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1 e proteolytic signature were investigated in germ-free adult mice and in dams colonized with HC, pre-
2 n of the microbiota in antibiotic-treated or germ-free adult mice results in significant deficits in
4 s present even in sterile rat embryo islets, germ-free adult rat islets, and neogenic tubular complex
5 aised (CONV-R) counterparts, and mice reared germ free and then colonized with CONV-R gut microbiota
6 mmunity structure (P < .001), with humanized germ-free and antibiotic-treated groups overlapping in b
11 diated diversification operate comparably in germ-free and conventional mice, indicating these unique
15 onic tip and crypt epithelial fractions from germ-free and conventionally raised mice and from mice d
17 temic infection with Listeria monocytogenes, germ-free and oral-antibiotic-treated mice display incre
21 ective role was observed in conventional and germ-free animal facilities, indicating that it does not
24 ystem, with for example the observation that germ-free animals harbor a poorly developed intestinal i
29 mor formation in 3 mouse colon tumor models (germ-free ApcMinDelta850/+;Il10-/- or ApcMinDelta850/+ a
31 consortium (Oligo-MM(12)) does not eliminate germ-free-associated clonotypes, yet does induce a conco
32 s to asthma was most pronounced in colonized germ-free BALB/c mice (genetically predisposed to asthma
33 rmite), and human-derived bacteria colonized germ-free bystander mice before mouse-derived organisms.
34 iota or a mouse cecal microbiota, along with germ-free "bystanders," revealed the success of particul
35 performed studies with conventional C57/BL6, germ-free C57/BL6, Nestin-creER(T2):tdTomato, Nestin-GFP
40 n asthma-resistant outbred mice and requires germ-free conditions before colonization with microbiota
43 Ig infusion, and analysis of mice raised in germ-free conditions reveal a negative feedback mechanis
44 Re-derivation of HDAC3(DeltaIEC) mice into germ-free conditions revealed that dysregulated IEC gene
45 lopment of intestinal carcinomas, even under germ-free conditions, and therefore does not involve mic
56 e acidic region was significantly reduced in germ-free Drosophila, indicative of a role of the gut ba
59 Based on studies using rodents raised in a germ-free environment, the gut microbiota appears to inf
64 st variation in colonization when individual germ-free flies were fed their own natural commensals (i
66 free than in SPF mice, and winner B cells in germ-free germinal centres are enriched in 'public' clon
71 tributes to tumor distribution, we generated germ-free (GF) Apc(Min/+) and Apc(Min/+) ;Il10(-/-) mice
73 report that I/R-induced intestinal injury in germ-free (GF) C57BL/6 wild-type (WT) mice is worse than
74 h broad-spectrum antibiotics (Abx) or use of germ-free (GF) donors and recipients resulted in prolong
75 a depletion by wide-spectrum antibiotics and germ-free (GF) female mice, we showed that the microbiot
76 ntrast to specific pathogen-free (SPF) mice, germ-free (GF) mice are resistant to Concanavalin A (Con
79 host microbiota to microglia homeostasis, as germ-free (GF) mice displayed global defects in microgli
80 crobiota in specific pathogen-free (SPF) and germ-free (GF) mice given more than 40 unique diets; we
81 ensals are not required for T1D progression, germ-free (GF) mice had a very low degree of sialitis, w
82 ination with CT, both antibiotic-treated and germ-free (GF) mice had reduced amounts of antigen-speci
87 er maturation upon bacterial colonization of germ-free (GF) mice that have implications for studies o
88 report that colonization of sexually mature germ-free (GF) mice with conventional specific pathogen-
93 development of PLZF(+) innate lymphocytes in germ-free (GF) neonatal mice is restored by colonization
94 he intestinal microbiota using mice that are germ-free (GF) or humanized (ex-GF mice colonized with h
95 gene expression, we evaluated mice that were germ-free (GF) or humanized (HM; ex-GF colonized with hu
96 PH by partial portal vein ligation (PPVL) in germ-free (GF) or mice colonized with altered Schaedler'
98 ion from the disease: MyD88-negative mice in germ-free (GF), but not in specific pathogen-free condit
99 typically, and functionally compared between germ-free (GF), specific pathogen-free, and GF mice reco
100 owth promotion phenotype is transferrable to germ-free hosts by LDP-selected microbiota, showing that
101 on tissue sections from immunocompromised or germ-free hosts, chronically infected hosts where the ti
107 ree and specific pathogen-free Il10(-/-) and germ-free Il10(-/-);Rag2(-/-) mice were infected with C.
116 llus reuteri This species induced DP IELs in germ-free mice and conventionally-raised mice lacking th
118 diet, to induce cholestatic liver disease in germ-free mice and germ-free mice conventionalized with
119 tes that were significantly downregulated in germ-free mice and have been reported to be related to n
120 duced mechanical hyperalgesia was reduced in germ-free mice and in mice pretreated with antibiotics.
122 om human donors with ASD or TD controls into germ-free mice and reveal that colonization with ASD mic
125 Enteritidis in neonatal chicks, phenocopying germ-free mice associated with adult chicken microbiota.
126 ly, it is phenocopied by pre-colonization of germ-free mice before Listeria infection with Prevotella
127 versal-dependent and could be transferred to germ-free mice by fecal microbiota transplantation.
128 ansferred from villin-TLR4 mice to wild-type germ-free mice caused increased H(2)O(2) production and
131 notypes and serum antibodies were reduced in germ-free mice compared with conventionally raised mice.
132 lestatic liver disease in germ-free mice and germ-free mice conventionalized with the microbiome from
141 Despite persistence of light-dark signals, germ-free mice fed low or high-fat diets exhibit markedl
142 emale twin pairs discordant for obesity into germ-free mice fed low-fat mouse chow, as well as diets
143 ia with a probiotic E. coli isolate protects germ-free mice from pathogen colonization, but the prote
146 Microbial sequencing and reconstitution of germ-free mice have indicated both positive and negative
147 thy donors, transfer of IBD microbiotas into germ-free mice increased numbers of intestinal Th17 cell
148 in NKT- and in MAIT-deficient as well as in germ-free mice indicates that these cells recognize dive
149 Transplantation of the cold microbiota to germ-free mice is sufficient to increase insulin sensiti
152 ally contains hundreds of bacterial species, germ-free mice mono-associated with a single Bacteroides
156 tration of specific microbial metabolites to germ-free mice promotes neuroinflammation and motor symp
158 Transfer of Ahr(-/-) microbiota to wild-type germ-free mice recapitulated the increase Verrucomicrobi
160 ith a favorable gut microbiome as well as in germ-free mice receiving fecal transplants from respondi
162 f faeces from specific-pathogen-free mice to germ-free mice restored germ-dependent clonotypes, direc
163 er, in vivo administration of NOD1 ligand to germ-free mice restored the numbers of hematopoietic ste
164 microbiota transplants from MS patients into germ-free mice resulted in more severe symptoms of exper
165 s and human microbiome transplantations into germ-free mice revealed that the KD-associated gut micro
166 exposure to polymer-rich luminal fluid from germ-free mice strongly compressed the mucus hydrogel, w
167 ota, activated a DUOX2 response in recipient germ-free mice that corresponded to abnormal colonizatio
169 opulation in both specific pathogen-free and germ-free mice that has not been described previously.
170 mpared through competition experiments in ex-germ-free mice that were either treated with omeprazole,
171 or undernourished Malawian donors into young germ-free mice that were fed a Malawian diet revealed th
173 RNA sequencing of luminal microbiota from ex-germ-free mice to show that inflamed Il10(-/-) mice main
174 model of auxotrophic Salmonella infection in germ-free mice to show that live bacterial virulence fac
176 fy their levels in the caecum of control and germ-free mice using two independent mass spectrometry m
177 ther, comparing cutaneous gene expression in germ-free mice vs. conventionally raised mice suggests t
178 s or mice (IBD, metabolic syndrome, etc.) to germ-free mice was found to be sufficient to transfer so
180 stinal microbiota, which when transferred to germ-free mice was sufficient to induce exacerbated inte
182 ing gut microbial community structure, adult germ-free mice were colonized with a consortium of 15 se
183 and osteoclast and osteoblast biology, young germ-free mice were colonized with cultured bacterial st
187 explore this association, we colonized young germ-free mice with a consortium of bacterial strains cu
190 ids modulate intestinal health, we colonized germ-free mice with a sphingolipid-deficient Bacteroides
191 antibiotic-induced microbial depleted and in germ-free mice with and without fecal microbial transfer
192 anscription factor cFos, and colonization of germ-free mice with bacteria that produce short-chain fa
196 egulate food allergy in humans, we colonized germ-free mice with feces from healthy or cow's milk all
199 in a mammalian gut environment, we colonized germ-free mice with microbial communities from human, ze
202 ally, we demonstrate that supplementation of germ-free mice with short-chain fatty acids, major produ
204 hted by anatomical and functional changes in germ-free mice, affecting the gut epithelium, immune sys
205 l studies employing dietary choline or TMAO, germ-free mice, and microbial transplantation collective
206 ells derived from specific pathogen-free and germ-free mice, and stratify cells into phenotypic subpo
207 mma6(+) and Vgamma4(+) cells was reversed in germ-free mice, and their activation state was decreased
208 tary tryptophan restriction are abrogated in germ-free mice, but are independent of canonical host se
209 airment of antiviral immunity was evident in germ-free mice, but neutralization of Ym1, a chitinase-l
213 IgA responses can be recapitulated in young germ-free mice, colonized with faecal microbiota obtaine
214 EGFP, CCR2(-/-), CD11c-EYFP, CD11c-EYFP-DTR, germ-free mice, CX3CR1(gfp/gfp), CX3CR1(gpf/wt), and CX3
215 favorable effects of nitrate were absent in germ-free mice, demonstrating the central importance of
217 diabetic mice; when transferred to recipient germ-free mice, oral microbiota from IL-17-treated donor
218 ve effects were lost in both Ifnar1(-/-) and germ-free mice, revealing essential roles for type I int
220 sals, coupled with microbial colonization of germ-free mice, showed the microbial porA gene facilitat
221 hese mucosal responses were also observed in germ-free mice, showing that they are independent of the
222 nase inhibitor blunted lactate production in germ-free mice, suggesting that lactate was predominantl
223 al bacterial composition and, by transfer to germ-free mice, that the oral microbiota of diabetic mic
225 +) intraepithelial lymphocytes purified from germ-free mice, their conventionally raised (CONV-R) cou
227 ensal colonization in antibiotic-treated and germ-free mice, using cultured commensals from the Actin
229 n this issue of the JCI, Li et al. show that germ-free mice, when chemically castrated, do not lose b
230 CCR9+ memory T cell frequency decreased in germ-free mice, whereas antibiotic treatment increased t
231 ow longitudinally the urine metabolome of ex-germ-free mice, which are colonized with two bacterial s
233 D-associated microbiome was transmissible to germ-free mice, with the gut microbial community structu
268 ed in specific-pathogen-free conditions into germ-free Nlrp12-deficient mice showed that NLRP12 and t
271 m cancer patients who responded to ICIs into germ-free or antibiotic-treated mice ameliorated the ant
275 icient states as compared to control in both germ-free or E. coli gut microbiota states was used to q
278 cs to suppress their native microbiome, were germ free, or received humanization without pretreatment
280 gnificant decrease in serum triglycerides in germ-free rats fed a high sugar diet compared to convent
282 the microbiota from Card9(-/-) to wild-type, germ-free recipients increases their susceptibility to c
283 (+) nTh17 cells are present in the thymus of germ-free RORgammat-gfp and IL-6(-/-) RORGamma: t-gfp mi
284 flora by fecal material transplantation into germ-free SAMP and the presence of the gut microbiome in
287 o asthma), only partially evident in outbred germ-free Swiss Webster mice, and marginal in convention
288 nce an altered environment compared with the germ-free system that includes reduced pH, depletion of
289 iated germinal centres is markedly higher in germ-free than in SPF mice, and winner B cells in germ-f
290 oPP to Il10(-/-) mice before transition from germ-free to SPF conditions reduced their development of
291 regulation of DUOX2 in intestinal tissues of germ-free vs conventional mice, mice given antibiotics o
292 ntibiotic treatment or colonizing littermate germ-free wild-type and NLRP6-deficient hosts with faeca
293 cognition protein 1) could be transferred to germ-free wild-type mice by colonization of mothers and
297 ferences in the number of secretory cells in germ-free zebrafish and their conventional counterparts,
300 d-type, and interleukin (Il)10(-/-) mice and germ-free zebrafish embryos were colonized with specific