ライフサイエンスコーパス: oral infection

1 ntestine, where bradyzoites must enter after oral infection.

2 trol the parasite and succumb within 2 wk of oral infection.

3 obial and antibody responses associated with oral infection.

4 vation, resulting in reduced defense against oral infection.

5 important for efficient T cell responses to oral infection.

6 ia within the liver and spleen of mice after oral infection.

7 differentiation of gut mucosal T cells after oral infection.

8 infection can be recapitulated following an oral infection.

9 toneal dose of CDDO at the time of T. gondii oral infection.

10 e expression due to Porphyromonas gingivalis oral infection.

11 compared with CX3CR1(gfp/gfp) mice following oral infection.

12 compared to noninfected controls, following oral infection.

13 ing and/or contributing to susceptibility to oral infection.

14 n the Peyer's patches as early as 3 hr after oral infection.

15 al colon of the gastrointestinal tract after oral infection.

16 y the gut mucosal immune responses following oral infection.

17 itionally regarded as a chronic inflammatory oral infection.

18 ors of bone loss consequent to P. gingivalis oral infection.

19 uantitative study of the fate of prions upon oral infection.

20 were conducted with insect larvae by use of oral infection.

21 th maximal migration occurring 48-54 h after oral infection.

22 pathogenic infection in its vector following oral infection.

23 ive further blood meals after their original oral infection.

24 s was present in saliva within two days post-oral infection.

25 nly encountered first during childhood as an oral infection.

26 ues and the spleen after an otherwise lethal oral infection.

27 enes replication foci only after a secondary oral infection.

28 egy to control alveolar bone loss induced by oral infection.

29 ntal disease-induced oxidative stress during oral infection.

30 lly favor CC17 GBS meningitis following mice oral infection.

31 re numerically stable for >1 y after initial oral infection.

32 protection against lethal Y. enterocolitica oral infection.

33 mouse macrophages and during S. typhimurium oral infection.

34 olonized the intestine and deeper tissues in oral infection.

35 g passage through the host stomach following oral infection.

36 al of B. microti in a murine model following oral infection.

37 n an NRAMP(R), C3H/HeN murine model of acute oral infection.

38 O resulting from the host immune response to oral infection.

39 parasite that is usually transmitted through oral infection.

40 wing, severe and progressive tooth decay, or oral infections.

41 The deceased had fewer teeth and more oral infections.

42 and hypofunction which causes xerostomia and oral infections.

43 reptococci and may be implicated in some non-oral infections.

44 sed in metainflammation are also reported in oral infections.

45 lymphoid organ that orchestrates immunity to oral infections.

46 ry T cell responses during both systemic and oral infections.

47 ed from extraoral infections as well as from oral infections.

48 erentially expressed in vaginal, rather than oral, infections.

49 terial challenge not only is associated with oral infection among children but also predicts increase

50 ervational Study, evaluated the influence of oral infection and age on the associations between osteo

51 rong rationale for studying the link between oral infection and AMD pathogenesis in individuals with

52 The possible association between oral infection and chronic inflammation and cardiovascul

53 showed reduced lethality in a mouse model of oral infection and persisted in significantly lower numb

54 /-) mice led to impaired immune responses to oral infection and to oral vaccination.

55 The link between oral infections and adverse systemic conditions has attr

56 and potentially causal associations between oral infections and cardiometabolic diseases (CMDs), con

57 rticles as a multifaceted agent for treating oral infections and improving dental materials, especial

58 athogens to distant body sites causing extra-oral infections and inflammation.

59 Akita/Ncf1 mice had increased prevalence of oral infections and more severe periodontitis compared w

60 tion of adhesion of bacteria responsible for oral infections and stomach ulcers.

61 oke or myocardial infarction enrolled in the Oral Infections and Vascular Disease Epidemiology Study

62 er-specific IgM and IgG antibodies following oral infection, and had significantly attenuated Citroba

63 and ROP16 promoted host resistance to acute oral infection, and Toxoplasma may possibly target the S

64 al route, and thus suitable animal models of oral infection are needed to investigate viral pathogene

65 al route, and thus suitable animal models of oral infection are needed to investigate viral pathogene

66 T cells provide protection against secondary oral infection are poorly understood.

67 Morphine markedly sensitized mice to oral infection, as assessed by survival, mean survival t

68 that can take time and expertise to diagnose oral infections based on X-ray images.

69 Neutrophils contribute to protection in oral infection but exacerbate vulvovaginal candidiasis.

70 barrier." Wild-type flies are refractory to oral infection by arboviruses, including Sindbis virus a

71 Mice are rendered susceptible to oral infection by injection with cortisone acetate and t

72 rise in serum IgA and IgG1 levels following oral infection by listeriae.

73 nflammasome does not result in resistance to oral infection by S. typhimurium, but rather, leads to i

74 esponses of adult mice and preweaned pups to oral infection by S. typhimurium.

75 ce has been reported to confer resistance to oral infection by Salmonella typhimurium.

76 larvae also exhibit enhanced sensitivity to oral infection by the bacterial pathogen Pseudomonas ent

77 exhibited complete protection against lethal oral infections by Yersinia enterocolitica WA and Y. pse

78 efore, future studies must elucidate whether oral infections can increase the risk of CMDs independen

79 Oral infections caused by Candida species, the most comm

80 Maternal oral infection, caused by bacteria such as C. rectus or

81 The low-grade oral infection chronic periodontitis (CP) has been impli

82 s from the murine spleen and liver following oral infection compared to organisms grown under normal

83 zation and immune cell populations following oral infection confirmed characteristics previously desc

84 The precise mechanism by which oral infection contributes to the pathogenesis of extra-

85 Sensitivity to oral infection correlated with CD155 expression not only

86 Surprisingly, however, following oral infection, dectin-1 was not required for the contro

87 ally distinct from Trm cells generated after oral infection, demonstrating the critical contribution

88 have been proposed, including spread of the oral infection due to transient bacteremia resulting in

89 ferred significant protection against lethal oral infection, equivalent to that conferred by whole he

90 The Oral Infections, Glucose Intolerance and Insulin Resista

91 ORIGINS (the Oral Infections, Glucose Intolerance and Insulin Resista

92 The "one pathogen, one disease" paradigm of oral infections has been replaced by a holistic concept

93 Oral infections have been postulated to produce cytokine

94 ese findings further support the notion that oral infections have extraoral effects and document that

95 In contrast to oral infection, i.p. infected CD73(-/-) mice were highly

96 te to the central nervous system (CNS) after oral infection in C57BL/6J mice expressing either wild-t

97 haryngeal candidiasis (OPC), the most common oral infection in human immunodeficiency virus-positive

98 measures of pathology for 4 weeks following oral infection in mice.

99 his animal model to track viral spread after oral infection in real time.

100 peutic implications in the treatment of this oral infection in the severely immunocompromised host.

101 infection that enables the natural route of oral infection in weaned and nonimmunocompromised 21-day

102 ype in an adult A129 mouse model and reduced oral infections in mosquitoes.

103 nuated in adult A129 mouse model and reduced oral infections in mosquitoes.

104 livary immunoglobulins might better estimate oral infections in this relationship.

105 he function of this signaling pathway during oral infection, in which mucosal immunity assumes a pred

106 Factors associated with HR oral infection included being male (adjusted odds ratio

107 coccus micros in the pathogenesis of various oral infections, including oropharyngeal abscesses and p

108 plication of nanoparticles in the control of oral infections, including their use in photodynamic the

109 Systemic bone density and oral infection independently influenced oral bone loss i

110 Oral infection induced the highest proportion of gamma i

111 though their specific causal relationship to oral infection-induced chronic inflammatory diseases is

112 The results support a potential oral infection-inflammation pathway.

113 the three mouse strains tested suggests that oral infection is a useful model for studying the host r

114 hermore, induction of T(H)17 immunity during oral infection is dependent on TLR1 and results from the

115 participants developing enteric fever after oral infection, marked transcriptional and cytokine resp

116 his creates a confounding relationship among oral infections, metainflammation, and genetics.

117 arcZ double mutant has phenotypes in a mouse oral infection model consistent with increased expressio

118 dies also reinforce the utility of the mouse oral infection model in dissecting the pathobiology of p

119 ack individual species within a dual-species oral infection model in mice with both temporal and spat

120 xpression was upregulated in a P. gingivalis oral infection model, and reduced IFN-gamma and IL-17 we

121 on and survival of P. gingivalis in a murine oral infection model.

122 This study presents an EV-A71 oral infection murine model that efficiently infects wea

123 suggesting that PPs are required neither for oral infection nor for CpG-induced resistance against or

124 We find that oral infection of adult females with the enteric pathoge

125 as a complete cycle for full virulence after oral infection of BALB/c mice.

126 After oral infection of calves, the Salmonella serotype Typhim

127 ns lacking these proteins were tested during oral infection of calves.

128 Oral infection of conventional mice with a Deltalmo2776

129 BALB/c mice received an oral infection of Heligmosomoides polygyrus third-stage

130 yphimurium is attenuated for virulence after oral infection of immunocompromised gp91phox(-/-) mice t

131 nd PIF2 (Ac022), like P74, are essential for oral infection of lepidopteran larval hosts of Autograph

132 enerated signature-tagged mutants during the oral infection of mice and calves.

133 After oral infection of mice with Listeria monocytogenes, prol

134 s of these observations were revealed during oral infection of mice with S. typhimurium, wherein endo

135 urine Salmonella infection, wherein low-dose oral infection of mice with Salmonella enterica subsp. e

136 Oral infection of mice with serovar Typhimurium demonstr

137 type 2 mucosal immune response that follows oral infection of mice with the nematode parasite, Helig

138 patches, the liver, and the spleen following oral infection of mice with WT, dam mutant, or flagellin

139 ere recovered from the liver or spleen after oral infection of mice, ADAR, PKR, Mx, and CIITA express

140 We examined the role of this deletion in oral infection of mosquitoes by constructing infectious

141 for infectivity via intraperitoneal but not oral infection of naive mice.

142 Here, we report that oral infection of neonatal mice with low doses of virule

143 ntibody responses to HuNoV and RRV following oral infection of suckling mice.

144 Oral infection of susceptible C57BL/6 mice with Toxoplas

145 Oral infection of susceptible mice with Toxoplasma gondi

146 stomatitis (DS) is a persistent and chronic oral infection of the denture-bearing palatal mucosa.

147 , SPI2 mutant ST are highly attenuated after oral infection of the same mice, revealing a role for SP

148 cleopolyhedrovirus (AcMNPV), is critical for oral infection of Trichoplusia ni larvae.

149 y, we examined the effect of EHDV serotype-2 oral infection on the survival and reproduction of Culic

150 Dentists deal with oral infections on a regular basis.

151 train II+ROP16I) promotes host resistance to oral infection only in the context of endogenous GRA15 e

152 understanding immunity to T. cruzi following oral infection or oral vaccination, knowing that the rou

153 Furthermore, animals with DIO exposed to oral infection or systemic inoculation of live P. gingiv

154 ealthy subjects or persons who had syphilis, oral infections, or rheumatoid arthritis were tested by

155 ons who had syphilis, periodontitis or other oral infections, or rheumatoid arthritis were tested wit

156 erns may help explain the immunopathology of oral infections, particularly with regard to inflammator

157 emic inflammatory state elicited by a common oral infection (periodontitis) could enhance treatment r

158 Using Yersinia enterocolitica, we show that oral infection promotes T(H)17 immunity, whereas systemi

159 In both strains, oral infection resulted in focal meningitis and ventricu

160 specific animal husbandry techniques and an oral infection route showed cftr(-/-) mice but not WT mi

161 Neonates are susceptible to oral infection, showing higher infection rates for wild-

162 Oral infection studies have identified many of the key p

163 Mouse oral infection studies indicate that E2~Ub conjugates ac

164 Biofilm-induced inflammatory osteolytic oral infections, such as periodontitis and peri-implanti

165 one loss than did immunocompetent mice after oral infection, suggesting that lymphocytes contribute t

166 Chronic oral infections that elicit host responses leading to pe

167 In oral infections the SPI-2 mutant was not observed in the

168 We demonstrated that after oral infection, the parasite rapidly recruited inflammat

169 In metabolic inflammation and oral infections, the innate immune system is activated t

170 nity to these proteins has been shown in non-oral infections to contribute to protection.

171 Oral infection was assessed from subgingival plaque samp

172 In this study, a mouse model of oral infection was characterized to assess the roles of

173 Bone loss after oral infection was decreased in mice deficient in major

174 An animal model of oral infection was developed using transgenic mice expre

175 ss, in general, but neither bone density nor oral infection was significantly associated with mean al

176 ral mucosal constructs, and a mouse model of oral infection, we demonstrated that S. oralis augmented

177 To identify novel regulators of KSHV oral infection, we performed a transcriptome analysis of

178 ased susceptibility to bone resorption after oral infection, while a hypomorphic defect in beta(2)-in

179 trate that morphine withdrawal sensitizes to oral infection with a bacterial pathogen and predisposes

180 e, and WT C57BL/6 mice all survived an acute oral infection with a low dose of mildly virulent strain

181 Oral infection with A. actinomycetemcomitans increased L

182 us, MRE16sp, poorly infects mosquitoes after oral infection with an equivalent titer.

183 ion (odds ratio, 14.6; 95% CI, 6.3 to 36.6), oral infection with any of 37 types of HPV (odds ratio,

184 In oral infection with bradyzoite cysts, the Deltasrs9 stra

185 Importantly, oral infection with C. albicans stimulates the phosphory

186 Lcn2 is strongly upregulated following oral infection with C. albicans, and its expression is a

187 we evaluated the role of Lcn2 in immunity to oral infection with C. albicans.

188 ination of infection than Cnlp+/+ mice after oral infection with C. rodentium.

189 During oral infection with Candida, a large number of pro-infla

190 IEL can be isolated at specific times after oral infection with cysts containing bradyzoites.

191 signs of the hemolytic uremic syndrome after oral infection with Escherichia coli O157:H7 or other Sh

192 g-treated mice, tooth extraction followed by oral infection with Fusobacterium nucleatum caused BONJ-

193 show that rhesus macaques are susceptible to oral infection with human noroviruses from two different

194 The present study demonstrates that oral infection with hyperyersiniabactin (Ybt) producing

195 Following oral infection with L. monocytogenes, Rc3h1(gt/gt) --> N

196 ction nor for CpG-induced resistance against oral infection with L. monocytogenes.

197 We found that oral infection with Listeria monocytogenes induced a rob

198 o intestinal epithelium-derived OVA, because oral infection with Listeria monocytogenes-encoding OVA

199 Maternal periodontal disease is a chronic oral infection with local and systemic inflammatory resp

200 e M cells, renders BALB/c mice refractory to oral infection with MNV.

201 Recent studies demonstrated that oral infection with P. gingivalis induces both periodont

202 st cells to local bone destruction following oral infection with P. gingivalis Mast cell-deficient mi

203 re resistant to alveolar bone loss following oral infection with P. gingivalis, and thus establish a

204 In a murine model of pregnancy and oral infection with P. gingivalis, C57BL/6J mice develop

205 After oral infection with P. gingivalis, mice with DIO had a s

206 ly more susceptible to atherosclerosis after oral infection with P. gingivalis.

207 d that antibiotic treatment of mice prior to oral infection with poliovirus reduced viral replication

208 thritis, concomitant periodontitis caused by oral infection with Porphyromonas gingivalis enhances ar

209 el in which alveolar bone loss is induced by oral infection with Porphyromonas gingivalis, a gram-neg

210 el in which alveolar bone loss is induced by oral infection with Porphyromonas gingivalis.

211 be induced in specific-pathogen-free mice by oral infection with Porphyromonas gingivalis.

212 sal and systemic humoral immune responses to oral infection with reovirus.

213 In specific response to oral infection with rhesus rotavirus, IL-6(-) and IL-6(+

214 icrobiota, and reduced insect survival after oral infection with S. marcescens.

215 hine withdrawal on spontaneous sepsis and on oral infection with Salmonella enterica serovar Typhimur

216 and proinflammatory cytokines in response to oral infection with Salmonella in newly hatched chickens

217 y hatched chickens 6, 12, 24, and 48 h after oral infection with Salmonella serovar Typhimurium.

218 did the progeny of nonvaccinated hens after oral infection with Salmonella strains.

219 liver but remained lowest in brain following oral infection with Salmonella.

220 icient mice, which are already sensitized to oral infection with Shigella flexneri, leads to further

221 LB/c) that fail to develop ileitis following oral infection with T. gondii were rendered susceptible

222 After oral infection with T. gondii, susceptible wild-type (WT

223 inflammatory response that ensues following oral infection with T. gondii.

224 ere resistant to chronic toxoplasmosis after oral infection with T. gondii.

225 ne response in alveolar bone loss induced by oral infection with the human gram-negative anaerobic ba

226 ited in certain strains of inbred mice after oral infection with the intracellular protozoan parasite

227 Oral infection with the nematode parasite Heligmosomoide

228 avirulent and protective against subsequent oral infection with the virulent serovar Typhimurium SR-

229 anemic and exhibit delayed growth following oral infection with third-stage Ancylostoma ceylanicum h

230 Oral infection with Toxoplasma gondii results in dysbios

231 After acute oral infection with Toxoplasma gondii, both WT and Crtam

232 RB6-8C5 MAb-treated mice succumbed to oral infection with Toxoplasma gondii, similar to Ccr2(-

233 Using a model of lethal oral infection with Toxoplasma gondii, we examined the f

234 Oral infection with Toxoplasma triggers an inflammasome

235 loped severe necrotizing hepatitis following oral infection with Trichinella spiralis.

236 et within the iIEL population in response to oral infection with virulent or avirulent Salmonella.

237 his study examined the effect of morphine on oral infection with virulent Salmonella typhimurium.

238 In response to oral infection with virulent type 1 or avirulent type II

239 r's patches and mesenteric lymph nodes after oral infection with Y. enterocolitica.

240 rences in 50% lethal dose (LD(50)) following oral infection with Y. enterocolitica.

241 We report that oral infection with Yersinia pseudotuberculosis results

242 Moreover, Cnlp+/+ mice were protected from oral infections with C. rodentium inocula that infected

243 s or with all three species in polymicrobial oral infections with or without Fusobacterium nucleatum.

244 treatment, HAART) suffer significantly fewer oral infections with the opportunistic fungal pathogen C