared to conventional animals, such as Salmonella enterica serovar
               Typhimurium or Listeria monocytogenes, owing to the lack of colonization resistance provided by the
                         [72]
               microbiome .

               Probiotics belonging to Lactobacillus and Bifidobacterium have a long history of use in foods and
               supplements, contributing to the balance of the gut microbiota [130,131] . There are several applications where
               these probiotics are recommended, such as infant colic, allergies, and antibiotic administration .
                                                                                                       [132]
               Colonization resistance limits the growth of probiotic bacteria, which usually only transit through the GI
               tract; permanent colonization is uncommon for probiotics . Moreover, transient colonization is highly
                                                                  [133]
               individualized during the consumption of probiotics . Usually, probiotic applications do not consider
                                                             [134]
               colonization resistance or probiotic interactions with other members of the microbiota, which outnumber
               probiotics by at least 1,000 times . Some studies have suggested that colonization is not necessary for its
                                           [74]
               effects on the host .
                              [132]
               CONCLUSIONS
               Microbial interactions represent the inner connections of the gut microbiota and contribute to its protective
               role through colonization resistance against pathogens, ARB, or probiotics. Antibiotics and a low-fiber diet
               play a role against colonization resistance, resulting in dysbiosis with a concomitant reduction in BPB and
               an increased chance of colonization by foreign microbes. Bifidobacterium species are key members of the
               gut microbiota and participate in multiple cross-feeding interactions with species of the same genus and
               other distant species, for example, by sharing SCFAs or monosaccharides. While there are few examples
               showing how some bifidobacteria display beneficial effects to the host and a balanced gut ecosystem, the
               mechanisms, microbial interactions, or metabolites involved in their protective role are largely unknown
               and remain the subject of future studies.


               DECLARATIONS
               Authors’ contributions
               Made substantial contributions to the conception and design of the study and performed data analysis and
               interpretation: Serebrinsky-Duek K, Riquelme E, Saa PA, Martin AJM, Garrido D
               Performed data acquisition and provided administrative, technical, and material support: Riquelme E, Saa
               PA, Martin AJM, Garrido D


               Availability of data and materials
               Not applicable.

               Financial support and sponsorship
               ANID Fondecyt Regular 1230764, 1190074 and 1191526, ANID Fondequip EQM190070; Centro Ciencia &
               Vida, FB210008, Financiamiento Basal para Centros Científicos y Tecnológicos de Excelencia de ANID.
   66   67   68   69   70   71   72   73   74   75   76