ライフサイエンスコーパス: bacterial burden

1 he outcome of disease, often irrespective of bacterial burden.

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

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

4 sthma harbored significantly lower bronchial bacterial burden.

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

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

7 powerful host defense mechanism that reduces bacterial burden.

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

9 spleens, the main subsets controlling early bacterial burden.

10 ockdown in zebrafish results in an increased bacterial burden.

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

12 is important for inhibiting inflammation and bacterial burden.

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

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

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

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

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

18 in exacerbated lung granuloma pathology and bacterial burden.

19 increased survival, despite having a higher bacterial burden.

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

21 of IL-1beta, IL-6, and IL-12, and increasing bacterial burden.

22 eltafakA mutant is not due to an increase in bacterial burden.

23 idered an indirect assessment of periodontal bacterial burden.

24 ant reductions observed in dermonecrosis and bacterial burden.

25 uced weight loss, systemic inflammation, and bacterial burden.

26 rea, and skin of the chest and arm to assess bacterial burden.

27 k infection, which correlated with increased bacterial burdens.

28 WT-derived macrophages exhibited comparable bacterial burdens.

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

30 nd extensive exfoliation and reduced bladder bacterial burdens.

31 MAIT cell-targeted immunotherapy to control bacterial burdens.

32 ted a significant positive relationship with bacterial burdens.

33 nociceptive neurons significantly increased bacterial burden 10 days postinfection and delayed patho

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

35 tential to offer infected patients with high bacterial burdens a therapeutic hope against infection w

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

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

38 hAAT reduces the bacterial burden after infection.

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

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

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

42 with M. tuberculosis HN878 exhibit increased bacterial burden and are unable to control tissue-damagi

43 filtration in mouse eyes, but, increased the bacterial burden and caused more retinal tissue damage.

44 end our previous report of reduced bronchial bacterial burden and compositional complexity in subject

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

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

47 rs of disease severity, predicting increased bacterial burden and delayed culture conversion in PTB.

48 omarkers of greater disease severity, higher bacterial burden and delayed sputum culture conversion i

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

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

51 balance necessary for granulomas to control bacterial burden and disease pathology in M. tuberculosi

52 p. was associated with a substantial loss in bacterial burden and diversity, particularly in the anae

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

54 Interventions to reduce bacterial burden and EED may improve long-term growth in

55 usions: Key features of the lung microbiome (bacterial burden and enrichment with gut-associated bact

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

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

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

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

60 ced certain proinflammatory gene expression, bacterial burden and Il-22 expression was unaffected.

61 from the probiotic Bacillus subtilis reduces bacterial burden and inflammation during S. aureus blood

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

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

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

65 Increased bacterial burden and pathology was also found in lungs o

66 Bacterial burden and pulmonary immunopathology of chimer

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

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

69 challenge, vaccinated mice exhibited reduced bacterial burden and splenomegaly, along with distinct e

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

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

72 stered nebulized bacteriophages reduced lung bacterial burdens and improved survival of methicillin-r

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

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

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

76 This was consistent with reduced bacterial burdens and more efficient bacterial killing b

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

78 with nonmucoid early CF isolates maintained bacterial burdens and mounted immune responses similar t

79 ine infection results in uniformly high lung bacterial burdens and poorly organized granulomas.

80 dose (50-100 CFU) that correlated with lung bacterial burdens and predicted Mtb infection outcomes a

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

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

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

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

85 t mice, assessment of lipoprotein fractions, bacterial burden, and inflammation in juvenile mice.

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

87 mucus obstruction, MUC5B protein expression, bacterial burden, and neonatal mortality.

88 ate interactions between immune networks and bacterial burden, and to integrate these identified path

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

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

91 9; 95% CI, 1.78-9.41; P = .0011), and higher bacterial burden (aOR, 9.32; 95% CI, 6.30-13.96; P < .00

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

93 een at this time, despite carrying a similar bacterial burden as the liver.

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

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

96 he ID93/GLA-SE vaccine significantly reduced bacterial burden at 16 weeks post-challenge while the BC

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

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

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

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

101 e at day 5 postinfection was interesting, as bacterial burdens began to decline by this point, yet th

102 ody protected mice by significantly reducing bacterial burden both systemically and within reproducti

103 Bacterial burdens, bronchoalveolar lavage fluid (BALF) c

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

105 cline and rifampicin for five days decreased bacterial burden by three log(10) in the liver.

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

107 In a murine infection model using a high bacterial burden, ceftazidime-avibactam-fosfomycin signi

108 Primary predictors were the bacterial burden, community diversity, and community com

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

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

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

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

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

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

115 1 x 10(8) CFU/mouse) and postinfection lung bacterial burden did not appreciably impact the kinetics

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

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

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

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

120 loss and roughly 10-fold-increased systemic bacterial burden during L. monocytogenes-induced enteroc

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

122 The bacterial burden during primary infection was significan

123 a murine septic model of infection to reduce bacterial burden during staphylococcal infection.

124 influenza-infected lung, which increases the bacterial burden during superinfection.

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

126 d that GAS transmission correlated with high bacterial burdens during the acute symptomatic phase of

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

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

129 as effective as female mice at reducing the bacterial burden either with a chronic infection or when

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

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

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

133 ice challenged with Brucella display reduced bacterial burden following infection, but the underlying

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

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

136 Patients with increased lung bacterial burden had fewer ventilator-free days (hazard

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

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

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

140 Bacterial burden, host cytokine response, and histologic

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

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

143 ce development and are effective in reducing bacterial burden in a mouse model of skin MRSA infection

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

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

146 r hours later, control mice developed higher bacterial burden in blood and organs compared with mice

147 Bacterial burden in blood, lung, liver, and spleen was n

148 irway inflammation had a significantly lower bacterial burden in both BALF and lung tissue than did S

149 2 h postinfection, significantly reduced the bacterial burden in both the liver and spleen.

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

151 mice show both reduced weight loss and lower bacterial burden in circulating blood.

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

153 Bacterial burden in hyperglycaemic animals was greater t

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

155 ed in low lipoproteins and decreased hepatic bacterial burden in juvenile mice.

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

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

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

159 At 3 days post S. aureus infection, bacterial burden in lungs, spleen, and kidneys was signi

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

161 pe (WT) and B2m KO mice but failed to reduce bacterial burden in MHC-II KO mice.

162 -1452-NH3 is well tolerated in vivo, reduces bacterial burden in mice and rescues mice from lethal in

163 isingly, these T cells were unable to reduce bacterial burden in mice.

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

165 he antibiotic induces a 3-4 log reduction in bacterial burden in mouse models of peritonitis, pneumon

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

167 In vivo, CD200R deficiency leads to enhanced bacterial burden in neutrophils, suggesting CD200R norma

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

169 Unexpectedly, bacterial burden in prostates challenged with either UPE

170 ted with greater disease severity and higher bacterial burden in PTB.

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

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

173 t significantly reduces splenomegaly and the bacterial burden in spleen and lung tissues.

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

175 -26 decreased inflammation, lung damage, and bacterial burden in the airways by increasing macrophage

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

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

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

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

180 llenge, resulting in significantly decreased bacterial burden in the FRT, accelerated Chlamydia clear

181 present in humans, functioning to reduce the bacterial burden in the gastrointestinal tract while als

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

183 ad greater weight loss, and showed increased bacterial burden in the kidney and peritoneal cavity fol

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

185 tion of Pla results in a decreased Y. pestis bacterial burden in the lung and failure to progress int

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

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

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

189 ticosteroids that permitted higher levels of bacterial burden in the lungs were more likely to have p

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

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

192 Loss of ldh decreased bacterial burden in the nasopharynx and enhanced bactere

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

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

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

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

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

198 ony forming units/mL, respectively), and the bacterial burden in tissues and fluids was lower.

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

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

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

202 f an apramycin-5-O-glycoside in reducing the bacterial burden in vivo.

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

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

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

206 esult was recapitulated in vivo, with higher bacterial burdens in murine tissues when infected with p

207 es a lethal or sublethal infection with high bacterial burdens in peritoneal cavity, blood and tissue

208 th infections influence disease severity and bacterial burdens in TB is not well understood.

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

210 The decreased bacterial burdens in the C5aR2(-/-) mice correlated with

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

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

213 Animal survival correlated with reduced bacterial burdens in the lung (1.2 x 10(6) cfu/g of tiss

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

215 ice, and support reduced pathology and lower bacterial burdens in the lung, spleen, and liver.

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

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

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

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

220 f mucin with iron significantly enhanced the bacterial burdens in the peritoneal cavity and lung.

221 C5aR2(-/-) mice had significantly lower bacterial burdens in the spleens and livers on both day

222 nfection with C. muridarum results in higher bacterial burdens in the upper genital tract at earlier

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

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

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

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

227 ls, neutrophil-depleted mice had higher lung bacterial burdens, increased incidence of bacteremia, an

228 bined B and T cell deficiency did not impact bacterial burden, indicating that B cells only enhance s

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

230 Their survival, bacterial burden, inflammation level, and effectiveness

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

232 Sputum bacterial burden inversely associated with bronchial exp

233 Controlling bacterial burden is essential to surviving infection.

234 ly when the threshold density-the acceptable bacterial burden-is sufficiently high, an effect that ma

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

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

237 e including reduced morbidity and mortality, bacterial burden, maintenance of alveolar macrophages, a

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

239 ce adhesin FnbA contributes to the increased bacterial burden observed in the purR mutant.

240 bergenin treatment significantly reduced the bacterial burden of a multidrug-resistant TB strain.

241 osa lux signals to noninvasively monitor the bacterial burden of both strains.

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

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

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

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

246 We found an association between increasing bacterial burden on the patient and HCP glove or gown co

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

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

249 y and epithelial disruption independently of bacterial burden or toxin expression.

250 Currently most assays require high bacterial burdens or prolonged enrichment to achieve acc

251 Ss+ was also associated with higher bacterial burdens (OR, 7.57; 95% CI, 4.18-14.05; P < .00

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 te of infection that leads to an increase in bacterial burden post- implantation and develops patholo

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

257 In patients with IPF, lung bacterial burden predicts fibrosis progression, and micr

258 fected with a mucoid CF isolate carried high bacterial burdens, produced significantly more interleuk

259 The distinct kinetics of thrombosis and bacterial burden provides a test of the hypothesis that

260 il numbers, had the highest correlation with bacterial burden (r > 0.6), whereas T-helper effector sy

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

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

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

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

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

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

267 entified a strong, negative correlation with bacterial burden, suggesting that C. trachomatis activel

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

269 2) developed larger lesion sizes with higher bacterial burden than mice infected with CA-MRSA (SF8300

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

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

272 targeting Ly6G reverts lung inflammation and bacterial burden to levels comparable to those of WT mic

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

274 ction caused by KP35 is important to control bacterial burden, to prevent lung damage, to modulate cy

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

276 ring influenza infection exhibited increased bacterial burdens upon superinfection with either MRSA o

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

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

279 Bacterial burden was evaluated by enumerating colony-for

280 The bacterial burden was increased in Il2rg (KO/)Tg(+) juven

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

282 Bacterial burden was quantified using both colony-formin

283 The greatest lesion size and bacterial burden was seen with a CC398 strain that produ

284 The host response, rather than the bacterial burden, was the principal determinant of the d

285 infected mice exhibited highly heterogeneous bacterial burdens, well-circumscribed granulomas that sh

286 The dissemination and bacterial burden were measured after intraperitoneal inf

287 reflecting inflammation, tissue injury, and bacterial burden were measured.

288 When bacterial burdens were equivalent in intravaginally and

289 Tissue bacterial burdens were examined by PCR analysis.

290 Elevated bacterial burdens were found in the spleens of CO92 Delt

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

292 Skap2-/- mice had 100-fold higher bacterial burden when compared to wild-type and burden w

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

294 ce (MIIG.TNF-alpha(-/-)) exhibited increased bacterial burdens when compared with MIIG mice.

295 Scnn1b-Tg mice carried higher bacterial burdens when infected with biofilm-grown rathe

296 nts precede vaccine-induced reduction of the bacterial burden, which occurs only after the colocaliza

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

298 with IPF have altered lung microbiota, with bacterial burden within the lungs associated with mortal

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.