ライフサイエンスコーパス: oral infection

1 obial and antibody responses associated with oral infection.

2 vation, resulting in reduced defense against oral infection.

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

4 important for efficient T cell responses to oral infection.

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

6 enes replication foci only after a secondary 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 to noninfected controls, following oral infection.

12 egy to control alveolar bone loss induced by 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 were conducted with insect larvae by use of oral infection.

20 ntal disease-induced oxidative stress during 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 nly encountered first during childhood as an oral infection.

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

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

27 mouse macrophages and during S. typhimurium oral infection.

28 olonized the intestine and deeper tissues in oral infection.

29 g passage through the host stomach following oral infection.

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

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

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

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

34 parasite that is usually transmitted through oral infection.

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

36 ntestine, where bradyzoites must enter after oral infection.

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

38 The deceased had fewer teeth and more oral infections.

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

40 sed in metainflammation are also reported in oral infections.

41 lymphoid organ that orchestrates immunity to oral infections.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

70 Oral infections caused by Candida species, the most comm

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

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

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

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

75 Sensitivity to oral infection correlated with CD155 expression not only

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

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

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

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

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

81 Oral infections have been postulated to produce cytokine

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

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

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

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

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

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

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

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

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

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

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

93 Oral infection induced the highest proportion of gamma i

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

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

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

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

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

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

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

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

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

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

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

105 After oral infection of calves, the Salmonella serotype Typhim

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

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

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

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

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

111 After oral infection of mice with Listeria monocytogenes, prol

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

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

114 Oral infection of mice with serovar Typhimurium demonstr

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

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

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

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

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

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

121 Oral infection of susceptible C57BL/6 mice with Toxoplas

122 Oral infection of susceptible mice with Toxoplasma gondi

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

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

125 Dentists deal with oral infections on a regular basis.

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

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

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

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

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

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

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

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

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

135 Oral infection studies have identified many of the key p

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

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

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

139 Chronic oral infections that elicit host responses leading to pe

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

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

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

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

144 Oral infection was assessed from subgingival plaque samp

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

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

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

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

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

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

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

152 Oral infection with A. actinomycetemcomitans increased L

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

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

155 In oral infection with bradyzoite cysts, the Deltasrs9 stra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 Oral infection with the nematode parasite Heligmosomoide

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

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

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

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

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

199 Oral infection with Toxoplasma triggers an inflammasome

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

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

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

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

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

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

206 We report that oral infection with Yersinia pseudotuberculosis results

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

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

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