ライフサイエンスコーパス: germ-free

1 n the intestinal wall of all rats (including germ free).

2 ate-term fetal piglets or piglets maintained germ-free.

3 Here we demonstrate that germ-free adult pregnant mice inoculated with a gut micr

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 Depletion of intestinal Th17 cells in germ-free and antibiotic-treated mice ameliorated renal

7 In germ-free and antibiotic-treated mice, LRCs colonized in

8 mic, biochemical, and physiologic studies of germ-free and cocolonized Gpr41-/- and +/+ littermates d

9 diated diversification operate comparably in germ-free and conventional mice, indicating these unique

10 d attenuated responses to gluten compared to germ-free and conventional SPF mice.

11 of DCs were similar in mesenteric lymph from germ-free and conventionally housed mice.

12 onic tip and crypt epithelial fractions from germ-free and conventionally raised mice and from mice d

13 Oral tolerance was induced by DNFB gavage in germ-free and mice deficient in several TLRs.

14 temic infection with Listeria monocytogenes, germ-free and oral-antibiotic-treated mice display incre

15 induced inflammation in wild-type mice, and germ-free and Pseudomonas fluorescens-monoassociated int

16 ause wild-type (WT) colonic macrophages from germ-free and specific pathogen-free (SPF)-derived mice

17 Germ-free and specific pathogen-free Il10(-/-) and germ-

18 Conversely, colonic macrophages from germ-free and SPF-derived colitis-prone Il10(-/-) mice d

19 ith a complete gut microbiota or were reared germ-free and then cocolonized as young adults with two

20 ective role was observed in conventional and germ-free animal facilities, indicating that it does not

21 Germ-free animal models have demonstrated that commensal

22 We present viscosity measurements in germ-free animals (devoid of gut microbes), animals colo

23 mice with a normal microbiome compared with germ-free animals and antibiotic-treated mice.

24 cally, we show that gut dendritic cells from germ-free animals are reduced in the ability to stimulat

25 Germ-free animals are susceptible to atherosclerosis, su

26 Here, we show that germ-free animals are unable to eradicate Citrobacter ro

27 ystem, with for example the observation that germ-free animals harbor a poorly developed intestinal i

28 Remarkably, germ-free animals harboring SFBs alone developed EAE, sh

29 Comparison with germ-free animals reveals that the immunomodulatory acti

30 experimental models of these diseases and in germ-free animals that help us understand the mechanisms

31 Monocolonization of germ-free animals with B. fragilis increases the suppres

32 Germ-free animals, induced for EAE, produce lower levels

33 Using germ-free animals, Rawls et al. reveal that the gut of a

34 verlapping membership in individually housed germ-free animals.

35 er in conventionally reared mice compared to germ-free animals.

36 endent manner, as assessed by antibiotic and germ-free approaches.

37 ed with conventionally reared axin1 mutants, germ-free axin1 mutants exhibit decreased intestinal epi

38 B6 and TCR transgenic animals, as well as in germ-free B6 mice.

39 rmite), and human-derived bacteria colonized germ-free bystander mice before mouse-derived organisms.

40 iota or a mouse cecal microbiota, along with germ-free "bystanders," revealed the success of particul

41 We therefore infected germ-free C57BL/6 mice aged 7-14 months with a BI/NAP1 s

42 We conclude that aged, germ-free C57BL/6 mice are susceptible to fulminant CDI

43 We colonized germ-free C57BL/6 mice with bacteria isolated from the s

44 Germ-free C57BL/6J-Rag(1tm1Mom) (Rag1(-/-)) mice were co

45 Germ-free Cd1d-/- mice exhibited a defect in Paneth cell

46 intestinal microbiota by oral antibiotics or germ-free condition can prevent arthritis in mice.

47 with methods for raising these animals under germ-free conditions can be used to monitor microbial mo

48 Mice maintained under germ-free conditions develop significantly attenuated EA

49 ensal bacteria, because mice re-derived into germ-free conditions expressed significantly less Nod2 i

50 Further, mice raised in germ-free conditions had hematopoietic abnormalities sim

51 Re-derivation of pIgR(-/-) mice in germ-free conditions or treatment with the anti-inflamma

52 Ig infusion, and analysis of mice raised in germ-free conditions reveal a negative feedback mechanis

53 Re-derivation of HDAC3(DeltaIEC) mice into germ-free conditions revealed that dysregulated IEC gene

54 bserved that under specific pathogen-free or germ-free conditions, intragastric administration of Pse

55 We find that, when maintained under germ-free conditions, mice do not display an age-related

56 Germ-free conditions, probiotics and antibiotics are eac

57 pithelial cells are significantly altered by germ-free conditions.

58 , and in wild-type mice that were kept under germ-free conditions.

59 icrobial flora and were not detectable under germ-free conditions.

60 pe were unchanged in dtp larvae reared under germ-free conditions.

61 ibiotic treatment and entirely averted under germ-free conditions.

62 Germ-free (control) or conventionally derived Il10(-/-)

63 ata with those from other symbioses, such as germ-free/conventionalized mice and zebrafish, revealed

64 e acidic region was significantly reduced in germ-free Drosophila, indicative of a role of the gut ba

65 r PI3K p110delta, wild-type mice raised in a germ-free environment markedly up-regulated colonic PI3K

66 Experiments in a germ-free environment showed that the late larval phenot

67 Based on studies using rodents raised in a germ-free environment, the gut microbiota appears to inf

68 sed when spin homozygotes are derived into a germ-free environment.

69 ated with certain antibiotics or raised in a germ-free environment.

70 l enterocolitis does not occur in a sterile (germ-free) environment and is prevented and treated by b

71 e flies were colonized while others remained germ-free even at extremely high bacterial doses.

72 Here, by employing a germ-free experimental system, we demonstrate the abilit

73 st variation in colonization when individual germ-free flies were fed their own natural commensals (i

74 Growth on germ-free food reduced AMP gene expression and rescued s

75 tion on neuroinflammation in cirrhosis using germ-free (GF) and conventional mice.

76 Recent comparisons of germ-free (GF) and normal specific-pathogen-free (SPF) m

77 In this article, we show that germ-free (GF) and Toll-like receptor-2 (Tlr2)-deficient

78 , in contrast to mice with a gut microbiota, germ-free (GF) animals are protected against the obesity

79 We observed that germ-free (GF) animals show delayed clearance of an apat

80 tributes to tumor distribution, we generated germ-free (GF) Apc(Min/+) and Apc(Min/+) ;Il10(-/-) mice

81 vestigate liver fibrosis in conventional and germ-free (GF) C57BL/6 mice.

82 report that I/R-induced intestinal injury in germ-free (GF) C57BL/6 wild-type (WT) mice is worse than

83 re housed in specific pathogen-free (SPF) or germ-free (GF) conditions and weaned onto diabetes-promo

84 ly attenuated in the K/BxN mouse model under germ-free (GF) conditions, accompanied by reductions in

85 h broad-spectrum antibiotics (Abx) or use of germ-free (GF) donors and recipients resulted in prolong

86 Germ-free (GF) mice and mice who had received a gut micr

87 the microbiota in colon tumor development in germ-free (GF) mice are limited.

88 ntrast to specific pathogen-free (SPF) mice, germ-free (GF) mice are resistant to Concanavalin A (Con

89 Germ-free (GF) mice display a significantly different in

90 Here, we report that germ-free (GF) mice display altered daily oscillation of

91 host microbiota to microglia homeostasis, as germ-free (GF) mice displayed global defects in microgli

92 crobiota in specific pathogen-free (SPF) and germ-free (GF) mice given more than 40 unique diets; we

93 ensals are not required for T1D progression, germ-free (GF) mice had a very low degree of sialitis, w

94 ination with CT, both antibiotic-treated and germ-free (GF) mice had reduced amounts of antigen-speci

95 Germ-free (GF) mice have reduced stool output.

96 Germ-free (GF) mice lost the gender bias (female-to-male

97 Transfer of OP but not OR microbiota to germ-free (GF) mice replicated the characteristics of th

98 Comparisons of conventionally raised and germ-free (GF) mice revealed a similar degree of allergi

99 er maturation upon bacterial colonization of germ-free (GF) mice that have implications for studies o

100 report that colonization of sexually mature germ-free (GF) mice with conventional specific pathogen-

101 We colonized germ-free (GF) mice with mouse microbiota (MMb) or human

102 In this study, we demonstrate that in germ-free (GF) mice, ablation of the otherwise fully fun

103 tiation factor 88-deficient (MyD88(-/-)) and germ-free (GF) mice, but not IL-1R(-/-) mice, exhibit im

104 Here, we show that in germ-free (GF) mice, invariant natural killer T (iNKT) c

105 In germ-free (GF) mice, sex steroid deficiency failed to in

106 We tested the hypothesis that germ-free (GF) mutltidrug resistance 2 knockout (mdr2(-/

107 he intestinal microbiota using mice that are germ-free (GF) or humanized (ex-GF mice colonized with h

108 gene expression, we evaluated mice that were germ-free (GF) or humanized (HM; ex-GF colonized with hu

109 PH by partial portal vein ligation (PPVL) in germ-free (GF) or mice colonized with altered Schaedler'

110 ue repair of excisional skin wounds by using germ-free (GF) Swiss mice.

111 ng zebrafish and relative ease of generating germ-free (GF) zebrafish make it an attractive model org

112 Germ-free (GF), antibiotic-treated (AVMN), and conventio

113 ion from the disease: MyD88-negative mice in germ-free (GF), but not in specific pathogen-free condit

114 typically, and functionally compared between germ-free (GF), specific pathogen-free, and GF mice reco

115 rences are not evident when germ-free WT and germ-free Gpr41 knockout animals are compared.

116 owth promotion phenotype is transferrable to germ-free hosts by LDP-selected microbiota, showing that

117 on tissue sections from immunocompromised or germ-free hosts, chronically infected hosts where the ti

118 rred under specific pathogen-free as well as germ-free housing conditions.

119 Moreover, feeding bacteria to germ-free hybrids reinstates lethality and recapitulates

120 microbiota did not induce HO-1 in colons of germ-free Il10(-/-) mice.

121 ree and specific pathogen-free Il10(-/-) and germ-free Il10(-/-);Rag2(-/-) mice were infected with C.

122 Using germ-free Il10(-/-);Rag2(-/-) mice, we observed that inn

123 In addition, germ-free intestines fail to take up protein macromolecu

124 stages of development or mono-association of germ-free larvae with individual constituents of the mic

125 Germ-free male and female Swiss-Webster mice that were 3

126 on BabA expression as shown by infection of germ free mice.

127 onfers in vivo resistance upon transfer into germ free mice.

128 n, steatosis, and hyperglycemia to wild type germ free mice.

129 We used germ-free mice (GF) to assess visceral sensitivity, spin

130 Restoring the microbiota of germ-free mice abrogated this protection.

131 TFH development is deficient in germ-free mice and can be restored by feeding TLR2 agoni

132 llus reuteri This species induced DP IELs in germ-free mice and conventionally-raised mice lacking th

133 Use of germ-free mice and faecal transplants indicated that suc

134 duced mechanical hyperalgesia was reduced in germ-free mice and in mice pretreated with antibiotics.

135 rance induced by DNFB gavage was impaired in germ-free mice and TLR4-deficient mice.

136 Germ-free mice are protected from CCM formation, and a s

137 versal-dependent and could be transferred to germ-free mice by fecal microbiota transplantation.

138 otic-treated mice, and antibiotic therapy of germ-free mice caused no additional abnormalities.

139 obiota from TLR5-deficient mice to wild-type germ-free mice conferred many features of metabolic synd

140 Studies using germ-free mice confirmed a critical role for dietary cho

141 Germ-free mice developed increased intraepithelial lymph

142 Tumors in antibiotic-treated or germ-free mice did not respond to CTLA blockade.

143 al microbiota, as antibiotic-treated mice or germ-free mice did not transmit infectious virus to thei

144 We reveal that germ-free mice display reduced proportions and different

145 ed in interleukin (IL)-10(-/-) and wild-type germ-free mice during transition to a conventional micro

146 Additionally, germ-free mice exhibit diminished retention of O2-sensit

147 Germ-free mice failed to induce IL-36gamma in response t

148 Cohoused and germ-free mice fed feces from REG3A-TG mice and given DS

149 Despite persistence of light-dark signals, germ-free mice fed low or high-fat diets exhibit markedl

150 emale twin pairs discordant for obesity into germ-free mice fed low-fat mouse chow, as well as diets

151 Germ-free mice fed selenium diets modified their selenop

152 iNKT cells isolated from germ-free mice had a less mature phenotype and were hypo

153 Germ-free mice had endogenous RvD1 and PD1 levels higher

154 Similar to meprin beta-deficient mice, germ-free mice have attached mucus as they did not shed

155 This study demonstrated that EHEC colonizes germ-free mice in large numbers, adheres to the intestin

156 d complementation of commensal bacteria into germ-free mice induced Nod2 expression.

157 Transplantation of the cold microbiota to germ-free mice is sufficient to increase insulin sensiti

158 d restored the reduced transport observed in germ-free mice known to have a marked reduction in intes

159 Moreover, colonization of germ-free mice leads to an increased ratio of Iglambda-e

160 A higher proportion of germ-free mice live to 600 days than their conventional

161 nterparts, and macrophages derived from aged germ-free mice maintain anti-microbial activity.

162 ally contains hundreds of bacterial species, germ-free mice mono-associated with a single Bacteroides

163 Upon monocolonization of germ-free mice or rats with SFB indigenous to mice (M-SF

164 R4(-/-)) or Myd88 (Myd88(-/-)), in wild-type germ-free mice or wild-type mice depleted of the microbi

165 ation by using antimicrobials or gnotobiotic germ-free mice overrides these protective benefits.

166 tration of specific microbial metabolites to germ-free mice promotes neuroinflammation and motor symp

167 By using germ-free mice raised and bred on an elemental diet devo

168 Transfer of Ahr(-/-) microbiota to wild-type germ-free mice recapitulated the increase Verrucomicrobi

169 ith a favorable gut microbiome as well as in germ-free mice receiving fecal transplants from respondi

170 d functions of iNKT cells in germ-free mice, germ-free mice reconstituted with specified bacteria, an

171 TLR4 inhibition confers resistance, whereas germ-free mice remain sensitive.

172 er, in vivo administration of NOD1 ligand to germ-free mice restored the numbers of hematopoietic ste

173 microbiota transplants from MS patients into germ-free mice resulted in more severe symptoms of exper

174 exposure to polymer-rich luminal fluid from germ-free mice strongly compressed the mucus hydrogel, w

175 Conventionalized germ-free mice subjected to selenium diets gave similar

176 ota, activated a DUOX2 response in recipient germ-free mice that corresponded to abnormal colonizatio

177 opulation in both specific pathogen-free and germ-free mice that has not been described previously.

178 mpared through competition experiments in ex-germ-free mice that were either treated with omeprazole,

179 or undernourished Malawian donors into young germ-free mice that were fed a Malawian diet revealed th

180 RNA sequencing of luminal microbiota from ex-germ-free mice to show that inflamed Il10(-/-) mice main

181 Intragastric exposure of germ-free mice to Sphingomonas bacteria, which carry iNK

182 Microbial colonization of germ-free mice triggers epithelial expression of RegIIIg

183 fy their levels in the caecum of control and germ-free mice using two independent mass spectrometry m

184 ther, comparing cutaneous gene expression in germ-free mice vs. conventionally raised mice suggests t

185 s or mice (IBD, metabolic syndrome, etc.) to germ-free mice was found to be sufficient to transfer so

186 ing gut microbial community structure, adult germ-free mice were colonized with a consortium of 15 se

187 Plasma extracts from germ-free mice were compared with samples from conventio

188 Germ-free mice were then colonized with E. rectale and/o

189 Young adult specific-pathogen-free and germ-free mice were used to delineate the commensal micr

190 Recolonization of germ-free mice with a complex microbiota restores defect

191 explore this association, we colonized young germ-free mice with a consortium of bacterial strains cu

192 this trait is transmissible: colonization of germ-free mice with an 'obese microbiota' results in a s

193 of Archaea to digestive health, we colonized germ-free mice with Bacteroides thetaiotaomicron, an ada

194 Recolonizing germ-free mice with dysbiotic poststroke microbiota exac

195 recolonization of the antibiotic-treated or germ-free mice with microbes.

196 in a mammalian gut environment, we colonized germ-free mice with microbial communities from human, ze

197 Co-housing germ-free mice with old, but not young, conventionally r

198 Conventionalization of germ-free mice with SF-derived microbiota confirmed thes

199 ally, we demonstrate that supplementation of germ-free mice with short-chain fatty acids, major produ

200 By colonizing adult germ-free mice with the cecal contents of neonatal and a

201 hted by anatomical and functional changes in germ-free mice, affecting the gut epithelium, immune sys

202 btained through the use of gene-deficient or germ-free mice, and discuss new potential therapeutic ap

203 l studies employing dietary choline or TMAO, germ-free mice, and microbial transplantation collective

204 ells derived from specific pathogen-free and germ-free mice, and stratify cells into phenotypic subpo

205 airment of antiviral immunity was evident in germ-free mice, but neutralization of Ym1, a chitinase-l

206 e epithelium of TLR4 knockout (KO), 5KO, and germ-free mice, but not in TLR2KO mice.

207 DR was localized to the surface epithelia of germ-free mice, but to crypt epithelial cells in convent

208 Germ-free mice, clean specific-pathogen-free (SPF) mice

209 IgA responses can be recapitulated in young germ-free mice, colonized with faecal microbiota obtaine

210 EGFP, CCR2(-/-), CD11c-EYFP, CD11c-EYFP-DTR, germ-free mice, CX3CR1(gfp/gfp), CX3CR1(gpf/wt), and CX3

211 Germ-free mice, fed a (15)N-labeled diet for two generat

212 , phenotypes, and functions of iNKT cells in germ-free mice, germ-free mice reconstituted with specif

213 A similar phenotype was observed in germ-free mice, mice depleted of intestinal microbiota,

214 diabetic mice; when transferred to recipient germ-free mice, oral microbiota from IL-17-treated donor

215 ve effects were lost in both Ifnar1(-/-) and germ-free mice, revealing essential roles for type I int

216 hese mucosal responses were also observed in germ-free mice, showing that they are independent of the

217 nase inhibitor blunted lactate production in germ-free mice, suggesting that lactate was predominantl

218 When transferred to germ-free mice, T3 microbiota induced greater adiposity

219 al bacterial composition and, by transfer to germ-free mice, that the oral microbiota of diabetic mic

220 However, in germ-free mice, the levels of LDC-induced, CT-specific I

221 +) intraepithelial lymphocytes purified from germ-free mice, their conventionally raised (CONV-R) cou

222 phenotypic markers and by their presence in germ-free mice, these preexisting memory-like CD44(hi) C

223 In antibiotics-treated or germ-free mice, tumor-infiltrating myeloid-derived cells

224 ensal colonization in antibiotic-treated and germ-free mice, using cultured commensals from the Actin

225 Using germ-free mice, we show that the frequency of Th17 cells

226 n this issue of the JCI, Li et al. show that germ-free mice, when chemically castrated, do not lose b

227 ow longitudinally the urine metabolome of ex-germ-free mice, which are colonized with two bacterial s

228 DP IELs are absent in germ-free mice, which suggests that their differentiatio

229 ntionalization experiments were performed in germ-free mice.

230 ither by means of antibiotic treatment or in germ-free mice.

231 abolites increases colonic and blood 5-HT in germ-free mice.

232 demonstrated by microbiota reconstitution of germ-free mice.

233 a samples that transmit immune phenotypes to germ-free mice.

234 that was reversed by conventionalization of germ-free mice.

235 the Christensenellaceae, and transplanted to germ-free mice.

236 ferred dramatic susceptibility to colitis in germ-free mice.

237 as absent in Rag1(-/-), IL-7Ralpha(-/-), and germ-free mice.

238 ses and anaphylaxis when reconstituted in WT germ-free mice.

239 growth in conventionally raised mice but not germ-free mice.

240 wer levels of miR-10a compared with those in germ-free mice.

241 Th1 response correcting the Th2 cell skew of germ-free mice.

242 ventionally reared mice (P<0.01) compared to germ-free mice.

243 sed mice, but provide no growth advantage in germ-free mice.

244 bial origin since no formate was detected in germ-free mice.

245 on a regular diet (MRD) and transferable to germ-free mice.

246 ed, while Sirt1 is upregulated, in aortas of germ-free mice.

247 Using a germ-free model, we show that colonization by commensals

248 or after the introduction of microbiota into germ-free models.

249 We used a germ-free mouse model to investigate the role of host fa

250 Using a germ-free mouse model, we found that faecal/gut microbio

251 t is dependent on commensal microbes because germ-free MyD88-negative NOD mice develop robust diabete

252 bust diabetes, whereas colonization of these germ-free MyD88-negative NOD mice with a defined microbi

253 Further, germ-free neonates had reduced skin Tregs indicating tha

254 in the bone marrow of antibiotic-treated and germ-free neonates.

255 Finally, germ-free Nfil3(-/-) mice do not develop colonic inflamm

256 ed in specific-pathogen-free conditions into germ-free Nlrp12-deficient mice showed that NLRP12 and t

257 Germ-free NMRI mice were colonized at birth from their g

258 MyD88-negative NOD donors attenuates T1D in germ-free NOD recipients.

259 Finally, germ-free NOD.aire(-/-) mice exhibited autoimmunity in a

260 The microbiota was ablated via germ-free or antibiotic approaches.

261 We examined studies with germ-free or antibiotic-treated laboratory animals, and

262 m cancer patients who responded to ICIs into germ-free or antibiotic-treated mice ameliorated the ant

263 Murine norovirus (MNV) infection of germ-free or antibiotic-treated mice restored intestinal

264 Thus, antibody responses in germ-free or antibiotic-treated mice were impaired, but

265 microbiota from antibiotic-treated donors to germ-free or germ-depleted mice.

266 d most investigations have been performed in germ-free or microbiome-depleted animals.

267 Germ-free or SPF-raised wild-type and Il10(-/-) mice wer

268 ing (beta7 integrin-/-), enteric microbiota (germ-free), or active for immune colitis (G alpha i2-/-

269 ents of the microbiota reverses all of these germ-free phenotypes.

270 ion was very low in fetal IPP and the IPP of germ-free piglets but increased 3- to 5-fold after colon

271 Germ-free piglets were consistently and extensively colo

272 lls from the bone marrow of 4- to 5-week old germ-free pigs.

273 Unlike wild-type controls, germ-free Rab11a-deficient mouse intestines failed to to

274 gnificant decrease in serum triglycerides in germ-free rats fed a high sugar diet compared to convent

275 59: Dietary Carbohydrate and Blood Lipids in Germ-Free Rats," led by Dr.

276 the microbiota from Card9(-/-) to wild-type, germ-free recipients increases their susceptibility to c

277 cecal transplantation conferred leanness to germ-free recipients.

278 to promote adiposity when transplanted into germ-free recipients.

279 (+) nTh17 cells are present in the thymus of germ-free RORgammat-gfp and IL-6(-/-) RORGamma: t-gfp mi

280 flora by fecal material transplantation into germ-free SAMP and the presence of the gut microbiome in

281 ignificantly increased in the ilea of 80% of germ-free SAMP1/Fc mice examined compared with specific

282 Conventionally reared and germ-free SCID C.B17 mice revealed a similar pattern in

283 that critically ill humans never exist in a germ-free state.

284 Investigations included an intestinal germ-free study and a C15:0/C17:0 diet dose response stu

285 nce an altered environment compared with the germ-free system that includes reduced pH, depletion of

286 litis-prone Il10(-/-) mice transitioned from germ-free to a conventional microbiota.

287 oPP to Il10(-/-) mice before transition from germ-free to SPF conditions reduced their development of

288 slocation via these two routes, we colonized germ-free transgenic mice expressing the human enterocyt

289 Colonization of germ-free transgenic zebrafish with a commensal microbio

290 regulation of DUOX2 in intestinal tissues of germ-free vs conventional mice, mice given antibiotics o

291 In germ-free wild-type mice colonized with enteric microbio

292 In colons of germ-free, wild-type mice, SPF microbiota induced produc

293 Germ-free, wild-type, and interleukin (Il)10(-/-) mice a

294 These differences are not evident when germ-free WT and germ-free Gpr41 knockout animals are co

295 l transplantations of these microbiotas into germ-free zebrafish and mouse recipients.

296 ferences in the number of secretory cells in germ-free zebrafish and their conventional counterparts,

297 Germ-free zebrafish colonized with isogenic P. aeruginos

298 In this study, we used a germ-free zebrafish embryo model to show that osmotic st

299 d-type, and interleukin (Il)10(-/-) mice and germ-free zebrafish embryos were colonized with specific

300 Exposure of germ-free zebrafish to heat-killed preparations of the m