ライフサイエンスコーパス: bacterial burden

1 Z B cells, preserves IgM levels, and reduces bacterial burden.

2 e death did not require a high intracellular bacterial burden.

3 ator, increased the number of BALF cells and bacterial burden.

4 is important for inhibiting inflammation and bacterial burden.

5 ed weight loss, and a more-rapid increase in bacterial burden.

6 s, also contribute to the elimination of the bacterial burden.

7 ible nitric oxide synthase level and a lower bacterial burden.

8 d the rate of positive results declined with bacterial burden.

9 IFN-alpha and IFN-beta resulted in a reduced bacterial burden.

10 in exacerbated lung granuloma pathology and bacterial burden.

11 increased survival, despite having a higher bacterial burden.

12 to MPYS-deficient mice decreases their liver bacterial burden.

13 ound that lesion size did not correlate with bacterial burden.

14 st survival and optimal long-term control of bacterial burden.

15 pe mice, although there was no difference in bacterial burden.

16 nti-TNF-alpha antibody resulted in increased bacterial burden.

17 he interactions of the host with the massive bacterial burden.

18 sthma harbored significantly lower bronchial bacterial burden.

19 ant proinflammatory responses, not increased bacterial burden.

20 myelination in the absence of changes in CNS bacterial burden.

21 termined by gross pathologic examination and bacterial burden.

22 vaccination without significantly impacting bacterial burden.

23 maging was used to noninvasively monitor the bacterial burden.

24 ting a direct response to Hla independent of bacterial burden.

25 sufficient wild-type mice, despite a similar bacterial burden.

26 powerful host defense mechanism that reduces bacterial burden.

27 s and Tlr7, we found an elevated respiratory bacterial burden.

28 spleens, the main subsets controlling early bacterial burden.

29 ockdown in zebrafish results in an increased bacterial burden.

30 k infection, which correlated with increased bacterial burdens.

31 e this phagocytic defect as well as decrease bacterial burdens.

32 nd extensive exfoliation and reduced bladder bacterial burdens.

33 WT-derived macrophages exhibited comparable bacterial burdens.

34 0 strains overproducing PVL caused increased bacterial burdens.

35 ected wild-type mice despite markedly higher bacterial burdens.

36 uclear leukocytes to the lung but had higher bacterial burdens.

37 d from liver and spleen, indicating elevated bacterial burdens.

38 tes host death and is associated with higher bacterial burdens.

39 ged mice suffered 1000-fold higher pulmonary bacterial burden, 2.2-fold higher levels of neutrophil r

40 if predatory bacteria can attenuate systemic bacterial burden administered intravenously.

41 ion of neutrophils in their lungs and higher bacterial burden after infection with M. tuberculosis.

42 hAAT reduces the bacterial burden after infection.

43 etion did not alter the clinical outcome and bacterial burden, although it moderately improved lung i

44 tment resulted in up to 85-fold reduction in bacterial burden and a 53% decrease in infection-induced

45 es with the number of airway neutrophils and bacterial burden and a genetic polymorphism that increas

46 ter rhinovirus infection, there is a rise in bacterial burden and a significant outgrowth of Haemophi

47 ion, huTNF KI mice survived, controlling the bacterial burden and activating bactericidal mechanisms.

48 with recombinant IL-8 significantly reduced bacterial burden and apoptosis.

49 ey U test was used to compare differences in bacterial burden and cytokine responses between trauma a

50 of bacterial infections, including increased bacterial burden and decreased diversity of microbial co

51 ed PMN recruitment and resulted in sustained bacterial burden and delayed wound healing.

52 to standard tuberculosis treatment increased bacterial burden and did not decrease the time to bacter

53 IkappaBNS (-/-) mice displayed an increased bacterial burden and diminished tissue damage.

54 tion sanroque mice demonstrated an increased bacterial burden and dysregulated inflammation in the lu

55 esponse promotes stable control of pulmonary bacterial burden and granuloma integrity, whereas TLR2 s

56 ing and, consequently, a higher plateau lung bacterial burden and greater immune pathology.

57 mouse oropharynx with significantly greater bacterial burden and had significantly reduced ability t

58 on in huTNF KI mice, leading to an increased bacterial burden and hyperinflammation.

59 accinated macaques were protected with lower bacterial burden and immunopathology.

60 d that simvastatin significantly reduces the bacterial burden and inflammatory cytokines in the infec

61 ore, dexamethasone significantly reduced the bacterial burden and influx of lymphocytes but not of ne

62 nificantly increased survival and diminished bacterial burden and kidney abscesses when mice were cha

63 processing of il1beta, results in increased bacterial burden and less infiltration of macrophages to

64 coagulant coumadin display increased hepatic bacterial burden and mortality following either i.p. or

65 eutrophil influx to the lung, increased lung bacterial burden and mortality in an Escherichia coli pn

66 Using NOD2/RIP2(-)/(-) mice, we observed bacterial burden and neutrophil accumulation in the lung

67 This correlated with increased lung bacterial burden and pathology and decreased survival co

68 al, and MyD88 signaling is required to limit bacterial burden and prolong survival during pulmonary i

69 Bacterial burden and pulmonary immunopathology of chimer

70 culosis-infected IL-21R KO mice had enhanced bacterial burden and reduced infiltration of Ag-specific

71 We found enhanced bacterial burden and reduced neutrophil and cytokine/che

72 mice with E. coli infection displayed higher bacterial burden and reduced neutrophil recruitment and

73 hold value of 28 can be used as a measure of bacterial burden and smear status in a high HIV burden s

74 ion of psaA leads to a decrease in the organ bacterial burden and to a significant increase in the 50

75 The outcome was measured by the analysis of bacterial burden and transcriptome-wide analysis of host

76 ion was evidenced by 2-log reduction of lung bacterial burden and was accompanied by less leukocytes

77 The expression of LAG3 coincides with high bacterial burdens and changes in the host type 1 helper

78 il-18(-/-) mice also suffered from increased bacterial burdens and exacerbated histopathology.

79 al transparency allows for rapid analysis of bacterial burdens and host survival in response to genet

80 Clecsf8-/- mice exhibit higher bacterial burdens and increased mortality upon M. tuberc

81 ion, impaired responses in the colon, higher bacterial burdens and increased mortality.

82 eron gamma (IFN-gamma), leading to increased bacterial burdens and inflammation.

83 17 cells into TCR alphabeta KO mice restored bacterial burdens and innate immune cell infiltrates to

84 ol were sufficient to significantly increase bacterial burdens and kidney pathology in mice infected

85 We found reduced lung bacterial burdens and less severe histopathological find

86 B7x(-/-) mice had significantly lower bacterial burdens and levels of inflammatory cytokines i

87 ibited significantly elevated lung and blood bacterial burdens and mortality.

88 chronic phase of infection and had increased bacterial burdens and severe pulmonary inflammation, wit

89 effects of IL-5 administration on survival, bacterial burden, and cytokine production after polymicr

90 t mice displayed reduced survival, increased bacterial burden, and exacerbated hemorrhagic pathology.

91 by worsening clinical correlates, high lung bacterial burden, and granulomatous immunopathology.

92 -CSF resulted in reduced survival, increased bacterial burden, and greater lung injury.

93 emonstrated by decreased survival, increased bacterial burden, and increased damage to their livers a

94 tion, enhanced immune cell access, decreased bacterial burden, and increased host survival, suggestin

95 cal T cell and cytokine responses, increased bacterial burden, and lower levels of inflammation.

96 s persistent bacteriuria, high-titer bladder bacterial burdens, and chronic inflammation.

97 sted as persistent bacteriuria, high bladder bacterial burdens, and chronic inflammation.

98 ignificantly short survival times, increased bacterial burdens, and severe organ pathology compared t

99 odulating inflammatory response, alleviating bacterial burdens, and suppressing thymocyte apoptosis.

100 This PcpA-dependent effect on bacterial burden appeared earlier (within 12 h) in the f

101 lta-sigH mutant is completely attenuated for bacterial burden as well as immunopathology in NHPs.

102 This regulation is independent of bacterial burden, as CD36 also limits dermonecrosis caus

103 cific operational taxonomic units as well as bacterial burden associated independently with IPF.

104 Inhalational antibiotics reduce the bacterial burden associated with a worse outcome.

105 use mortality (40% versus 10%) and increased bacterial burden at 8 and 20 h postinfection compared to

106 reduced inflammatory cytokine expression and bacterial burden at the site of infection, and improved

107 We found that differences in bacterial burden at the time of death did not explain th

108 n of S. aureus, it significantly reduced the bacterial burden at the wound infection site.

109 production, decreased weight loss, and lower bacterial burdens at 24 h postbacterial infection in com

110 7-H1-deficient mice had significantly higher bacterial burdens at day 21 and day 35 postinfection com

111 hly resistant to fatal disease and had lower bacterial burden, attenuated pathology, and prolonged su

112 Comparison of bacterial burdens between IL-17a(-/-) and wild-type mice

113 Bacterial burdens, bronchoalveolar lavage fluid (BALF) c

114 he same FimH inhibitor lowered their bladder bacterial burden by >1000-fold.

115 pigs and mice, InlP increased the placental bacterial burden by a factor of 3 log10 while having onl

116 PEP35 reduced the tissue bacterial burden by exclusively modulating the local neu

117 r MyD88-dependent signaling but dependent on bacterial burden, caspase-1/11, and neutrophil-dependent

118 y and extrapulmonary pathology, and a higher bacterial burden compared with glucose-intolerant and no

119 gy to increase long-term survival and reduce bacterial burden, compared with standard antibiotic chem

120 t to M. tuberculosis infection, with reduced bacterial burdens, compared with those of healthy donors

121 straightforward associations among salivary bacterial burdens, corresponding antibody formation, and

122 The increased bacterial burden could be only partially recapitulated b

123 allenge, indicated by dramatically increased bacterial burden, cytokine storm, striking histological

124 rine tuberculosis, where it exhibits a lower bacterial burden, delayed time to death, and decreased a

125 , CD14 deficiency is associated with greater bacterial burden despite the presence of highly activate

126 By 24 h, however, Die-P mice have increased bacterial burden, despite increased neutrophil recruitme

127 y susceptible with a progressive increase in bacterial burden, despite their ability to mount an infl

128 ngly associated with a diagnosis of IPF, BAL bacterial burden (determined by 16S quantitative polymer

129 one marrow chimeric mice exhibited increased bacterial burden, disorganized accumulation of lymphocyt

130 DeltaprrF1-prrF2 mutant is due to decreased bacterial burden during acute lung infection.

131 ls is a powerful defense mechanism to reduce bacterial burden during infection but this activity cann

132 In vivo, namH disruption did not affect the bacterial burden during infection of C57BL/6 mice or cel

133 nificantly improved capacity to restrain the bacterial burden during lethal listeriosis despite their

134 reased miR-718 expression is associated with bacterial burden during Neisseria gonorrhoeae infection

135 The bacterial burden during primary infection was significan

136 in the lung, IL-6 and IL-10 production, and bacterial burden during sepsis.

137 While fibrin limits the bacterial burden during sublethal listeriosis in wild-ty

138 ed bacterial lysis, and resulted in enhanced bacterial burdens during infection.

139 that although defective in establishing high bacterial burdens early during the infection process, T4

140 For patients with large bacterial burdens (eg, individuals with ventilator-requi

141 tically tagged PMNs, we observed that a high bacterial burden elicited a sustained mobilization of PM

142 C. rodentium infection resulted in a higher bacterial burden, enhanced intestinal damage, and greate

143 nfected mice showed significant reduction of bacterial burden, enhanced neutrophil recruitment, and a

144 ficantly decreased survival rates, increased bacterial burdens, exaggerated tissue injuries, and elev

145 When the hepatic bacterial burden exceeds 1x10(6) CFU, levels of hepatic

146 as evidenced by a 100-1000-fold reduction in bacterial burden following challenge.

147 h purified MrkA proteins also showed reduced bacterial burden following K. pneumoniae challenge.

148 ese, 77% of patients had a moderate or heavy bacterial burden (>/=2+).

149 day with standard therapy, translating to a bacterial burden half-life of 11.52 days vs 8.53 days, r

150 l molecules prevented efficient clearance of bacterial burden, highlighting a role for NLRP12 as a ne

151 pre-treatment infection severity (including bacterial burden, host cell activation and host cell dea

152 Bacterial burden, host cytokine response, and histologic

153 dx6-deficient mice exhibit no differences in bacterial burden, host immune response, or lung damage f

154 ure red blood cells correlated with elevated bacterial burdens, implying that extramedullary erythrop

155 dose of imipenem (IPM) robustly lowered the bacterial burden in a neutropenic Staphylococci murine i

156 creased survival was associated with reduced bacterial burden in affected tissues and with recruitmen

157 Lung transplant recipients had higher bacterial burden in BAL than control subjects, frequent

158 IPF is characterized by an increased bacterial burden in BAL that predicts decline in lung fu

159 2 h postinfection, significantly reduced the bacterial burden in both the liver and spleen.

160 es, restricted cytokine release, and reduced bacterial burden in C57BL/6 mice during sepsis.

161 Bacterial burden in Cftr morphants infected with a P. ae

162 decan-1 shedding significantly decreased the bacterial burden in corneal tissues.

163 y therapeutic compounds dramatically reduced bacterial burden in different organs.

164 Bacterial burden in hyperglycaemic animals was greater t

165 ansfer of immune WT CD8(+) T cells increased bacterial burden in IL-18Ralpha(-/-) mice following IOE

166 an pyroptosis, because we observed augmented bacterial burden in IL-1R and IL-18 knockout mice.

167 tokines and present with greater disease and bacterial burden in infected tissues.

168 mically to infected wild-type mice decreased bacterial burden in lung and liver at 24 h postinfection

169 fferences correlated with variability in the bacterial burden in lung and spleen of mice infected wit

170 tB resulted in a 1,000- and 100-fold reduced bacterial burden in lungs and lymph nodes, respectively,

171 on and analyzed the cellular composition and bacterial burden in lungs and spleens.

172 s associated with a significant reduction in bacterial burden in lungs, liver, and spleen of immunize

173 ory cytokine levels, leading to an increased bacterial burden in macrophages.

174 n also improves survival and reduces hepatic bacterial burden in mice challenged intraperitoneally wi

175 Cigarette smoke exposure increased the bacterial burden in mice infected with M. tuberculosis a

176 , XBP1 deficiency resulted in a much greater bacterial burden in mice infected with the TLR2-activati

177 Salmonella-infected cell and to regulate the bacterial burden in mice.

178 bination with light, CgoX activation reduces bacterial burden in murine models of SSTI.

179 rates, treatment, modified Centor score, and bacterial burden in patients with negative RADTs and pos

180 CL1 levels in tissues and blood could reduce bacterial burden in sepsis.

181 O rescues neutrophil numbers and reduces the bacterial burden in Sod2-deficient zebrafish.

182 s required to modulate lung inflammation and bacterial burden in TB.

183 riaxone)-treated mice, we further reduce the bacterial burden in the brain.

184 arance defect, with an almost 10-fold-higher bacterial burden in the bronchoalveolar lavage fluid 3 h

185 bacterial control, significant reductions in bacterial burden in the draining lymph nodes, spleen, an

186 but not IL-17 or IL-23 plus IL-1beta rescued bacterial burden in the ethanol group to control levels.

187 pathogen Listeria monocytogenes, most of the bacterial burden in the gut is extracellular.

188 ss and kidney abscesses, as well as a higher bacterial burden in the kidneys.

189 /-) mice, MPYS deficiency leads to increased bacterial burden in the liver upon Listeria monocytogene

190 nary K. pneumoniae infection and show higher bacterial burden in the lungs and dissemination.

191 al lung burden, and systemic IL-22 decreases bacterial burden in the lungs and peripheral organs by p

192 yed significantly reduced inflammation, less bacterial burden in the lungs and spleens, and extended

193 ted mice also exhibited significantly higher bacterial burden in the lungs compared to the control gr

194 of Nb infection substantially increases the bacterial burden in the lungs of co-infected mice.

195 el, we observed a PcpA-dependent increase in bacterial burden in the lungs, blood, liver, bronchoalve

196 mice exhibit no difference in survival time, bacterial burden in the lungs, or dissemination from wil

197 nduced more-severe splenomegaly and a higher bacterial burden in the spleens of B1a cell-deficient Br

198 -/-) mice had reduced survival and increased bacterial burden in their livers and spleens.

199 t strain exhibited a 4-log-unit reduction in bacterial burden in their lungs, as well as reduced lung

200 L-23p19 knockout (KO) mice have an increased bacterial burden in this organ, suggesting that IL-23 ma

201 er DHA + aspirin therapy influences specific bacterial burden in this setting is unknown.

202 ion resulted in significant reduction of the bacterial burden in tissue at 24 hours, along with prolo

203 ciated with retinol in vivo, and limited the bacterial burden in tissues after acute infection.

204 y and phagocytosis in neutrophils to control bacterial burden in tissues during CLP-induced polymicro

205 The ability of predatory bacteria to reduce bacterial burden in vivo within the lungs of rats has be

206 mine whether predatory bacteria could reduce bacterial burden in vivo, Klebsiella pneumoniae was inje

207 te antigen-specific reductions in the tissue bacterial burdens in animal models of S. aureus skin abs

208 her pathogen, MPYS deficiency did not impact bacterial burdens in infected spleens.

209 ultiplies within macrophages, with increased bacterial burdens in liver and spleen.

210 mixed bone marrow chimeras, we compared the bacterial burdens in lung myeloid cells that were capabl

211 in MyD88 KO mice was associated with greater bacterial burdens in lungs and distal organs, and the ab

212 specific deletion of Il22ra1 also had higher bacterial burdens in lungs compared with littermate cont

213 ific antibodies, resulted in a difference in bacterial burdens in organs of infected mice at 10 h pos

214 oles for Borrelia adhesins BBK32 and OspC in bacterial burdens in the bloodstream.

215 orferi results in the inefficient control of bacterial burdens in the heart and increased Lyme cardit

216 Fibgamma(Delta5) mice exhibited reduced bacterial burdens in the hearts and kidneys, a blunted h

217 , IFNAR1(-/-) and wild-type mice had similar bacterial burdens in the liver and spleen following food

218 annii exhibit increased survival and reduced bacterial burdens in the liver and spleen.

219 of neutrophils abrogated the differences in bacterial burdens in the livers but not the spleens of C

220 parts, and exhibited significantly increased bacterial burdens in the lung and spleen.

221 TLR9(-/-) mice have significantly increased bacterial burdens in the lungs, as well as decreased pro

222 R9(-/-) mice exhibit significantly increased bacterial burdens in the lungs, increased extrapulmonary

223 e determined the contributions of each AT to bacterial burdens in the lungs, liver, and spleen.

224 e colonized with sfb, as indicated by higher bacterial burdens in the lungs, lung inflammation, and m

225 d to levels in B6 mice, leading to increased bacterial burdens in the spleens of L. monocytogenes-inf

226 nriched blood cultures (5/10; phase II), and bacterial burdens in tissues starting 14 to 21 days post

227 These data indicate that the enhanced bacterial burdens in Tpl2(-/-) mice are not caused prima

228 nt of bacteria in granulomas, and control of bacterial burdens in vivo.

229 ly, depletion of NK/NKT cells also increased bacterial burdens in XID mice.

230 ented bacteria-killing capability (decreased bacterial burden) in neutropenic recipient mice in both

231 matory response to the bacteria, rather than bacterial burden, in a T cell independent manner.

232 NLRC4-dependent regulation of intracellular bacterial burden, inflammasome assembly, pyroptosis, and

233 PcpA was strongly associated with increased bacterial burden, inflammation, and negative regulation

234 Controlling bacterial burden is essential to surviving infection.

235 In agreement with the increased bacterial burden, KO mice showed poorer survival than WT

236 cus pneumoniae via the intranasal route, and bacterial burdens, leukocyte counts, and cytokine levels

237 neumonia was associated with diminished lung bacterial burden, limited innate responses within the lu

238 ed K. pneumoniae-colonized mice to increased bacterial burden, liver abscess and necrosis, and lethal

239 infected with amrZ mutants exhibited reduced bacterial burden, morbidity, and mortality.

240 sessed by corneal imaging, clinical scoring, bacterial burden, neutrophil infiltration, and CXCL2 exp

241 dinal measurements of the dynamic changes in bacterial burden, neutrophil recruitment and bone damage

242 Bacterial burden observed at 24 h was mathematically mod

243 bacterial expansion and explains the higher bacterial burden observed in these mice.

244 Increases in both bacterial persistence and bacterial burden occurred prior to this mutation, and a

245 se biofilm bacteria showed a 100-fold higher bacterial burden of nasal-associated lymphoid tissue in

246 that during wiping they reduced the biofilm bacterial burden of S. aureus (CFU cm(-2)) by three logs

247 Though the bacterial burden of the airway was significantly lower t

248 h exacerbations associated with an increased bacterial burden of the organism.

249 Total postchallenge nasopharyngeal virulent bacterial burden of vaccinated animals was substantially

250 Contusion to soft tissue had no effect on bacterial burden or cytokine response in a mouse model o

251 ic neutralization of IL-17A did not increase bacterial burden or delay bacterial clearance.

252 tion TB, suppression of IDO activity reduced bacterial burden, pathology, and clinical signs of TB di

253 In the absence of IL-18, bacterial burdens persist, eventually triggering other s

254 to determine the effect of contusion on iGAS bacterial burden, phenotype, and host cytokine response.

255 Baseline bacterial burden predicted the rate of decline in lung v

256 Catheter-associated bacterial burdens progressively increased, with maximal

257 ld-type (WT) mice based on assessment of the bacterial burden, recall response, phenotype of recruite

258 T helper-1-type immune responses, decreased bacterial burden, reduced the duration of conventional c

259 n in both dermonecrotic injury and cutaneous bacterial burden relative to controls.

260 ethal dose, at a lethal dose of E. coli, the bacterial burdens remained high in GRK5 KO mice relative

261 tionship was observed between the cumulative bacterial burden score of periodontal disease-related pa

262 The mean bacterial burden (+/-SD) at which granulocyte-mediated k

263 d by an approximately three log reduction in bacterial burdens, significantly diminished clinical man

264 mast cell stabilizer, reduced BALF cells and bacterial burden similar to the levels seen in Wsh mice;

265 d with ID93/SE, as assessed by reductions in bacterial burden, survival, and pathology.

266 TTP was a more sensitive measure of bacterial burden than CFU/mL.

267 rensis infection, with greater mortality and bacterial burden than that of wild-type mice.

268 cells exhibited earlier mortality and higher bacterial burdens than control mice, underexpressed indo

269 MHC II(+/+) cells had lower bacterial burdens than did MHC II(-/-) cells.

270 were more susceptible and exhibited greater bacterial burdens than similarly vaccinated wild-type mi

271 (rolipram and cilomilast) and the impact on bacterial burden, time to clearance, and relapse when ty

272 er levels of plazomicin exposure reduced the bacterial burden to <5 log10 CFU/g, allowing granulocyte

273 e therapeutic effect necessary to reduce the bacterial burden to a level below the half-saturation po

274 tative measures of culturable and cumulative bacterial burden to show that most lung lesions are prob

275 sistant Sdc1(-/-) mice increased the corneal bacterial burden to that of the susceptible WT mice, sug

276 significant effect on the risk of death, but bacterial burden upon diagnosis was higher in patients r

277 of pneumococcal pneumonia and improvement of bacterial burden upon IL-22 administration.

278 r microscopy, and liquid culture to quantify bacterial burden using cycle threshold values, smear gra

279 Total DNA was extracted, bacterial burden was assessed by quantitative PCR, and a

280 on of cells with Mycobacterium tuberculosis, bacterial burden was determined.

281 Bacterial burden was evaluated by enumerating colony-for

282 it/mL) among groups (p=.057), and the lowest bacterial burden was found in endotracheal tubes treated

283 g1(-/-) mice that lack T cells, reduction in bacterial burden was no longer observed.

284 An increased pulmonary bacterial burden was observed in alcohol-intoxicated mic

285 val in the sepsis model, whereas decrease of bacterial burden was observed in the superficial skin an

286 The increased bacterial burden was preceded by reduced CCL2 chemokine

287 Bacterial burden was quantified using both colony-formin

288 The dissemination and bacterial burden were measured after intraperitoneal inf

289 Tissue bacterial burdens were examined by PCR analysis.

290 Elevated bacterial burdens were found in the spleens of middle-ag

291 clinically relevant concentrations; observed bacterial burdens were modeled using 3-dimensional respo

292 mouse model of intranasal infection, similar bacterial burdens were observed after 48 h in the lungs

293 ve blood cultures 14 days post-challenge and bacterial burdens were observed in the lung, liver and/o

294 Whereas bacterial burdens were similar in IRAK-M-deficient and w

295 gene-deficient mice did not exhibit a lower bacterial burden when compared with wild-type mice, alth

296 levels of hepatic fibrin correlate with the bacterial burden, which also correlates with levels of h

297 odentium, Tpl2(-/-) mice experienced greater bacterial burdens with evidence of dissemination to the

298 enes in the two pathways resulted in reduced bacterial burden within DCs.

299 h a single species, despite having a similar bacterial burden within the urinary tract.

300 ns host tissues to become tolerant to a high bacterial burden, without compromising host fitness.