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1 mescales of host-microbe interactions in the gut.
2 are not typically retrieved from the chicken gut.
3 lexity relative to other niches, such as the gut.
4 microbial community structure in an infant's gut.
5 ormal accumulation of apoptotic cells in the gut.
6 he biogeography of symbiotic bacteria in the gut.
7 wn to provide colonization resistance in the gut.
8 central homeostatic mechanism of the insect gut.
9 nge the balance of commensal bacteria in the gut.
10 the gastro-oesophageal junction in the human gut.
11 n in the fruit fly (Drosophila melanogaster) gut.
12 ia, including those in the mouth, lungs, and gut.
13 also interact with bacteria in the mammalian gut.
14 major source of nutrients for E. coli in the gut.
15 increasing the stability of higher-diversity guts.
19 Vgamma9/Vdelta2 T cells are abundant in the gut and recognize microbiota-associated metabolites, we
21 oorganisms (microbiota), particularly in the gut, and at least 20% of the small molecules in human bl
22 DNA in blood, lymph nodes (LN), spleen, and gut, and contained replication-competent and infectious
23 mation within diabetic islets, brain, liver, gut, and muscle; the role of inflammation in fibrosis an
26 h must integrate each component of the brain-gut axis and the influence of biological sex, early-life
27 ic targeting of the gut microbiota for brain-gut axis disorders, opening new avenues in the field of
28 tion of neurotoxicants that affect the brain-gut axis via the vagus nerve, and then travel to higher
30 mmunities, we observed widespread sharing of gut bacteria between predator-prey host-species pairs, i
32 (2017) report the identification of specific gut bacteria that protect from Salmonella infection by p
35 provide a proof of concept that introducing gut bacteria to a herbivore may provide a novel approach
37 intestinal permeability and translocation of gut bacteria trigger various polyaetiological diseases a
42 nstrate that host plants influence herbivore gut bacterial communities and consequently affect the he
45 Overall, our study suggests that increasing gut bacterial diversity and relative abundances of Fusob
48 of phylogenetically diverse, sequenced human gut bacterial strains introduced into adult gnotobiotic
50 a quantitative perspective of the early-life gut Bifidobacterium colonization and shows how factors s
51 tinal cell suspensions and ILC3s sorted from gut biopsy specimens of patients with IBD were also anal
52 otility, and metabolites that stimulate the "gut-brain axis" to alter neural circuits, autonomic func
54 and peripheral immune pathways in microbiota-gut-brain communication during health and neurological d
56 te directly to CDI-associated lesions of the gut, but other bacterial factors are needed for the bact
59 hether barrier deregulations, similar to the gut, characterize other vital organs in obese individual
62 ss-diverse microbiome and loss of protective gut commensal strains (of the family Lachnospiraceae) an
65 results on the potential involvement of bee gut communities in pathogen protection and nutritional f
70 lammation, which is believed to be driven by gut-derived inflammatory mediators carried via mesenteri
71 de-1 highlights the therapeutic potential of gut-derived signals acting via nonphysiologic mechanisms
72 However, it is still largely unknown how gut dysbiosis affects the onset and progression of CNS a
79 and how MFSD2A regulates lipid metabolism of gut endothelial cells to promote resolution of intestina
81 strategy of C. difficile in the challenging gut environment still remains incompletely understood.
86 strates that autocrine IL-6 signaling in the gut epithelium regulates crypt homeostasis through the P
89 protein adequacy as well as energy intakes, gut function, clinical outcomes, and how well nutritiona
90 7A/B, localizes to lysosome-like organelles (gut granules) in the intestine under copper overload con
93 the intestinal lamina propria contribute to gut homeostasis through the immunomodulatory interleukin
94 and autoantibody responses by increasing the gut-homing alpha4beta7 integrin expression on Tfh cells.
95 disruption of retinoid homeostasis affected gut-homing and differentiation of lymphocytes and displa
97 -dependently slow gastric emptying and alter gut hormone secretion compared with a control but have n
98 trasonography), and blood glucose and plasma gut-hormone concentrations [insulin, glucagon, ghrelin,
99 dministration of a long-acting analog of the gut-hormone glucagon-like peptide-1 highlights the thera
100 arnesoid X receptor and TGR5, the BA-induced gut hormones, fibroblast growth factor 19 and glucagon-l
103 y B cells due to their redistribution to the gut, increases of the activated B cells and circulating
104 w that CX3CR1-deficient mice fail to resolve gut inflammation despite high production of IL10 and hav
105 anisms by which Entamoeba histolytica drives gut inflammation is critical for the development of impr
107 Urinary fluorophore and sugar ratios reflect gut injury in an indomethacin dose dependent manner.
108 Hirschsprung disease, leading to absence of gut innervation and severe gastrointestinal symptoms.
109 There is increasing evidence that brain-gut interactions are altered during development of infla
112 ding pH-shift produced protein isolates from gutted kilka (Clupeonella cultriventris) and silver carp
114 collected and microbiota were analyzed using Gut Low-Density Array quantitative polymerase chain reac
118 nt of gut microbiota in lung diseases by the gut-lung axis has been widely observed, but the underlyi
119 DNA viral community from publicly available gut metagenome data sets from human populations with dif
126 es of 2 self-proteins and a related order of gut microbes may provide a link between mucosal and join
127 infections exert on populations of commensal gut microbes of veterinary species is a field of researc
129 Metabonomic studies implicated variations in gut microbial activities that mapped onto tacrine-induce
130 l stiffness and exerts a beneficial shift in gut microbial communities in a rat model that mimics hum
131 ducing dysbiosis and that the FODMAP-altered gut microbial community leads to intestinal pathology.
132 al roles in animal health, and shifts in the gut microbial community structure can have detrimental i
133 l sociality) are associated with patterns of gut microbial composition (diversity and similarity) bet
134 in strong responders, based on differential gut microbial composition (e.g., Lactobacillus, Bacteroi
137 Patients were characterized by a form of gut microbial dysbiosis that is more prominent than prev
139 163), soluble CD14 (sCD14), CRP, IL-6, and a gut microbial translocation marker (intestinal fatty aci
140 hanges in circulating metabolites, including gut microbial, tryptophan, plant component, and gamma-gl
141 annotation of a diversity of endogenous and gut microbially derived metabolites affected by both die
143 his article we review the current methods of gut microbiome analysis and the resulting data regarding
144 etween observed dramatic fluctuations in the gut microbiome and intensified medication due to a flare
145 gated the impact of diazinon exposure on the gut microbiome composition and its metabolic functions i
149 evaluate the effects of azithromycin on the gut microbiome diversity of children from an antibiotic-
151 ry analyses of neuroimaging data suggest the gut microbiome has minimal effects on regional brain vol
153 nt in order to determine if dysbiosis of the gut microbiome impacts honeybee health, and we performed
154 iet rich in fat and simple sugars alters the gut microbiome in a manner that contributes to host adip
155 our results highlight the importance of the gut microbiome in honeybee health, but they also provide
156 re we show that high salt intake affects the gut microbiome in mice, particularly by depleting Lactob
157 or further investigations on the role of the gut microbiome in promoting or preventing ACVD as well a
158 e composition and functional capacity of the gut microbiome in relation to cardiovascular diseases ha
159 ich integrates unique information about host-gut microbiome interactions, gastrointestinal functional
160 definitively decreases the diversity of the gut microbiome of children in an antibiotic-naive commun
165 with our intestinal counterpart, pushing the gut microbiome toward a dysbiotic layout, where microbio
169 ia effects on (a) circadian biology, (b) the gut microbiome, and (c) modifiable lifestyle behaviors,
171 ey metabolites and signaling molecules (e.g. gut microbiome-to-intestine-to-blood-to-liver-to-kidney-
178 e tests for RI associated with diet-specific gut microbiomes in D. melanogaster Despite observing rep
179 pite observing replicable differences in the gut microbiomes of flies maintained on different diets,
182 ve disease removed harmful bacteria from the gut microbiota and attenuated SLE-like disease in lupus-
184 s, as a critical factor that is regulated by gut microbiota and determines thrombus growth in Tlr2(-/
188 stablishing a strong association between the gut microbiota and obesity in humans, a causal relations
192 vealed that Clostridia added to mouse infant gut microbiota are sufficient to limit colonization of p
193 In conclusion, drug discovery targeting the gut microbiota as well as the characterization of microb
194 rmula with specific prebiotics modulated the gut microbiota closer to that of breast-fed infants.
195 role of fat content in the diet in altering gut microbiota community by shifting phylotype compositi
196 Thus, ultrafine particles ingestion alters gut microbiota composition, accompanied by increased ath
200 base supporting therapeutic targeting of the gut microbiota for brain-gut axis disorders, opening new
203 ability of prebiotics to specifically modify gut microbiota in children with overweight/obesity or re
209 siological activities, and the importance of gut microbiota in supplying micronutrients to animals.
214 g ACVD as well as other related diseases.The gut microbiota may play a role in cardiovascular disease
215 Further, some of the predicted pomegranate gut microbiota metabolites modulated (14)C-D-glucose and
220 ing immune system and the not-yet-stabilized gut microbiota of young children to facilitate its persi
225 Science, Wang et al. (2017) reveal that the gut microbiota regulates the expression of circadian-clo
226 in Ruminococcus and Dorea were identified as gut microbiota signatures of NAFL onset and NAFL-NASH pr
227 polysaccharides play extensive roles in host-gut microbiota symbiosis beyond dietary polysaccharide d
228 A diet high in fiber led to changes in the gut microbiota that played a protective role in the deve
229 g cells (pAPCs) recognize and respond to the gut microbiota through multiple pattern-recognition rece
230 ce elements such as copper and zinc, altered gut microbiota to more pathogenic bacteria, increased in
234 er-Bone Axis intriguingly implies the normal gut microbiota's osteoimmunomodulatory actions are partl
235 s bone mass, mechanisms governing the normal gut microbiota's osteoimmunomodulatory effects on skelet
238 ints to a strong association between sex and gut microbiota, bile acids (BAs), and gastrointestinal c
239 tibility, environmental factors, and altered gut microbiota, leading to dysregulated innate and adapt
240 iminution correlates with alterations in the gut microbiota, particularly enrichment of Propionibacte
241 tis model, we show that a constituent of the gut microbiota, segmented filamentous bacteria (SFB), di
242 bution of one of the main metabolites of the gut microbiota, the short-chain fatty acid acetate.
243 nate antimicrobial defenses and disrupts the gut microbiota, which leads to overgrowth of indigenous
245 ractions occurring between parasites and the gut microbiota, with a profound impact on both host immu
246 asma trimethylamine N-oxide (TMAO) levels, a gut microbiota-dependent metabolite associated with coro
247 cant interest in recent years has focused on gut microbiota-host interaction because accumulating evi
256 Diabetes has a significant impact on the gut microbiota; however, studies in the oral cavity have
257 ludes luminal content, senses changes in the gut microenvironment, and releases immune regulators tha
258 ppreciation for the contribution of resident gut microorganisms-the gut microbiota-to human health ha
262 ated surfaces of the body, in particular the gut mucosa, are the major sites where immune cells traff
265 sis), consistent with a single origin of the gut, nerve cells, and muscle cells in the stem lineage o
267 Inhibiting the activity of Pol III in the gut of adult worms or flies is sufficient to extend life
270 tem in maintaining immune homeostasis in the gut/pancreas and reveals a conversation between the nerv
272 associated with amelioration of age-related gut pathology and functional decline, dampened protein s
274 athetic-gut communication is associated with gut pathology, dysbiosis, and inflammation and plays a k
275 a hallmark of CD, and anti-TG2 IgA-producing gut PCs accumulate in patients upon gluten ingestion.
277 evidence to the EE hypothesis that increased gut permeability and inflammation adversely affects subs
278 vented chronic morphine induced increases in gut permeability, colonic mucosal destruction, and colon
281 ous mechanical and chemical stimuli in nerve-gut preparations in mouse, or following antagonism of Na
282 toxins bind sequentially to different larval gut proteins facilitating oligomerization, membrane inse
290 duced T-cell clonotypes from total blood and gut TCR repertoires in an unbiased manner using immunose
291 troduction of beta-cell autoantigens via the gut through Lactococcus lactis (L. lactis) has been demo
294 , as shown by the reductions of FITC-dextran gut translocation, serum interleukin-6 (IL-6) levels, ba
296 at investigating the biological role of the gut virome in human physiology, and the importance of ou
298 ogy of cancers in different locations of the gut, where colon cancer is primarily driven by inflammat
299 GF or HGF expanded into self-organizing mini-guts with similar levels of efficacy and contained all d
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