ライフサイエンスコーパス: bacterial killing

1 sinophils achieve an efficient extracellular bacterial killing.

2 bind via Fab, facilitating opsonization and bacterial killing.

3 tophagy degradation, accompanied by enhanced bacterial killing.

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

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

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

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

8 Lack of CFTR reduces bacterial killing.

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

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

11 nced phagocytosis and NADPH oxidase-mediated bacterial killing.

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

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

14 t neutrophils were impaired in intracellular bacterial killing.

15 translation, causes apoptosis, and restricts bacterial killing.

16 with bacteria and phagolysosomes to enhance bacterial killing.

17 lar machinery responsible for the control of bacterial killing.

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

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

20 NETs instead of increasing histone-mediated bacterial killing.

21 n species production during phagocytosis and bacterial killing.

22 iously unrecognized deficit in extracellular bacterial killing.

23 protein translocation early in the course of bacterial killing.

24 sential to the production of lactoferrin and bacterial killing.

25 gamma production in macrophages and mediated bacterial killing.

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

27 le heparan sulfate proteoglycans and impairs bacterial killing.

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

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

30 ed no protection against complement-mediated bacterial killing.

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

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

33 le associated with macrophage activation and bacterial killing.

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

35 ing their ability to generate superoxide for bacterial killing.

36 polymerization, inhibited leukocyte-specific bacterial killing.

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

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

39 endent and -independent resistance to innate bacterial killing.

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

41 tinuous bacterial multiplication balanced by bacterial killing.

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

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

44 presence of cath is necessary for efficient bacterial killing.

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

46 nt degradation of membrane phospholipids and bacterial killing.

47 hlorination by normal neutrophils paralleled bacterial killing.

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

49 associated with successful phagocytosis and bacterial killing.

50 at neither compound is sufficient to mediate bacterial killing.

51 factors predicted to influence intracellular bacterial killing.

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

53 egulation of oxidant production important in bacterial killing.

54 owed inactivation of daptomycin and enhanced bacterial killing.

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

56 from the liver accurately parallels hepatic bacterial killing.

57 dual accumulation of colistin resulted in no bacterial killing.

58 tor-mediated enhancements in degradation and bacterial killing.

59 nted hypercapnic inhibition of autophagy and bacterial killing.

60 ctivated Salmonella-infected macrophages for bacterial killing.

61 lenge, in keeping with reduced intracellular bacterial killing.

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

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

64 radative enzymes, ultimately contributing to bacterial killing.

65 species production and results in increased bacterial killing.

66 1-T6SS co-regulated vgrG genes, vgrG1abc, to bacterial killing.

67 changed this interaction, inducing efficient bacterial killing.

68 selective reduction of delayed intracellular bacterial killing.

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

70 sulting in increased apoptosis and defective bacterial killing.

71 ereby leading to increased degranulation and bacterial killing.

72 t severely pneumonic mice, despite effective bacterial killing.

73 nt of concentrations associated with maximal bacterial killing.

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

75 ndent oxidant generation, degranulation, and bacterial killing.

76 on, allowing for phagosome acidification and bacterial killing.

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

78 -1alpha inhibited NET-mediated extracellular bacterial killing.

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

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

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

82 revealed impaired phagocytosis and defective bacterial killing activities.

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

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

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

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

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

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

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

90 The bacterial killing and clearance capabilities observed in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 zed roles of neutrophils in phagocytosis, in bacterial killing, and in mediating the inflammatory res

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

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

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

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

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

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

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

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

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

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

124 tions of paromomycin, using an intracellular bacterial killing assay, and found that C. parvum infect

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 Enhanced bacterial killing by CPPD-induced NETs demonstrates thei

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

160 mediated methionine oxidation contributes to bacterial killing by neutrophils.

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

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

163 Bacterial killing by PLA2 requires Ca2+ and catalytic ac

164 Bacterial killing by PMN extracts was substantially inhi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 Bacterial killing depended on exosome structural integri

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

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

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

183 2] and epidermal growth factor [EGF]) and/or bacterial killing (e.g., inducible nitric oxide synthase

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

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

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

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

188 ainst Escherichia coli, caused three logs of bacterial killing in 4 hours, and cured mice infected wi

189 1599 and clarithromycin provided additional bacterial killing in a mouse model of acute tuberculosis

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

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

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

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

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

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

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

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

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

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

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

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

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

203 -1 are essential for IL-1beta production and bacterial killing in the cornea.

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

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

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

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

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

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

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

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

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

213 e coincubated with diluted (4%) human blood, bacterial killing-induced total IL-6 release was signifi

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

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

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

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

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

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

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

221 1 ectodomains to inhibit neutrophil-mediated bacterial killing mechanisms in an HS-dependent manner t

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

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

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

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

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

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

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

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

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

231 ith C7- or C9-depleted serum did not enhance bacterial killing or PL degradation during phagocytosis

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

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

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

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

236 /3-deficient neutrophils demonstrated intact bacterial killing, phagocytosis, and chemotaxis; however

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

238 lammatory cytokines but also accelerates the bacterial killing rate.

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

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

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

242 However, because bacterial killing required a low NaCl concentration and

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

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

245 However, imipenem-induced bacterial killing resulted in significantly less IL-6 re

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

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

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

249 e kinetics of phagosome- lysosome fusion and bacterial killing suggests that a nonlysosomal mechanism

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

251 basis for the previously described defect in bacterial killing that is present in the cystic fibrosis

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

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

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

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

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

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

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

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

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

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

262 Complete bacterial killing was demonstrated at approximately 5 mi

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

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

265 ATP-mediated bacterial killing was independent of reactive nitrogen a

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

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

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

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

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

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

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

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

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