ライフサイエンスコーパス: bacterial killing

1 sulting in increased apoptosis and defective bacterial killing.

2 ereby leading to increased degranulation and bacterial killing.

3 t severely pneumonic mice, despite effective bacterial killing.

4 nt of concentrations associated with maximal bacterial killing.

5 on of IGF-1, whereas IGF-1 blockade worsened bacterial killing.

6 ndent oxidant generation, degranulation, and bacterial killing.

7 bacteria to determine the effect of IGF-1 on bacterial killing.

8 -1alpha inhibited NET-mediated extracellular bacterial killing.

9 sinophils achieve an efficient extracellular bacterial killing.

10 bind via Fab, facilitating opsonization and bacterial killing.

11 tophagy degradation, accompanied by enhanced bacterial killing.

12 ytic activity against H. ducreyi and similar bacterial killing.

13 ed in decreased IFN-gamma induction and poor bacterial killing.

14 t were unable to compensate for the impaired bacterial killing.

15 te mediates the stressor-induced increase in bacterial killing.

16 Lack of CFTR reduces bacterial killing.

17 equences on the mucosal barrier and invasive bacterial killing.

18 IL-12 and IFN-gamma production and improved bacterial killing.

19 /(-) neutrophils show impaired intracellular bacterial killing.

20 nced phagocytosis and NADPH oxidase-mediated bacterial killing.

21 is an effector mechanism for WP1130-mediated bacterial killing.

22 us may inhibit CXCR2-independent pathways of bacterial killing.

23 t neutrophils were impaired in intracellular bacterial killing.

24 translation, causes apoptosis, and restricts bacterial killing.

25 lar machinery responsible for the control of bacterial killing.

26 rectly binds to NOD2 to inhibit NOD2-induced bacterial killing.

27 a conserved "EPN" motif that is critical for bacterial killing.

28 NETs instead of increasing histone-mediated bacterial killing.

29 n species production during phagocytosis and bacterial killing.

30 promoted WT but not REG3gamma-deficient IEC bacterial killing.

31 iously unrecognized deficit in extracellular bacterial killing.

32 protein translocation early in the course of bacterial killing.

33 sential to the production of lactoferrin and bacterial killing.

34 gamma production in macrophages and mediated bacterial killing.

35 vitro, whereas db/db blood was defective in bacterial killing.

36 le heparan sulfate proteoglycans and impairs bacterial killing.

37 on in the small intestine, thereby enhancing bacterial killing.

38 on, alveolar neutrophil emigration, and lung bacterial killing.

39 ed no protection against complement-mediated bacterial killing.

40 ining p40(phox) as an essential component in bacterial killing.

41 le associated with macrophage activation and bacterial killing.

42 onses to PMA or opsonized zymosan and normal bacterial killing.

43 ing their ability to generate superoxide for bacterial killing.

44 polymerization, inhibited leukocyte-specific bacterial killing.

45 mission by a mechanism that does not require bacterial killing.

46 and C meningococci, which leads to increased bacterial killing.

47 s, which was mirrored by a small decrease in bacterial killing.

48 ation, actin polymerization, chemotaxis, and bacterial killing.

49 tinuous bacterial multiplication balanced by bacterial killing.

50 ell aggregation, motility, invasiveness, and bacterial killing.

51 t sufficient, for the observed efficiency of bacterial killing.

52 presence of cath is necessary for efficient bacterial killing.

53 ies alone was found to be not sufficient for bacterial killing.

54 nt degradation of membrane phospholipids and bacterial killing.

55 hlorination by normal neutrophils paralleled bacterial killing.

56 ive chemotaxis, adherence, phagocytosis, and bacterial killing.

57 associated with successful phagocytosis and bacterial killing.

58 at neither compound is sufficient to mediate bacterial killing.

59 factors predicted to influence intracellular bacterial killing.

60 of membrane phospholipids (PL) required for bacterial killing.

61 egulation of oxidant production important in bacterial killing.

62 was sufficient to be solely responsible for bacterial killing.

63 den, and host macrophages use Cu to increase bacterial killing.

64 veal several essential steps in PGRP-induced bacterial killing.

65 lenge, in keeping with reduced intracellular bacterial killing.

66 species production and results in increased bacterial killing.

67 selective reduction of delayed intracellular bacterial killing.

68 on, allowing for phagosome acidification and bacterial killing.

69 ins, potentially explaining one mechanism of bacterial killing.

70 with bacteria and phagolysosomes to enhance bacterial killing.

71 however, this response did not contribute to bacterial killing.

72 bacterial resistance to neutrophil-mediated bacterial killing.

73 endent and -independent resistance to innate bacterial killing.

74 owed inactivation of daptomycin and enhanced bacterial killing.

75 (PGE2), and exhibit defective intracellular bacterial killing.

76 dual accumulation of colistin resulted in no bacterial killing.

77 tor-mediated enhancements in degradation and bacterial killing.

78 nted hypercapnic inhibition of autophagy and bacterial killing.

79 ctivated Salmonella-infected macrophages for bacterial killing.

80 t, suggesting Die-P phagocytes have impaired bacterial killing.

81 G2b, but not IgM, resulted in cell-dependent bacterial killing.

82 radative enzymes, ultimately contributing to bacterial killing.

83 1-T6SS co-regulated vgrG genes, vgrG1abc, to bacterial killing.

84 changed this interaction, inducing efficient bacterial killing.

85 protein 3 (NALP3) inflammasome, intensifying bacterial killing.

86 s above 1 mg/L within 1 h caused significant bacterial killing (~5 log10CFU/mL), while the gradual ac

87 oxygen species production during phagocytic bacterial killing, a process also known as oxidative bur

88 Good synergism between the bacterial killing activities of hepcidin and moronecidin

89 plasmid, the CapsidCas13a(s) exhibit strong bacterial killing activities upon recognizing target gen

90 revealed impaired phagocytosis and defective bacterial killing activities.

91 , we found that citrullination decreased the bacterial killing activity of histones and nucleosomes,

92 Despite the potent bacterial killing activity of HOCl, individuals who fail

93 red in ordered complexes while retaining its bacterial killing activity.

94 l extra-cellular trap (NET), and compromised bacterial killing activity.

95 the rate and extent of PL degradation and/or bacterial killing after addition of PLA2.

96 ection model, col-aaPEG displayed acceptable bacterial killing against P. aeruginosa ATCC 27853 and n

97 infection through regulation of PMN number, bacterial killing and balancing pro- and anti-inflammato

98 The bacterial killing and clearance capabilities observed in

99 pecifically target HDP induction, facilitate bacterial killing and disrupt the UPEC infection cycle.

100 environments, our model fits the kinetics of bacterial killing and gives similar lower limits (CNCs)

101 ine protease that plays an important role in bacterial killing and immune regulation.

102 erse immune functions, including both direct bacterial killing and immunomodulatory effects.

103 howed faster monocyte recruitment, increased bacterial killing and improved healing upon a secondary

104 It is involved in bacterial killing and in the delivery of three toxins, T

105 CF macrophages exhibit reduced bacterial killing and increased inflammatory signaling.

106 ontact lenses, to rabbit corneas resulted in bacterial killing and limited inflammation.

107 o explore the capacity of PGI(2) to regulate bacterial killing and phagocytosis in macrophages, and o

108 Our results suggest that vimentin impedes bacterial killing and production of ROS, thereby contrib

109 Under these conditions, IFN-gamma decreased bacterial killing and promoted the production of monocyt

110 We developed a 96-well-based bacterial killing and protease inactivation assay that d

111 ammation, and were associated with increased bacterial killing and reduced bacteremia, in part throug

112 ear cells from patients with sepsis enhanced bacterial killing and respiratory burst.

113 Treatment with recombinant IL-6 enhanced bacterial killing and resulted in the control of wound i

114 O production using iNOS inhibitors decreases bacterial killing and shifts the cell death program from

115 ammatory cytokines and had reduced levels of bacterial killing and T-cell activation than cells from

116 l control, suggesting that a balance between bacterial killing and tissue damage is required for surv

117 ophils to the corneal stroma, and subsequent bacterial killing and tissue damage.

118 ning how inflammasomes mediate intracellular bacterial-killing and clearance in host macrophages rema

119 NOs and beta-defensin-2 production, impaired bacterial killing, and a susceptible phenotype.

120 otype and levels of lysosomal acidification, bacterial killing, and agonist-induced secretory respons

121 ncluding phagocyte stimulation and response, bacterial killing, and apoptosis.

122 Treprostinil inhibited phagocytosis, bacterial killing, and cytokine generation in AMs to a m

123 ure significantly reduced phagocyte-mediated bacterial killing, and exposure to high temperatures inc

124 properties, such as migration, phagocytosis, bacterial killing, and formation of reactive oxygen spec

125 is, neutrophil extracellular trap formation, bacterial killing, and induction of apoptosis.

126 prostinil on the regulation of phagocytosis, bacterial killing, and inflammatory mediator production

127 and LC3, stimulation of autophagy increases bacterial killing, and inhibition of autophagy increases

128 utrophils and cytokines, alveolar macrophage bacterial killing, and leukotriene B(4) synthesis.

129 ished alveolar macrophage (AM) phagocytosis, bacterial killing, and production of TNF-alpha and cyste

130 veolar macrophages to CF BAL fluid decreased bacterial killing, and this was reversed by the addition

131 nd -DR, and CXCR2, chemotaxis, phagocytosis, bacterial killing, and tumor necrosis factor-alpha/inter

132 Lys appear to have optimal chain lengths for bacterial killing as shortening Lys or lengthening Arg i

133 exhibit no defects in cytokine production or bacterial killing as was observed in SLAM-/- macrophages

134 ted only with inadequate alveolar macrophage bacterial killing, as indicated by significantly decreas

135 stinal epithelial cells were evaluated using bacterial killing assays and transwell experiments, resp

136 ovel explanation of the defect in neutrophil bacterial killing associated with vascular prosthetic gr

137 ice, suggesting CR3-dependent differences in bacterial killing between sexes.

138 In contrast, IL-17A promoted bacterial killing but did not affect MCP-1 production.

139 host defense against pathogens by promoting bacterial killing, but also as signaling agents coordina

140 phil and macrophage product, is important in bacterial killing, but also drives inflammatory reaction

141 ges to extracellular ATP (ATP(e)) results in bacterial killing, but the molecular mechanisms remain i

142 gnificantly (P<0.05) decreased intracellular bacterial killing by a mouse alveolar macrophage cell li

143 significantly increased capacity to mediate bacterial killing by abundant production of reactive oxy

144 st to GINs but similar to PBNs, the enhanced bacterial killing by AINs accompanied both better granul

145 that ACs suppress in vitro phagocytosis and bacterial killing by alveolar macrophages and that this

146 eroxide and hydrogen peroxide production and bacterial killing by alveolar macrophages.

147 n also decreased PGE2-induced suppression of bacterial killing by AMs.

148 41C change results in longer time needed for bacterial killing by antibiotic treatment and shows evid

149 (A549) cells, thus increasing the extent of bacterial killing by antibiotics.

150 ss or cognitive impairment, despite adequate bacterial killing by antibiotics.

151 ncreased bacterial replication and decreased bacterial killing by antimicrobial peptides.

152 We found a significant decrease in bacterial killing by CF alveolar macrophages compared wi

153 membrane is a key factor in the mechanism of bacterial killing by CM15.

154 Enhanced bacterial killing by CPPD-induced NETs demonstrates thei

155 As judged from flow cytometric assays, bacterial killing by GA occurred within minutes.

156 aenoic acid impairs superoxide formation and bacterial killing by immune cells.

157 Chi3l1 augments macrophage bacterial killing by inhibiting caspase-1-dependent macr

158 erial genes, the esx-3 region, in evasion of bacterial killing by innate immunity.

159 reactive species is thought to contribute to bacterial killing by interaction with diverse targets an

160 H(2)S-producing enzymes were used to assess bacterial killing by leukocytes.

161 cement of FcgammaR-mediated phagocytosis and bacterial killing by LTB(4) was also PTX-sensitive, wher

162 reduced bacterial burdens and more efficient bacterial killing by Ly6B.2(+) myeloid cells and macroph

163 P2X7R signaling protects through enhancing bacterial killing by macrophages, which is independent o

164 bacteria, acting in part via a modulation of bacterial killing by macrophages.

165 p53 inhibition boosts bacterial killing by mouse neutrophils and oxidant gener

166 MgrA, which in turn leads to a reduction in bacterial killing by moxifloxacin, a substrate of the No

167 Bacterial killing by MSC was found to be mediated in par

168 findings define a mechanism of nonoxidative bacterial killing by NE and point to OmpA as a bacterial

169 cubation with bacteria, and are deficient in bacterial killing by NETs.

170 es adhesion and biofilm formation, decreases bacterial killing by neutrophil extracellular traps, and

171 owed previously that the competition between bacterial killing by neutrophils and bacterial growth in

172 f reactive oxygen species, and intracellular bacterial killing by neutrophils remains intact.

173 cterial growth) and a second-order reaction (bacterial killing by neutrophils).

174 ied production of IL-6, which promotes rapid bacterial killing by neutrophils.

175 mediated methionine oxidation contributes to bacterial killing by neutrophils.

176 n system (T6SS), and prevents T6SS-dependent bacterial killing by P. aeruginosa.

177 nd kills Gram-negative bacteria and supports bacterial killing by phagocytes.

178 ggests that this protein may be a target for bacterial killing by phagocytes.

179 shown that B. parapertussis is able to avoid bacterial killing by polymorphonuclear leukocytes (PMN)

180 tudy, we tested whether PGE(2) could inhibit bacterial killing by polymorphonuclear neutrophils (PMN)

181 Of note, this binding was required for bacterial killing by sphingosine, as revealed by genetic

182 rmed cariogenic biofilms, markedly enhancing bacterial killing by the antimicrobial agent (3-log incr

183 sic molecular insights into MAC assembly and bacterial killing by the immune system.

184 These include enhancing bacterial killing by the innate immune system.

185 h both P2 and Crp4 target the cell envelope, bacterial killing by these peptides appears to occur by

186 uginosa with rMIF is associated with reduced bacterial killing by tobramycin.

187 activity and apoptosis in vivo and increased bacterial killing by treated cells.

188 In the presence of erythrocytes, bacterial killing by VPO1 is slightly reduced.

189 trary to Cas9-based antimicrobials that lack bacterial killing capacity when the target genes are loc

190 articipates in phagosomal pH control and has bacterial killing capacity.

191 ion, indicating that the initial step of the bacterial killing cascade proceeds through LPS-mediated

192 y consolidation while maintaining equivalent bacterial killing compared to WT mice.

193 to acidify, and the cells were deficient in bacterial killing compared with wild type controls.

194 atalase in mitochondria results in defective bacterial killing, confirming the role of mROS in bacter

195 us density, hyperinflammation, and defective bacterial killing could all cause P. aeruginosa to grow

196 ction in patients with CF, and that assaying bacterial killing could report on the benefit of therape

197 r magnetic resonance spectroscopy as well as bacterial killing curves against Pseudomonas aeruginosa

198 Bacterial killing defects in HO-1-deficient murine macro

199 that both donor-derived AMs and PMNs display bacterial killing defects post-BMT.

200 Bacterial killing depended on exosome structural integri

201 The rate of bacterial killing depended on the concentration of neutr

202 under some conditions, altered on subsequent bacterial killing, depending on the mode of killing.

203 vated glucose, which together with defective bacterial killing due to aberrant HCO3(-) transport and

204 2] and epidermal growth factor [EGF]) and/or bacterial killing (e.g., inducible nitric oxide synthase

205 the CaM/iNOS complex that promotes effective bacterial killing following infection by Salmonella typh

206 imental to bacterial survival such as direct bacterial killing, generation of antimicrobial peptides,

207 wn to evade host-specific IFN-gamma-mediated bacterial killing; however, IFN-gamma-deficient mice exh

208 ecule compound (AVE3085) enhanced macrophage bacterial killing, improved bacterial clearance, and inc

209 1599 and clarithromycin provided additional bacterial killing in a mouse model of acute tuberculosis

210 lving defective phagosomal acidification and bacterial killing in alveolar macrophages.

211 echanisms, such as mucociliary clearance and bacterial killing in CF airways.

212 of host cells, but the importance of direct bacterial killing in controlling in vivo infection remai

213 a-stimulated chemotaxis are required for PMN bacterial killing in fibrin gels, and that fMLP inhibits

214 Defective bacterial killing in IFN-gamma-activated LRG-47-/- macro

215 eloperoxidase, H(2)O(2,) RNS production, and bacterial killing in K. pneumoniae-infected CXCL1(-/-) n

216 nced proinflammatory cytokine expression and bacterial killing in macrophages and boosted protection

217 he deubiquitinase inhibitor WP1130 increases bacterial killing in macrophages by enhancing iNOS local

218 e NALP3 inflammasome, as CO did not increase bacterial killing in macrophages isolated from NALP3-def

219 Rac1, thereby leading to ROS production and bacterial killing in macrophages.

220 ynthesis and PGE2 receptor blockade enhanced bacterial killing in Mphis.

221 ng, phagosomal maturation, and intracellular bacterial killing in neutrophils.

222 This serum also induced bacterial killing in opsonophagocytosis assays, suggesti

223 expressing macrophages, thus promoting early bacterial killing in pneumococcal pneumonia.

224 rate that MDP fails to enhance intracellular bacterial killing in SAMP mice.

225 ammation but likely contributes to decreased bacterial killing in the cornea.

226 -1 are essential for IL-1beta production and bacterial killing in the cornea.

227 epithelial cells of transgenic mice enhanced bacterial killing in the lung in vivo, and was associate

228 ole and mechanism of AM apoptosis-associated bacterial killing in the lung.

229 t production likely contributes to effective bacterial killing in the lungs of SP-D-/- mice.

230 phage proinflammatory cytokine secretion and bacterial killing in vitro in a PGE2-dependent manner vi

231 ase activity of lysozyme is not required for bacterial killing in vitro or in vivo.

232 se activity) of lysozyme is not required for bacterial killing in vivo.

233 Reducing ASL pH diminished bacterial killing in wild-type pigs, and, conversely, in

234 ranule mobilization, resulting in inadequate bacterial killing, in particular, of gram-negative Esche

235 augment periodontal treatment by increasing bacterial killing, inactivating bacterial virulence fact

236 D was able to inhibit innate immune-mediated bacterial killing independently of other S. aureus prote

237 We show that bacterial killing is dependent upon the presence of gamm

238 tested the hypothesis that stressor-enhanced bacterial killing is due to increases in the production

239 than wild-type mice to lung infections, and bacterial killing is enhanced in transgenic mice overexp

240 Rapid oxidative bacterial killing is followed by a sustained period of n

241 One correlate of bacterial killing is the fusion of phagosomes with lysos

242 Anti-inflammatory strategies that impair bacterial killing may be helpful in cases in which antib

243 This impairment of bacterial killing may contribute to the apparent suscept

244 1 ectodomains to inhibit neutrophil-mediated bacterial killing mechanisms in an HS-dependent manner t

245 ction of FPR2, reduced potential to generate bacterial-killing neutrophil extra-cellular trap (NET),

246 not mediated by their contribution to direct bacterial killing, nor by increased neutrophil recruitme

247 Deposition of iC3b and C5b-9 and bacterial killing occurred when bacteria were treated wi

248 nsified focus on dosage regimens targeted at bacterial killing of both the fully susceptible bacteria

249 organisms including Pseudomonas aeruginosa; bacterial killing of LL-37 was sensitive to NaCl and was

250 istance to hydrogen peroxide and accelerated bacterial killing of macrophages.

251 oglitazone) showed enhanced phagocytosis and bacterial killing of PAO1.

252 gen species production (26 to 71% increase), bacterial killing of these periodontal pathogens (22 to

253 Conventional antibiotics typically target bacterial killing or growth inhibition, resulting in str

254 nanostructured surfaces and bacteria lead to bacterial killing or prevention of bacterial attachment

255 defects in mucosal barrier function, innate bacterial killing, or immunoregulation.

256 found that neutrophil functions involved in bacterial killing, other than NETosis, remained intact.

257 nitude of the inflammatory response, reduced bacterial killing (p < 0.05), reduced early myeloid cell

258 here k is the second-order rate constant for bacterial killing, p is the neutrophil concentration, g

259 /3-deficient neutrophils demonstrated intact bacterial killing, phagocytosis, and chemotaxis; however

260 am-negative bacterial pathogens, facilitates bacterial killing, promotes activation of the lipid A se

261 lammatory cytokines but also accelerates the bacterial killing rate.

262 on of proinflammatory cytokines, but not the bacterial killing rate.

263 ed to study multiple bactericidal processes: bacterial killing, reactive oxygen species (ROS) generat

264 associated lymphoid tissue and correlates of bacterial killing, reduced checkpoint signaling, and the

265 Mast cells required TLR2 for effective bacterial killing, regulation of the hydrolytic enzyme c

266 The late phase of bacterial killing required both caspase-induced generati

267 he site of infection, and ex vivo phagocytic bacterial killing required expression of the NOD1 signal

268 acity to form bactericidal pores; therefore, bacterial killing requires both in situ conversion of C5

269 neutrophils, a critical oxidant involved in bacterial killing, requires chloride anions.

270 al crystal structures, binding analyses, and bacterial killing studies of inhibitors that target both

271 nd some early defense mechanisms involved in bacterial killing, such as the complement system, can al

272 Silencing of ATP7A expression attenuated bacterial killing, suggesting a role for ATP7A-dependent

273 Purified VPO1 and VPO1 in plasma mediate bacterial killing that is dependent on chloride and H(2)

274 vation of phox by phorbol ester or bacteria, bacterial killing, TNF-induced granule exocytosis and ph

275 increase of LL-37 was sufficient to restore bacterial killing to normal levels.

276 ant catabolism, cell adhesion, phagocytosis, bacterial killing, Toll-receptor signaling, and expressi

277 irpin RNA reduces ROS production and impairs bacterial killing under conditions where p67(phox) level

278 o a proposed mechanism of membrane lysis and bacterial killing via an ion channel activity of CecA.

279 ection, TB granulomas are often hypoxic, and bacterial killing via NOS2 in these conditions is likely

280 idal activity was indicated by the fact that bacterial killing was abrogated by the NADPH oxidase inh

281 by NETs was visualized microscopically, and bacterial killing was assessed by bacterial culture.

282 In SP-D-/- mice, bacterial killing was associated with increased lung inf

283 In contrast, in the absence of SP-A, bacterial killing was decreased and associated with incr

284 Complete bacterial killing was demonstrated at approximately 5 mi

285 Bacterial killing was dependent on IL-6 released from MC

286 Bacterial killing was dependent on the presence of IFN-g

287 intratracheal infection with K. pneumoniae, bacterial killing was enhanced 9-fold in lysozyme(tg) mi

288 No apparent defect in phagocytosis or bacterial killing was found.

289 Intracellular bacterial killing was markedly impaired in MUNC13-4 KO n

290 However, a small but significant decrease in bacterial killing was observed in lungs of homozygote SP

291 stically significant increase (P = 0.036) in bacterial killing was observed in the cimetidine rinse g

292 Protein chlorination associated with bacterial killing was unaffected by the presence of nitr

293 ar ROS status is pivotal to inflammation and bacterial killing, we determined the role of DJ-1 in bac

294 itric oxide (NO) and superoxide (O(2)(-)) in bacterial killing, were reexamined in cell-free radical-

295 in the airspaces of transgenic mice enhanced bacterial killing whereas lysozyme deficiency resulted i

296 cells appear to have a greater capacity for bacterial killing, which may contribute to control of ba

297 PMN effector functions, leading to decreased bacterial killing, which may contribute to the innate su

298 s really efficient in enhancing PMN-mediated bacterial killing, while topical administration of such

299 lar polysaccharide transport, enabled potent bacterial killing with antiserum.

300 veal DJ-1 impairs optimal ROS production for bacterial killing with important implications for host s