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1                                              K. pneumoniae can evade serum killing and phagocytosis p
2                                              K. pneumoniae challenge resulted in significantly increa
3                                              K. pneumoniae has become a common pathogen of monomicrob
4                                              K. pneumoniae infection of mice lacking Nlrp3 results in
5                                              K. pneumoniae infection of STAT6 knockout mice resulted
6                                              K. pneumoniae is ubiquitous in the environment and can c
7                                              K. pneumoniae may establish these infections in vivo fol
8                                              K. pneumoniae must acquire iron to replicate, and it uti
9                                              K. pneumoniae were confirmed to belong to the same clone
10                                    Of the 15 K. pneumoniae strains detected in the study, four were d
11 teristics of four infections caused by KPC-3 K. pneumoniae strains.
12                              A total of 3846 K. pneumoniae cultures were identified, with an overall
13 ta-lactamase-producing clinical isolates (39 K. pneumoniae and 30 K. oxytoca isolates).
14 d recovery from infection with each of the 5 K. pneumoniae strains, revealing a contribution of these
15  with abscesses caused by community-acquired K. pneumoniae in the kidneys and spleen without liver in
16  neutrophil recruitment in response to acute K. pneumoniae infection and thereby increases the lung K
17                                 In addition, K. pneumoniae-induced late NF-kappaB activation and phos
18 inetobacter spp., C. freundii, E. aerogenes, K. pneumoniae, P. aeruginosa, and S. marcescens) became
19 resistance to bacterial dissemination, after K. pneumoniae infection or cecal ligation and puncture s
20 ntratracheal rG-CSF to MCP-1(-/-) mice after K. pneumoniae infection rescued survival, bacterial clea
21  CRAMP exerted bactericidal activity against K. pneumoniae in vitro.
22 howed potent bacteriostatic activity against K. pneumoniae, which was dependent on lipocalin 2 (LCN2)
23 ch to identify protective antibodies against K. pneumoniae Several monoclonal antibodies were isolate
24  underlying KC-mediated host defense against K. pneumoniae have not been explored.
25 to the role of NLRC4 in host defense against K. pneumoniae infection.
26 ctive role of Mincle in host defense against K. pneumoniae pneumonia by coordinating bacterial cleara
27 nt cells contributes to host defense against K. pneumoniae.
28 wever, polymyxin B MICs are elevated against K. pneumoniae isolates with increasing frequency, leavin
29  CCL8 in lung antibacterial immunity against K. pneumoniae and suggest new mechanisms of orchestratin
30 hils and in regulating host immunity against K. pneumoniae infection.
31 nd SP-B(N) conferred more protection against K. pneumoniae infection than each protein individually.
32 nge conferred significant protection against K. pneumoniae infection.
33 bacteriovorus acting therapeutically against K. pneumoniae in serum, informing future research into t
34                                          All K. pneumoniae strains tested positive for K. pneumoniae
35 ent in spectra from retrospectively analyzed K. pneumoniae outbreak isolates, concordant with results
36  most common pathogens were GAS (n = 16) and K. pneumoniae (n = 15).
37     The CFU of recoverable P. aeruginosa and K. pneumoniae isolates were decreased, but the biofilm b
38 s or decreasing the CFU of P. aeruginosa and K. pneumoniae within a biofilm.
39 us collection of 196 isolates of E. coli and K. pneumoniae (PRIMERS II) were examined.
40 1-producing E. coli in blood and E. coli and K. pneumoniae in rectal specimens, both containing the s
41 tamase (ESBL)-producing Escherichia coli and K. pneumoniae isolates using MinION allowed successful i
42 ce variation between the FimH of E. coli and K. pneumoniae results in significant differences in func
43 d sisomicin suppressed growth of E. coli and K. pneumoniae, with N1MS exhibiting superior activity ag
44 tment to the airspace in response to LPS and K. pneumoniae by impairing both chemokine induction in t
45  cytokine expression induced by both LPS and K. pneumoniae.
46 rum amyloid A2 (SAA2) and that SAA2 had anti-K. pneumoniae bactericidal activity in vitro.
47  candidate target in the development of anti-K. pneumoniae drugs.
48 he resurgence of severe community-associated K. pneumoniae infections has led to increased recognitio
49                    Analysis of the available K. pneumoniae genomes revealed that this pathogen's geno
50 KC in bone marrow-derived macrophages before K. pneumoniae challenge decreases bacteria-induced produ
51          Neutrophil depletion in mice before K. pneumoniae infection reveals no differences in the pr
52 omparisons have revealed differences between K. pneumoniae strains, but the impact of genomic variabi
53 eceptor Mincle in pneumonic sepsis caused by K. pneumoniae.
54 th care environment, patient colonization by K. pneumoniae precedes infection, and transmission via c
55 ibility to acute intrapulmonary infection by K. pneumoniae, regardless of strain.
56 ates from a collection of well-characterized K. pneumoniae and E. coli strains and salvage rectal swa
57                                     We chose K. pneumoniae for our in vivo model, since K. pneumoniae
58 ive) were compared with those of the classic K. pneumoniae (cKP) isolates.
59 rains are an emerging variant of "classical" K. pneumoniae (cKP) that cause organ and life-threatenin
60                       A total of 46 clinical K. pneumoniae isolates with KPC genotypes, all modified
61 e 43816 strain and 4 newly isolated clinical K. pneumoniae strains.
62                                 The clinical K. pneumoniae strains, including one carbapenem-resistan
63 for bacteria including E. faecalis, E. coli, K. pneumoniae and S. aureus.
64  100 genome copies of A. baumannii, E. coli, K. pneumoniae, and P. aeruginosa.
65 ae to human clinical infections, we compared K. pneumoniae isolates from retail meat products and hum
66 d-type, magA-deficient, or magA-complemented K. pneumoniae into the posterior segments of mouse eyes.
67 vascular-magnitude fluid dynamic conditions, K. pneumoniae spontaneously develops into multicellular
68                           These data confirm K. pneumoniae colonization is a significant risk factor
69           Of note, 25/26 cultures containing K. pneumoniae that were reported as not detected by the
70                                 In contrast, K. pneumoniae-infected Rag2(-/-)Il2rg(-/-) mice failed t
71              pal-, lppA-, and ompA-deficient K. pneumoniae strains were constructed using an unmarked
72 mans can become infected with many different K. pneumoniae strains that vary in genetic background, a
73 e specific than (18)F-FDG in differentiating K. pneumoniae lung infection from lung inflammation.
74 erum sensitivity and virulence of 3 distinct K. pneumoniae (hypermucoviscous K1, research K2, and car
75                                       During K. pneumoniae infection, we observed subtle differences
76  in neutrophil-mediated host immunity during K. pneumoniae pneumonia and illustrate that G-CSF could
77 rophil influx into the alveolar space during K. pneumoniae infection was delayed early but increased
78 ndent mechanism critical for survival during K. pneumoniae bacteremia.
79          NDM-1-producing Enterobacteriaceae (K. pneumoniae and Escherichia coli) were clinically and
80 zation by vancomycin-resistant Enterococcus, K. pneumoniae, and E. coli.
81 henotype in the pathogenesis of experimental K. pneumoniae endophthalmitis.
82 so showed reduced bacterial burden following K. pneumoniae challenge.
83 MCP-1 treatment in MCP-1(-/-) mice following K. pneumoniae infection rescued impairment in survival,
84 is a critical mediator of survival following K. pneumoniae infection and sepsis and suggest that IL-6
85 erstand potential contributions of foodborne K. pneumoniae to human clinical infections, we compared
86 Norgen) and 80 CFU/ml urine, on average, for K. pneumoniae (Norgen).
87                       NLRC4 is essential for K. pneumoniae-induced production of IL-1beta, IL-17A, an
88  we present a detailed genomic framework for K. pneumoniae based on whole-genome sequencing of more t
89                                 Further, for K. pneumoniae (KpI), the entity most frequently associat
90 ll K. pneumoniae strains tested positive for K. pneumoniae carbapenemase (KPC) genes by real-time PCR
91 ed in 88 patients with cultures positive for K. pneumoniae hospitalized in the Beijing You'an Hospita
92               Periodic patient screening for K. pneumoniae colonization has the potential to curb the
93 ng potential carbon and nitrogen sources for K. pneumoniae and of 99% in predicting nonessential gene
94 sults support MrkA as a promising target for K. pneumoniae antibody therapeutics and vaccines.
95     The conjugation frequency of OXA-48 from K. pneumoniae and E. coli in the gut of low-complexity-m
96 b OXA-48-containing IncL/M-type plasmid from K. pneumoniae to E. coli belonging to the novel ST666 in
97                                    PqqE from K. pneumoniae was cloned into Escherichia coli and expre
98 ) were Klebsiella pneumoniae and 74 harbored K. pneumoniae carbapenemase (56.1%), 54 metallo-beta-lac
99                             OXA-48-harboring K. pneumoniae isolates belonging to ST14 were isolated d
100             Five of 7 eyes had <100 CFU HMV- K. pneumoniae at 27 hours PI.
101 viscous (HMV+) or nonhypermucoviscous (HMV-) K. pneumoniae.
102 88 blocking peptide exhibited attenuation in K. pneumoniae-induced neutrophil influx and enhanced bac
103 gulated promoters have been characterized in K. pneumoniae, and nine NAC-regulated promoters have bee
104 ltered type 3 fimbrial surface expression in K. pneumoniae.
105 ddition, FimH-dependent biofilm formation in K. pneumoniae is inhibited by heptyl mannose, but not me
106  fimbria production and biofilm formation in K. pneumoniae.
107 2,) RNS production, and bacterial killing in K. pneumoniae-infected CXCL1(-/-) neutrophils.
108 e investigated the role of TRIF and MyD88 in K. pneumoniae pneumonia.
109 ons of the chromosome associated with NAC in K. pneumoniae.
110         The large size of the NAC regulon in K. pneumoniae indicates that NAC plays a larger role in
111   Furthermore, fluoroquinolone-resistance in K. pneumoniae clinical isolates is reversed by expressio
112       The majority of bla(KPC) genes were in K. pneumoniae isolates, which fell into 14 clonal groups
113               The epidemic curve of incident K. pneumoniae cases showed a bimodal distribution of cas
114 nction against invading pathogens, including K. pneumoniae.
115 bacteriophage (NTUH-K2044-K1-1) that infects K. pneumoniae NTUH-K2044 (capsular type K1) was isolated
116 ial cell characteristics in an international K. pneumoniae isolate collection (n = 48), with a range
117  NF-kappaB and MAPKs following intratracheal K. pneumoniae infection.
118 educed survival in response to intratracheal K. pneumoniae administration.
119  that in the eye, the K1 capsule of invasive K. pneumoniae significantly contributes to the ability o
120 ead to the emergence of untreatable invasive K. pneumoniae infections; our data provide the whole-gen
121                                 The isolated K. pneumoniae strains (n = 10) were of capsular polysacc
122  the virulence gene profiles of the isolated K. pneumoniae strains.
123 ass and reduced the CFU of E. coli isolates, K. pneumoniae isolates were observed to have a reduction
124 e used for the diagnosis and treatment of K1 K. pneumoniae infections.
125 s administered orogastrically in serotype K1 K. pneumoniae-colonized mice and the outcome was compare
126                                 Wild-type K1 K. pneumoniae caused significant ocular disease.
127                              In the kidneys, K. pneumoniae outcompeted E. coli in healthy mice but in
128 alveolar macrophages with LPS or heat-killed K. pneumoniae recapitulated the increase in IL-10 produc
129  most common resistance mechanisms were KPC (K. pneumoniae carbapenemases) beta-lactamases encoded by
130 pneumoniae into three distinct species, KpI (K. pneumoniae), KpII (K. quasipneumoniae), and KpIII (K.
131 lly, we demonstrated that the decreased lung K. pneumoniae burden associated with allergic airway inf
132            We showed that the decreased lung K. pneumoniae burden was independent of IL-4, IL-5, and
133 nflammation significantly decreased the lung K. pneumoniae burden and postinfection mortality.
134 iae infection and thereby increases the lung K. pneumoniae burden.
135 E. coli lipid A, whereas only LpxL2 mediated K. pneumoniae lipid A acylation.
136                          In MyD88(-/-) mice, K. pneumoniae-induced early NF-kappaB and MAPK activatio
137 ta(2)-microglobulin expression during murine K. pneumoniae bacteremia.
138 m-susceptible from carbapenem-nonsusceptible K. pneumoniae isolates without the need for MHT, while t
139 ains were identified, responsible for 12% of K. pneumoniae infections in ICU.
140                                Nearly 25% of K. pneumoniae clinical isolates in a US network of LTACH
141                               In sum, 49% of K. pneumoniae infections were caused by the patients' ow
142 r for infection in ICU, and indicate 50% of K. pneumoniae infections result from patients' own micro
143                    Overall, 33.0% (29/88) of K. pneumoniae isolates were hvKP.
144 e screened for rectal and throat carriage of K. pneumoniae shortly after admission.
145                      In contrast to cases of K. pneumoniae bacteremia with primary liver abscesses in
146                          Three categories of K. pneumoniae isolates were identified: enterobactin pos
147                         Optimal clearance of K. pneumoniae from the host lung requires TNF and IL-17A
148                 While pulmonary clearance of K. pneumoniae is preserved in neutrophil-depleted mice,
149 ophils and CCR2(+) monocytes to clearance of K. pneumoniae pulmonary infection.
150 ter microbiota depletion, early clearance of K. pneumoniae was impaired, and this could be rescued by
151 sion causes neutrophil-mediated clearance of K. pneumoniae, the mechanisms underlying KC-mediated hos
152  in an epidemic multidrug-resistant clone of K. pneumoniae (ST258).
153 uggest that MrkD1P allows for competition of K. pneumoniae with P. aeruginosa in a mixed-species biof
154 nstrate the site-threatening consequences of K. pneumoniae endophthalmitis and the importance of the
155 ified self ligands, is a host determinant of K. pneumoniae pathogenicity.
156 vides new insights into host determinants of K. pneumoniae pathogenicity and raises the possibility t
157 gate the evolution and spatial dispersion of K. pneumoniae in support of hospital infection control.
158 ounts, as well as increased dissemination of K. pneumoniae to blood and liver, compared with control-
159               Although the adhesin domain of K. pneumoniae TOP52 FimH (FimH(52)) is highly homologous
160 dy was to determine whether the incidence of K. pneumoniae bloodstream infection (BSI) was higher dur
161  This molecule is a competitive inhibitor of K. pneumoniae OHCU decarboxylase with a K(i) of 30 +/- 2
162 potential, and host-pathogen interactions of K. pneumoniae.
163                                    The IR of K. pneumoniae BSI during the 4 warmest months of the yea
164 essures may lead to an increase in the IR of K. pneumoniae BSI during the warmest months of the year.
165  2.23/10,000 patient-days, whereas the IR of K. pneumoniae BSI for the other 8 months was 1.55/10,000
166 ed this assay to screen clinical isolates of K. pneumoniae and Klebsiella oxytoca for the presence of
167 stant gram-negative bacteria, 12 isolates of K. pneumoniae that exhibited nonsusceptibility to extend
168 factor among clinical bacteremia isolates of K. pneumoniae.
169 observed reduced phagocytosis and killing of K. pneumoniae in AMs from l/l mice that was associated w
170 blish the first report, to our knowledge, of K. pneumoniae containing bla(KPC-3) in an LTCF caring fo
171 ocytes are rapidly recruited to the lungs of K. pneumoniae-infected mice and produce TNF, which marke
172 sion of MGL1 was upregulated in the lungs of K. pneumoniae-infected mice, and the deficiency of this
173 ed an increased influx in pneumonic lungs of K. pneumoniae-infected mice.
174 selective alternatives for the management of K. pneumoniae pneumonia.
175  this study, an experimental murine model of K. pneumoniae endophthalmitis was established, and the r
176 ld-type and O-antigen or capsular mutants of K. pneumoniae were grown as broth culture in a Taylor-Co
177  airway inflammation decreased the number of K. pneumoniae-induced airway neutrophils and lung IL-17A
178 ve diminished survival and higher numbers of K. pneumoniae following i.p. infection.
179 icillin/ampicillin may lead to overgrowth of K. pneumoniae in the intestine and predispose to KPLA.
180 onal differences seen in the pathogenesis of K. pneumoniae UTI compared to E. coli UTI.
181 y and constitute an increasing proportion of K. pneumoniae strains, indicating an increasing propensi
182 h linearly predictive of increasing rates of K. pneumoniae BSI.
183 like receptor (TLR)-dependent recognition of K. pneumoniae.
184                        To assess the role of K. pneumoniae capsule in endophthalmitis, the authors in
185 rred protection against several serotypes of K. pneumoniae, including the recently described multidru
186 ide genome-wide support for the splitting of K. pneumoniae into three distinct species, KpI (K. pneum
187 have used the rodent-adapted 43816 strain of K. pneumoniae and demonstrated that neutrophils are esse
188 model for KPPR1, a highly virulent strain of K. pneumoniae.
189 e is known about the population structure of K. pneumoniae, so it is difficult to recognize or unders
190          In vivo, we found that treatment of K. pneumoniae-infected mice with SP-A and SP-B(N) confer
191 gulatory gene fimK promotes the virulence of K. pneumoniae strain TOP52 in murine pneumonia.
192 P-2 and activation of NF-kappaB and MAPKs on K. pneumoniae infection.
193 ene in genomic DNA extracted from E. coli or K. pneumoniae clinical isolates within a few minutes.
194 ice but in diabetic mice E. coli outcompeted K. pneumoniae and caused severe pyelonephritis.
195 hat E. coli had a significant advantage over K. pneumoniae in the bladders of healthy mice and less o
196 p-PCR indicated that all bla(KPC-3)-positive K. pneumoniae strains were genetically related (>/=98% s
197 ty of method 1 for detection of KPC-positive K. pneumoniae and E. coli in 149 rectal swab specimens w
198    In addition, we evaluated 13 KPC-positive K. pneumoniae isolates by using each of these methods an
199 (ESBL/Omp strains), and 42 blaKPC-possessing K. pneumoniae (KPC-Kp) isolates were evaluated.
200        Ampicillin administration predisposed K. pneumoniae-colonized mice to increased bacterial burd
201 t Klebsiella pneumoniae strains that produce K. pneumoniae carbapenemase (KPC) have spread globally i
202 bsiella pneumoniae (Kp) strains that produce K. pneumoniae carbapenemases (KPCs) has become a signifi
203                         Five NDM-1-producing K. pneumoniae colonizing and/or clinically infecting pat
204                  We report a NDM-1-producing K. pneumoniae outbreak in Ontario, Canada.
205 nts were identified carrying NDM-1-producing K. pneumoniae, all of them epidemiologically linked with
206  interpretations for carbapenemase-producing K. pneumoniae differ by methodology.
207 lebsiella pneumoniae carbapenemase-producing K. pneumoniae followed a similar path some 20 years late
208 lebsiella pneumoniae carbapenemase-producing K. pneumoniae infectious episodes in 22 polytrauma inten
209  by highly resistant carbapenemase-producing K. pneumoniae.
210  clinical strains of carbapenemase-producing K. pneumoniae.
211 lebsiella pneumoniae carbapenemase-producing K. pneumoniae; and present strategies used to halt the s
212 69/638 isolates) and 67.7% of ESBL-producing K. pneumoniae isolates (155/229 isolates).
213 lla pneumoniae carbapenemase (KPC)-producing K. pneumoniae has become endemic in many US hospitals.
214 lla pneumoniae carbapenemase (KPC)-producing K. pneumoniae were studied.
215 ce then, regional outbreaks of KPC-producing K. pneumoniae (KPC-Kp) have occurred in the USA, and hav
216 with imipenem for detection of KPC-producing K. pneumoniae and E. coli in surveillance specimens.
217 e, the international spread of KPC-producing K. pneumoniae is primarily associated with a single mult
218 factor that is prevalent among KPC-producing K. pneumoniae isolates and promotes respiratory tract in
219 nt progresses in understanding KPC-producing K. pneumoniae that are contributing to our knowledge of
220  for susceptibility testing of KPC-producing K. pneumoniae, as Vitek 2 did not provide reliable resul
221 outbreak of colistin-resistant KPC-producing K. pneumoniae.
222  signaling in host defense against pulmonary K. pneumoniae infection has not been elucidated.
223 F and MyD88 signaling triggered by pulmonary K. pneumoniae infection in the lungs and demonstrate the
224 ost defense functions of KC during pulmonary K. pneumoniae infection using KC(-/-) mice.
225 (-/-) mice are more susceptible to pulmonary K. pneumoniae infection and show higher bacterial burden
226 endered germfree mice resistant to pulmonary K. pneumoniae infection, abrogated IL-10 production, and
227  DNase I footprinting studies using purified K. pneumoniae ArgP protein indicated that ArgP bound the
228 -generation cephalosporin-resistant (Ceph-R) K. pneumoniae, and susceptible K. pneumoniae isolates ca
229 bacteria were unable to significantly reduce K. pneumoniae burden in the blood or prevent disseminati
230  transmitting virulent, antibiotic-resistant K. pneumoniae from food animals to humans.
231 describe an outbreak of carbapenem-resistant K. pneumoniae containing the blaOXA-232 gene transmitted
232 atients with blaOXA-232 carbapenem-resistant K. pneumoniae infections were identified at a tertiary c
233 Here, we describe three carbapenem-resistant K. pneumoniae isolates recovered from pediatric patients
234 atients with blaOxa-232 carbapenem-resistant K. pneumoniae isolates, including 9 with infections, 7 a
235 e to infection with the carbapenem-resistant K. pneumoniae ST258 strain.
236 bruary 2013, twenty-one multi-drug resistant K. pneumoniae strains, were collected from patients hosp
237 erapeutic strategy even for highly resistant K. pneumoniae infections, and underscore the effect humo
238 eat infections caused by multidrug resistant K. pneumoniae.
239  most prevalent cause of multidrug-resistant K. pneumoniae infections in the United States and other
240  evolutionary changes in multidrug-resistant K. pneumoniae, demonstrating the highly recombinant natu
241                                      We show K. pneumoniae has a large accessory genome approaching 3
242  of respiratory and fecal specimens, showing K. pneumoniae species and clonal group identification an
243 e K. pneumoniae for our in vivo model, since K. pneumoniae increases IL-17A expression and gammadelta
244                                  Meat-source K. pneumoniae isolates were more likely than clinical is
245 gion has contributed to the success of ST258 K. pneumoniae.
246 e hypothesis that carbapenem-resistant ST258 K. pneumoniae is a single genetic clone that has dissemi
247 genome of these isolates revealed that ST258 K. pneumoniae organisms are two distinct genetic clades.
248 y providing an alternative tool for studying K. pneumoniae pathogenesis and control within the lung.
249 tant (Ceph-R) K. pneumoniae, and susceptible K. pneumoniae isolates causing bloodstream infections at
250      Interestingly, a carbapenem-susceptible K. pneumoniae ST278 (KpN06) was obtained 1 month later f
251                                We found that K. pneumoniae carries an extra gene of unknown function
252                   Our findings indicate that K. pneumoniae Pal and LppA proteins are important in the
253 rt alerts clinicians to the possibility that K. pneumoniae bacteremia combined with multiple abscesse
254                    Our results revealed that K. pneumoniae capsule polysaccharide (CPS) was necessary
255            Recently our group has shown that K. pneumoniae dampens the activation of inflammatory res
256                       It has been shown that K. pneumoniae infections are characterized by reduced ea
257     The time-scaled phylogeny suggested that K. pneumoniae strains isolated during the study period m
258                                          The K. pneumoniae strain was a hypermucoid K2 serotype carry
259  model of UTI demonstrated that although the K. pneumoniae strain TOP52 required FimH(52) for invasio
260 n minimal medium has been proposed to be the K. pneumoniae ArgP protein.
261 Klebsiella pneumoniae isolates harboring the K. pneumoniae carbapenemase gene (bla(KPC)) are creating
262                   A knockout mutation of the K. pneumoniae argP gene was generated and used to assess
263      Herein we show that coexpression of the K. pneumoniae atsB gene with a plasmid that encodes gene
264 tting revealed "low-level" production of the K. pneumoniae carbapenemase, and rep-PCR indicated that
265 tance plasmids, particularly variants of the K. pneumoniae carbapenemase.
266                      The pathogenesis of the K. pneumoniae cystitis isolate TOP52 was compared to tha
267                               Mutants of the K. pneumoniae strain IA565 lacking the plasmid-borne mrk
268        Phylogenetic analysis showed that the K. pneumoniae ST278 from patient 2 was likely a descenda
269 ctors of 30-day mortality rates, whereas the K. pneumoniae susceptibility phenotype was not.
270                                        Thus, K. pneumoniae appears programmed for minimal expression
271 ver, whether CCR2(+) monocytes contribute to K. pneumoniae clearance from the lung.
272 naling in hematopoietic cells contributes to K. pneumoniae-induced lung inflammation.
273 e of multidrug resistance, especially due to K. pneumoniae carbapenemases (KPCs).
274 ations in CD36 may predispose individuals to K. pneumoniae syndromes.
275 ate that CD36 enhances LPS responsiveness to K. pneumoniae to increase downstream cytokine production
276 a281 knockout) mice were more susceptible to K. pneumoniae bacteremia.
277 ignificantly increased susceptibility toward K. pneumoniae pneumonia.
278  postinfection, eyes infected with wild-type K. pneumoniae retained significantly less retinal A-wave
279 ted with the magA mutant than with wild-type K. pneumoniae.
280  the weak inflammatory response of untreated K. pneumoniae-infected mice.
281               Finally, while the widely used K. pneumoniae model strain 43816 produces rapid dissemin
282                         To determine whether K. pneumoniae must produce Lcn2-resistant siderophores t
283 type 1 pili, which may explain, in part, why K. pneumoniae is a less prevalent etiologic agent of UTI
284 ith E. coli, 2/3 with K. oxytoca, 16/17 with K. pneumoniae, and 0/1 with Proteus spp.
285 and protection from pulmonary challenge with K. pneumoniae.
286 th wild-type neutrophils when incubated with K. pneumoniae.
287       However, MyD88(-/-) mice infected with K. pneumoniae showed a much more remarkable phenotype, i
288                 TRIF(-/-) mice infected with K. pneumoniae showed impaired survival and reduced bacte
289 ild type mice were created and infected with K. pneumoniae via the airways.
290 g and improved survival after infection with K. pneumoniae compared with wild-type controls, an effec
291 d the lungs of l/l mice after infection with K. pneumoniae in vivo.
292 ncreases in susceptibility to infection with K. pneumoniae or E. coli.
293 l depletion markedly worsened infection with K. pneumoniae strain 43816 and three clinical isolates b
294 /-) mice undergoing pulmonary infection with K. pneumoniae was compared.
295 ificantly more susceptible to infection with K. pneumoniae, confirming the likely in vivo relevance o
296 type mice after intratracheal infection with K. pneumoniae.
297 challenge prior to acute lung infection with K. pneumoniae.
298 une defense against pulmonary infection with K. pneumoniae.
299 hat, during pulmonary infection of mice with K. pneumoniae, conventional NK cells are required for op
300 els of IL-22 in the lungs postinfection with K. pneumoniae.

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