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1 iotics and alterations in fecal microbiota ("microflora").
2 make up the microbiota (previously known as microflora).
3 se to gain a metabolic advantage over intact microflora.
4 , appears to reflect microaspiration of oral microflora.
5 etween the immune system of the host and gut microflora.
6 ese factors may include subsets of commensal microflora.
7 h might impact the intestinal homeostasis of microflora.
8 ted by an immune response to bacteria in the microflora.
9 infections that do not belong to the vaginal microflora.
10 in the mutant mice required the presence of microflora.
11 broad spectrum of antibiotics to reduce gut microflora.
12 btained from volunteers with healthy vaginal microflora.
13 ct is in intimate contact with the commensal microflora.
14 ignal transducer for TLRs in response to the microflora.
15 s and inflammation triggered by the resident microflora.
16 n part by an aberrant response to intestinal microflora.
17 s evolved in the presence of diverse enteric microflora.
18 to excessive immunologic responses to normal microflora.
19 ate immune responses of the colon to enteric microflora.
20 een the host immune system and its commensal microflora.
21 growth of selected members of the intestinal microflora.
22 vitamins that are synthesized by the normal microflora.
23 ffering microbiologic effects on the vaginal microflora.
24 esponsive to food antigens and the commensal microflora.
25 s evolved in the presence of diverse enteric microflora.
26 may contribute to the maintenance of vaginal microflora.
27 the appendix to sequester it from intestinal microflora.
28 rom interactions between GALT and intestinal microflora.
29 t is commonly found as a member of the human microflora.
30 ated and perpetuated by the intestinal tract microflora.
31 nic inflammation in response to inflammatory microflora.
32 rmal role as a benign inhabitant of the oral microflora.
33 g upon probing, and reducing the subgingival microflora.
34 n human colon xenografts that lack a luminal microflora.
35 phabeta TCR(+) IELs even in the absence of a microflora.
36 ditis, despite being part of the normal oral microflora.
37 f periodontal disease and to the periodontal microflora.
38 in the establishment and ecology of the oral microflora.
39 sence of CpsB cross-reactive antigens in the microflora.
40 ent of the normal mouse and human intestinal microflora.
41 labeled cells of strain 299R from other leaf microflora.
42 athogenic bacteria without disturbing normal microflora.
43 rabbits and thereby acquired a different gut microflora.
44 ges in antibiotic susceptibility of the host microflora.
45 esponsiveness toward the lumenal prokaryotic microflora.
46 ased production of ethanol by the intestinal microflora.
47 produced by the epithelium or H2S-generating microflora.
48 al, a function dependent on licensing by gut microflora.
49 d by higher eukaryotes from the diet and gut microflora.
50 ions of bacterial RNA derived from symbiotic microflora.
51 isease in individuals with a compromised gut microflora.
52 cleanliness of the mouse colony and the gut microflora.
53 , ion concentrations, nutrient quantity, and microflora.
54 gy and mortality compared to mice deplete of microflora.
55 to environmental microbes and the commensal microflora.
56 with non-pathogenic members of the commensal microflora.
57 elieved to be under the influence of the gut microflora.
58 iols by beta-lyases that originate from oral microflora.
59 ic acids) were biodegraded by the endogenous microflora.
60 considered factors that maintain the normal microflora.
61 osedly induced by beta -lyases from the oral microflora.
62 each trial were fermented only by indigenous microflora.
64 s demonstrate a transition in the intestinal microflora accompanied by a dynamic change of its abilit
65 a isoflavone concentrations and modified gut microflora activities [beta-glucoside hydrolysis and equ
67 Here we report that the intestinal bacterial microflora and a functional Toll-like receptor 4 (TLR4),
68 s pathway involves synergy between commensal microflora and a sex-dependent liver enzyme, flavin-cont
69 new evidence for a possible role of altered microflora and altered host microbial interactions may p
70 the large intestine of mice is dependent on microflora and coincident with modulation of the host im
71 m affects both composition of the intestinal microflora and colonization of the gastrointestinal trac
72 S. aureus is a common inhabitant of the skin microflora and colonizes the nares and other human mucos
73 sential for the maintenance of the commensal microflora and combating invasive bacterial infection.
74 completely dependent on the presence of gut microflora and could be established by colonization with
76 ice showed no significant decline in the gut microflora and developed EAE similar to untreated mice,
77 stinal mucosa is exposed to a diverse normal microflora and dietary Ags and is a common site of entry
80 we characterized the Drosophila melanogaster microflora and examined the occurrence of enterococci in
83 for eukaryotes in the maintenance of normal microflora and in protection from pathogenic bacteria.
84 contributed colitis-predisposing intestinal microflora and increased intestinal ATP, whereas Nod2 de
85 the upper respiratory tract, where resident microflora and inhaled environmental microbes may contin
87 lex and dynamic interaction between the oral microflora and its host, which may lead, ultimately, to
89 species are normal members of the human gut microflora and most are regarded as safe when administer
90 the host genetic susceptibility, intestinal microflora and mucosal immune responses through the patt
91 alter the interaction of the host with both microflora and pathogens, promoting prolonged production
93 so harboring the highest burden of commensal microflora and representing a major portal of pathogen e
94 ompetence in endogenous populations of human microflora and temper gut disorders provoked by bacteria
95 ates the composition of intestinal commensal microflora and that it suppresses bacterial infection an
97 ve dialogue between members of the commensal microflora and the host mucosal immune system is rapidly
99 inter-kingdom signaling between the enteric microflora and the immune system to promote commensalism
101 teractions between components of the mucosal microflora and the mucosal immune system can involve eit
102 composition and diversity of the subgingival microflora and their oligotypes in health and levels of
103 distinctive in their selective effect on the microflora and their propensity to produce flatulence.
104 to normally harmless antigens in the mucosal microflora and therefore responses to antigens that by t
105 gests that changes in the composition of gut microflora and/or deranged epithelial barrier function e
107 elates with alterations in fecal microbiota (microflora) and widespread use of antibiotics (the "hygi
109 s form associations with neighboring plants, microflora, and microfauna, while humans maintain symbio
110 te the relationship between GALT, intestinal microflora, and modulation of the antibody repertoire.
111 y considered a benign inhabitant of the oral microflora, and yet it is a primary etiological agent in
113 bacteria normally present in the intestinal microflora are able to trigger redistribution of the cys
116 specific, currently unidentified intestinal microflora are required for Ab repertoire diversificatio
117 re undiversified, indicating that intestinal microflora are required for somatically diversifying the
118 rrant immune response and changes in the gut microflora are the main causes of inflammatory bowel dis
119 a daidzein metabolite produced by intestinal microflora) are antioxidants in vitro; equol is a partic
121 ent on both IFN-gamma and a normal commensal microflora, as indicated by experiments in IFN-gamma-kno
123 lecular analysis has revealed a more diverse microflora associated with endodontic infections than th
124 we have characterized GPX-DKO mice that have microflora-associated intestinal cancers, which are corr
126 d components and drugs, binding of commensal microflora, attachment and initiation of defense mechani
127 or was strongly limited by the environmental microflora because of the lack of oxygen, limiting the u
128 e relationship between humans and their oral microflora begins shortly after birth and lasts a lifeti
130 e performed comparing differences in vaginal microflora between the two treatment arms and between vi
131 Because of the complexity of the host and microflora biology and the associated chemistry, it is d
132 kely due to effects mediated through the gut microflora, bowel transit, and enhancement of gastrointe
134 ndida albicans is a normal part of the human microflora, but it is also an opportunistic fungal patho
135 OD2 regulates innate responses to intestinal microflora by downregulating multiple TLR responses and
136 resolving CDI symptoms, preservation of the microflora by fidaxomicin is associated with a lower lik
138 ecently described that alteration of the gut microflora can affect a population of Foxp3(+)T(reg) cel
139 mal inflammation after wounding and that the microflora can modulate specific cutaneous inflammatory
142 IC = 19/38 muM), selectivity over normal gut microflora, CC(50)s > 606 muM against mammalian cell lin
143 ded to determine if acid suppression-related microflora changes predict clinical infection risk; thes
144 environmental samples such as the human gut microflora, combined with the sustained exponential grow
145 ent and with the presence of a different gut microflora compared to mice maintained in SPF facilities
147 mixture (B-GOS) on immune function and fecal microflora composition in healthy elderly subjects.
150 ion feedbacks involving landscapes and their microflora could contribute to appraising the impact tha
153 As this low level of epsps in the intestinal microflora did not increase after consumption of the mea
154 The current evidence suggests that the oral microflora differs between individuals who are fully ede
155 ts; vaginal abrasions and effects on vaginal microflora; effects on the reproductive, digestive, or u
157 riasis, and rosacea with an imbalance of the microflora even in the absence of classical infection.
158 onauts, increase microbial proliferation and microflora exchange, alter virulence and decrease antibi
161 rum antibiotics-as well as transplanting gut microflora from a protective environment-attenuated infl
162 tatins, thus, leading to a shift of the oral microflora from dysbiotic to a more homeostatic one.
164 obiome was observed, suggesting that the gut microflora has a direct impact on the drug metabolism ca
167 various anti-gingivitis treatments on plaque microflora, here a double blinded, randomized controlled
168 FMT is able to restore the wide diversity of microflora, improve C. difficile-related symptoms and pr
171 and molecular analyses were performed on the microflora in aspirate samples collected from 5 infected
173 d an unbiased metagenomic approach to survey microflora in CCD hives, normal hives, and imported roya
175 sue, as well as bacteria growing among mixed microflora in enrichment cultures and in pure culture on
179 e composition of the submucosal peri-implant microflora in healthy and peri-implant mucositis conditi
181 ignificantly affect the growth of select gut microflora in humans, which suggests the potential prebi
182 ppreciation of the importance of the enteric microflora in IBD has led to a considerable interest in
184 s currently available on the role of the gut microflora in modulating isoflavone bioavailability or o
186 ctive in reducing the subgingival cultivable microflora in shallow periodontal pockets compared to cu
189 itional investigation revealed commensal gut microflora in the mesenteric lymph nodes and elevated LP
190 suggesting that AI-2 produced by indigenous microflora in the murine oral cavity may complement the
191 tem and its interactions with the intestinal microflora in the pathogenesis of inflammatory bowel dis
194 for interactions between GALT and intestinal microflora in the selective expansion of V(H)a B cells.
195 valuating critical components of the vaginal microflora in women with signs and symptoms of vaginitis
196 trobenzene sulfonic acid, colitis induced by microflora (in gnotobiotic interleukin-10(-/-)), and col
198 ses to distinct components of the intestinal microflora induce intestinal inflammation, we characteri
199 f oncogene-environment interaction, in which microflora-induced TLR activation regulates oncogene exp
200 the intention of identifying how the mucosal microflora influences specific functions of the mucosal
201 nfluence of the rich source of nutrients and microflora introduced with organic compost amendments.
204 However, the contribution of the intestinal microflora is beyond simple microbial translocation as a
206 we find that activation of TLRs by commensal microflora is critical for the protection against gut in
212 T) in which a healthy Lactobacillus-dominant microflora is replaced by BV-associated bacteria (BVAB),
213 ies have indicated that a subset of the oral microflora is responsible for endodontic infections.
214 bolic cluster present in the normal, colonic microflora is responsible for preventing C. difficile in
215 nctive taxa-a century later, the Torridonian microflora is still being characterized as primarily non
216 sponsiveness' towards the resident commensal microflora is thought to permit their successful colonis
217 I) was 0.83 (CI, 0.42-0.99) for conjunctival microflora isolates, 0.80 (CI, 0.54-0.94) for ocular inf
219 rinking water affects the composition of gut microflora, leading to an altered autoimmune response an
220 elative to naive GC-C+/+ mice, the commensal microflora load in uninfected GC-C-/- mice was decreased
221 n a balance in the composition of intestinal microflora; long-lived macrofauna have also been shown t
223 Concentrations of isoflavones and their gut microflora metabolites in the plasma, urine, and feces w
224 nto the bioactive natural products and human microflora metabolites of dietary ellagic acid derivativ
226 art from stimulating the growth of probiotic microflora, MOS impart anticancer and immunomodulatory e
228 molecular techniques for analysis of the gut microflora, new manufacturing biotechnologies, and incre
232 investigate peri-implant and intraconnection microflora of healthy implants restored with cemented an
233 ctively, these findings suggest that the gut microflora of the honey bee harbours bacterial members w
236 imately 4.0-6.5logcfu/g were recorded in the microflora of the salad, whereas the Pseudomonas spp. po
238 -frequency gene transfer from GM soya to the microflora of the small bowel before their involvement i
239 les indicate that dogs have a highly diverse microflora of the small intestine, with marked differenc
242 idermidis, a major constituent of the normal microflora on healthy human skin, acts as a barrier agai
244 f the resident non-pathogenic or 'commensal' microflora on mucosal immune function and gut health has
245 have a profound effect on the impact of this microflora on the regulation of nematode populations by
246 by CD4 T cells is induced by the intestinal microflora, oral delivery of specific Ag, and type I IFN
249 he abundance of cecal messenger RNA, luminal microflora, physiology, and behavior in a highly diverse
250 e under tissue and developmental control and microflora play a major role in their specific ontogeny
251 ecognized that innate immunity to intestinal microflora plays a significant role in mediating immune
253 unity-based mechanism for protecting the gut microflora, preserving its functional robustness during
254 This has led to the perception that the microflora proliferate in nutrient-rich periods during o
255 rvations indicate that the normal human skin microflora protects skin by various modes of action, a c
258 iotaomicron, a predominant member of the gut microflora, revealing a mechanism whereby intestinal com
259 ansition was associated with a change from a microflora rich in TLR4-stimulatory proteobacteria to on
261 erstanding of the impact of APOE genotype on microflora speciation and metabolism is completely lacki
262 However, it is unknown how the indigenous microflora stimulates the immune system and how this res
264 ns in shaping the composition of the enteric microflora, such polymorphisms may influence outcomes in
266 s a member of the mammalian gastrointestinal microflora that has become a leading cause of nosocomial
269 In particular, the capacity of autochthonic microflora that live on natural organic matter as the so
271 late the composition of the small intestinal microflora, that development of crypt organoid culture s
272 ons, such as circulating glucose levels, gut microflora, time of year, and even diurnal rhythm, which
273 aturally occurring or commercially available microflora to be added thus enhancing flavour developmen
275 oid tissues (GALTs) interact with intestinal microflora to drive GALT development and diversify the p
276 neered commensal bacteria within the vaginal microflora to inhibit heterosexual transmission of HIV.
279 ized here the ability of intestinal and oral microflora to stimulate individual pattern recognition r
282 nerally exists in harmony with the commensal microflora, under certain conditions, these organisms ma
284 immunostimulatory activity of the intestinal microflora varied among individual mice but was largely
285 major stimulatory activity of the intestinal microflora was still intact in NOD1-, NOD2-, TLR2-, TLR4
286 rstand how selenium regulates the intestinal microflora, we used high-throughput sequencing to examin
288 samples (sourdough breads prepared with wild microflora) were spoiled approximately at the 7th day.
290 errestrial organisms, as well as belowground microflora, whether and how soil symbionts regulate phot
291 HIV infection leads to changes in basal lung microflora, which may contribute to chronic pulmonary co
292 cosal surface is colonized by the indigenous microflora, which normally maintains an ecological balan
293 the microbial structure and assembly of oral microflora, while no significant difference was detected
295 inflammatory/antimicrobial mediators and/or microflora within cervical fluid at 22-24 weeks gestatio
296 gulating the innate inflammatory response to microflora within the lower bowel, likely through its ab
297 ated immune response to a dysbiotic resident microflora within the oral cavity leads to chronic perio
298 ter colonizing germ-free mice with commensal microflora without any known pathogens (SPF), <9% of GPX
299 s them to interact with and contain the oral microflora without eliciting a marked inflammatory respo
300 myces lactis occur as part of Stilton cheese microflora yet are not controlled during production.