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than the rodent (or zebrafish) GIT. Specifically,
although mice and rats have large ceca that serve as
sites of hindgut fermentation, dogs are functionally
monogastric, like humans. Dogs do possess a welldeveloped cecal structure when compared to the
human cecum (or appendix), although it is relatively
small compared to rodent ceca and the bacterial populations present in this region are of unknown relevance
to host health. Of importance for translational research,
privately owned dogs are often exposed to the same
environmental influences as humans and, in some
cases, may share compositional similarities to humans
in the same household,65,66 begging the question of
whether there is direct exchange between humans and
their pets or that both host species are exposed to the
same factors. Considering the functional capacity of
the canine microbiota, metagenomic analyses based on
the collective genomic content of the microbiota (rather
than marker genes such as 16S rRNA) suggest that dietinduced differences in the composition of the microbiota
do not necessitate changes in function, and that canine,
human, and mouse fecal microbiota demonstrate a high
degree of metabolic and phylogenetic similarity.67 The
functional or metabolic capacity of microbial communities can be interrogated using whole metagenome
sequencing or metatranscriptomic approaches to
reveal microbial genetic content and expression respectively,68 and metabolomic69 or metaproteomic70
approaches to quantify specific classes of molecules in
the gut. It is important to remember that these and other
functional outputs are essential adjuncts to composition-based studies.
For these and other reasons, microbiota-related
research using dogs as the model species is growing
and some of the most salient research focuses on gingival and periodontal disease, dental implants, and
inflammatory bowel disease. Links between the oral/
gingival microbiota and periodontal/gingival disease
are intuitive and dogs have proven to be apt model species for decades.71-73 Like humans (and unlike rodents),
dogs are subject to diet-induced periodontal disease74,75
and host genetics also influence susceptibility. Although
the cultivable oral microbiota of dogs differs depending
on whether saliva, gingival sulci, or plaque proper is
analysed,76-78 dominant genera include Streptococcus,
Staphylococcus,
Pseudomonas,
Actinomyces,
Pasteurella, Neisseria, and Porphyromonas, genera
repeatedly identified in the human oral microbiota.79,80
A recent culture-independent analysis of composite oral
samples (combined gingival, dental, buccal, and lingual
samples) collected from six privately owned dogs
revealed Porphyromonas spp. as the dominant colonizer
of the canine oral cavity, along with high relative abundance of Fusobacterium and Capnocytophaga spp.,
among others.81 The apparent discrepancies between

Laboratory Animals 53(3)
these two studies could be explained by differences in
sampling techniques, and the presence or absence of
microbiological culture prior to sequencing. Of particular interest are the changes associated with canine periodontal disease as similar changes may occur in
humans.82-85 For example, despite differences in the
composition of the oral microbiota between healthy
dogs and humans at the species level, the shift from
predominantly Gram-positive aerobic and facultative
anaerobic membership to greater numbers of Gramnegative anaerobic species during the development of
periodontal disease in both host species suggests
common ecological progression and mechanisms.83
Dogs (and cats) also develop chronic inflammatory
conditions very similar to human inflammatory bowel
disease. Considering the common environmental exposures with humans, there is interest in whether common
mechanisms are involved.86 Fusobacteria, Firmicutes,
Bacteroidetes, and Proteobacteria constitute the dominant phyla in the healthy canine fecal microbiota87,88
and associations between certain compositional
changes and incidence of idiopathic canine IBD have
been identified in multiple studies.89,90 Notably, these
studies support the notion that chronic inflammatory
conditions may be the result of dysbiosis in genetically
susceptible individuals, resulting from myriad pressures, and a decrease in the beneficial functions of the
GM such as production of short-chain fatty acids.90,91
As in the aforementioned studies on oral microbiota,
the fact that the relevant bacterial communities differ at
a finer taxonomic resolution between dogs and humans
may be irrelevant if common pathways are involved in
disease susceptibility. Thus, efforts to enhance the beneficial functions of the GM and prevent or ameliorate
inflammation via oral probiotics using canine models is
also a growing area of research.
Lastly, dogs may also represent an ideal model species for investigations of the microbiota present in other
internal organ systems such as the respiratory tract.
Although the lungs and lower airways were historically
regarded as sterile environments based on negative culture results, molecular approaches have revealed rich,
low-biomass bacterial communities in the healthy lungs
of humans,92 cats,93 dogs,94 sheep,95 and mice.96,97 This
newly appreciated factor potentially affecting human
development, physiology, and disease susceptibility
might be most appropriately studied in a canine
model based on the comparable size and environmental
exposures relative to humans. Moreover, the four
dominant genera found in the lungs of healthy
humans (i.e. Pseudomonas, Streptococcus, Prevotella,
and Fusobacterium)98 were all detected at appreciable
relative abundance in canine lung samples,94 suggesting
specific attributes of those taxa render them capable of
colonization in the lower airways of both species.



Laboratory Animals - June Issue

Table of Contents for the Digital Edition of Laboratory Animals - June Issue

Contents
Laboratory Animals - June Issue - Cover1
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Laboratory Animals - June Issue - Contents
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