ライフサイエンスコーパス: H. influenzae

1 H. influenzae and N. meningitidis accounted for 6.8% (5

2 H. influenzae causes predominantly mucosal infections.

3 H. influenzae displays various strategies to circumvent

4 H. influenzae infection also increased the binding of RV

5 H. influenzae is incapable of synthesizing sialic acid a

6 H. influenzae TolR(62-133) is a symmetrical dimer with a

7 H. influenzae type b (Hib) was historically responsible

8 at low concentrations (S. aureus, P < 0.001; H. influenzae, P < 0.0001) and in sputum-type specimens

9 in-1beta (M. catarrhalis, P = 1.6 x 10(-11); H. influenzae, P = 2.7 x 10(-7)).

10 IL-1beta (M. catarrhalis, P = 2.2 x 10(-12); H. influenzae, P = 7.1 x 10(-10)), TNF-alpha (M. catarrh

11 Our comparative analyses of H. somnus 129Pt, H. influenzae Rd, and H. ducreyi 35000HP revealed simila

12 itional S. aureus isolates and 25/92 (27.2%) H. influenzae isolates, which were more frequently disco

13 DNA sequence comparisons of the 21 H. influenzae sodC genes with sodC from H. haemolyticus

14 45% (123/273) S. pneumoniae, and 7% (19/273) H. influenzae.

15 sing 6 vaccine candidate S. pneumoniae and 3 H. influenzae protein antigens.

16 A total of 358 H. influenzae and H. haemolyticus isolates were genotype

17 A total of 656 H. influenzae strains, including 322 NTHI strains, have

18 wed by GBS (18.1%), N. meningitidis (13.9%), H. influenzae (6.7%), and L. monocytogenes (3.4%).

19 TNF-alpha (M. catarrhalis, P = 1.5 x 10(-9); H. influenzae, P = 5.9 x 10(-7)), and macrophage inflamm

20 P4 is also a component of a H. influenzae vaccine.

21 Thus, adult H. influenzae and H. haemolyticus carriers are colonized

22 ae nontypeable meningitis was observed after H. influenzae type b vaccine introduction.

23 spiratory burst and killing activity against H. influenzae and S. aureus compared to those transmigra

24 ntrolled asthma, azithromycin reduced airway H. influenzae load compared with placebo but did not cha

25 btained from normally sterile sites were all H. influenzae.

26 glycerol kinase and the chimeric, allosteric H. influenzae glycerol kinase were constructed with a no

27 prim/sulfamethoxazole and azithromycin among H. influenzae.

28 both evolutionary processes that occur among H. influenzae isolates during asymptomatic pharyngeal ca

29 In this study, we identified an H. influenzae lipoprotein having the ability to bind fac

30 Unlike an H. influenzae sapA mutant, strain 35000HPsapA was not mo

31 ollowed by meningococcus (34.6%: 53/153) and H. influenzae (19.0%: 29/153).

32 gococcal (n=1338), pneumococcal (n=455), and H. influenzae (n=991) meningitis, an estimated 11.0% (41

33 ged to meningococcus serogroup W (45.5%) and H. influenzae type b (54.5%), respectively.

34 moniae was cultured in 33 episodes (51%) and H. influenzae in 11 episodes (17%).

35 was higher for the presence of bocavirus and H. influenzae together (OR, 3.61; 95% CI, 1.90 and 6.86)

36 M. catarrhalis and H. influenzae colonization of the airways of asymptomati

37 Colonization with M. catarrhalis and H. influenzae induced a mixed T helper cell (Th) type 1/

38 tween H. influenzae colonization density and H. influenzae-confirmed pneumonia in children; the assoc

39 profiles of children with RSV infection and H. influenzae- and Streptococcus-dominated microbiota we

40 ection with sublethal doses of influenza and H. influenzae resulted in synergy between the two pathog

41 ction of S. pneumoniae, N. meningitidis, and H. influenzae in CSF, and that application of molecular

42 reptococcus pneumoniae, N. meningitidis, and H. influenzae were done.

43 tive for S. pneumoniae, N. meningitidis, and H. influenzae, only 10 were culture positive.

44 ccus pneumoniae, Neisseria meningitidis, and H. influenzae.

45 The most prevalent meningococcal and H. influenzae strains were serogroup W and serotype b, r

46 The majority of serotyped meningococcus and H. influenzae belonged to meningococcus serogroup W (45.

47 Pneumococcus, meningococcus, and H. influenzae accounted for 52.2%, 31.9%, and 16.0% of c

48 etection of pneumococcus, meningococcus, and H. influenzae was confirmed through microbiological tech

49 presence of pneumococcus, meningococcus, and H. influenzae.

50 oniae, Entrobacter species, K. pnemoniae and H. influenzae were each accounted 6.5% isolation rate.

51 achievements of siblings of pneumococcal and H. influenzae meningitis patients did not differ substan

52 n may apply particularly to pneumococcal and H. influenzae meningitis, whereas for meningococcal meni

53 6.6%) fewer meningococcal, pneumococcal, and H. influenzae meningitis patients were economically self

54 ine was maintained against S. pneumoniae and H. influenzae from 2008 through 2010, increased rates of

55 S. pneumoniae and H. influenzae, both of which frequently colonize the nas

56 nt causative pathogens are S. pneumoniae and H. influenzae.

57 nces for N. meningitidis, S. pneumoniae, and H. influenzae, respectively, were 7.5, 2.5, and 0.3.

58 bining two targets (H. haemolyticus purT and H. influenzae hpd, encoding protein D lipoprotein) was a

59 vaccines, pneumococcal vaccine serotypes and H. influenzae type b remain associated with bacterial me

60 ed increases in density of other species and H. influenzae carriage prevalence.

61 rs; Aspergillus species, 11%, 3.2 years; and H. influenzae, 9%, 3.1 years.

62 Analysis of 490 apparent H. influenzae strains, identified by standard methods, r

63 he recognition that some strains of apparent H. influenzae are H. haemolyticus substantially strength

64 pective study, selected isolates of apparent H. influenzae had an altered phenotype.

65 Strains of apparent H. influenzae obtained from a range of clinical sources

66 lus species; 860 isolates were identified as H. influenzae or H. haemolyticus based on the porphyrin

67 ollected, and 36 isolates were identified as H. influenzae using a gold standard methodology that com

68 onchitis, which are preceded by asymptomatic H. influenzae colonization of the human pharynx.

69 nfluenzae, carrier C predominantly with b(-) H. influenzae mutants, and carrier D with H. haemolyticu

70 nding protein of the Gram-negative bacterium H. influenzae, and when converted to plasmin, PE-bound p

71 conserved among all isolates presumed to be H. influenzae.

72 There is evidence for an association between H. influenzae colonization density and H. influenzae-con

73 ing N-Glc, to establish a connection between H. influenzae infection and MS.

74 essential factor in serum resistance of both H. influenzae strain Rd and nontypeable H. influenzae (N

75 er, in contrast to Hib, infections caused by H. influenzae serotype f (Hif) are emerging.

76 urrent meningitis, or with disease caused by H. influenzae.

77 e the dynamics of pharyngeal colonization by H. influenzae and an intimately related species, Haemoph

78 oyed by host cells in locations colonized by H. influenzae during pathogenesis that are likely to var

79 ing that these conditions are encountered by H. influenzae during pulmonary infection.

80 s of IgA proteases are variably expressed by H. influenzae during infection of the human airways.

81 ned the levels of HMW1 and HMW2 expressed by H. influenzae isolates collected serially from patients

82 most infections (67.3%: 66/98), followed by H. influenzae (23.5%: 23/98) and meningococcus (9.2%: 9/

83 cts of serum and to bloodstream infection by H. influenzae.

84 high extracellular molybdate concentration, H. influenzae makes use of parallel molybdate transport

85 . influenzae and S. pneumoniae and confirmed H. influenzae as nontypeable (NTHi).

86 s for detection of (i) N. meningitidis ctrA, H. influenzae hpd, and S. pneumoniae lytA (NHS assay); (

87 en developed to detect N. meningitidis ctrA, H. influenzae hpd, and S. pneumoniae lytA and serogroup-

88 ch is distinct from the previously described H. influenzae IgA protease.

89 leic acid diagnostics approaches that detect H. influenzae in RTIs have been described in the literat

90 bility to serve as biomarkers to distinguish H. influenzae from H. haemolyticus.

91 l activity against these genetically diverse H. influenzae strains.

92 Each H. influenzae strain uniquely produces only one of the f

93 Encapsulated H. influenzae type b (Hib) and type f (Hif) are the most

94 ) and hia (homologue of hsf, an encapsulated H. influenzae adhesin gene).

95 age, 99% identical to sodC from encapsulated H. influenzae but only 85% identical to sodC from H. hae

96 sodC gene has been reported in encapsulated H. influenzae strains belonging to phylogenetic division

97 re common in NTHI but absent in encapsulated H. influenzae) and hia (homologue of hsf, an encapsulate

98 in recent years a resurgence of encapsulated H. influenzae strains has also been observed, most notab

99 ore closely resembling those of encapsulated H. influenzae.

100 ain is 18%, approaching that of encapsulated H. influenzae.

101 th sodC from H. haemolyticus or encapsulated H. influenzae demonstrated that the sodC genes of the si

102 vestigation of P6 as a vaccine candidate for H. influenzae.

103 A 5.9 log10 copies/mL density cutoff for H. influenzae yielded 86% sensitivity and 77% specificit

104 NA gene demonstrated two distinct groups for H. influenzae and H. haemolyticus.

105 This novel interaction is important for H. influenzae resistance against complement activation a

106 pneumoniae ATCC 49619, and 2 to 8 mug/ml for H. influenzae ATCC 49247.

107 . pneumoniae ATCC 49619, and 16 to 20 mm for H. influenzae ATCC 49247.

108 The results indicate a role for H. influenzae arcA and dps in pre-emptive defence agains

109 orically differentiated H. haemolyticus from H. influenzae, but the recent recognition of significant

110 ot reliably distinguish H. haemolyticus from H. influenzae.

111 for rapid in silico serotype prediction from H. influenzae genome sequences.

112 insertion element associated with division I H. influenzae capsule serotypes.

113 insertion element associated with division I H. influenzae capsule serotypes.

114 ibed, expressed, and enzymatically active in H. influenzae.

115 serotype replacement may prevent changes in H. influenzae and S. aureus carriage among PCV7 recipien

116 clinical interventions, including changes in H. influenzae and S. aureus disease incidence following

117 ga, igaB, and both genes were constructed in H. influenzae strain 11P6H, a strain isolated from a pat

118 synthesis of the LPS oligosaccharide core in H. influenzae strain Rd/HapS243A, resulted in loss of Ha

119 fied and characterized IgA protease genes in H. influenzae and studied their expression and proteolyt

120 tified a second IgA1 protease gene, igaB, in H. influenzae that is present in addition to the previou

121 ed) showed an apparent transient increase in H. influenzae carriage but no further significant differ

122 pendent factors are likely to participate in H. influenzae pathogenesis.

123 nd 54 times, respectively, more prevalent in H. influenzae than in H. haemolyticus.

124 Comparison of predicted secreted proteins in H. influenzae to known DsbA substrates in other species

125 In this study, we evaluated the role in H. influenzae pathogenesis of DsbA, as well as HbpA, a s

126 emical features to the orthologous system in H. influenzae.

127 Hap and LPS biosynthesis that can influence H. influenzae interactions with the host.

128 Plasminogen, either attached to intact H. influenzae or bound to PE, was accessible for urokina

129 Invasive H. influenzae disease confirmed by positive culture from

130 44 years with laboratory-confirmed invasive H. influenzae disease during 2009-2012, encompassing 45,

131 n neonates had laboratory-confirmed invasive H. influenzae disease: 115 (97%) were NTHi, 2 were serot

132 171 women had laboratory-confirmed invasive H. influenzae infection, which included 144 (84.2%; 95%

133 cteristics, and outcome of neonatal invasive H. influenzae disease in England and Wales over a 5-year

134 s enhanced national surveillance of invasive H. influenzae disease in England and Wales.

135 lly responsible for the majority of invasive H. influenzae disease, and its prevalence has been marke

136 by a shift in capsular serotypes of invasive H. influenzae disease, with nontypeable strains replacin

137 s associated with a greater risk of invasive H. influenzae infection.

138 Three hundred and sixty invasive H. influenzae isolates were collected as part of Active

139 y isolates of S. pneumoniae (3329 isolates), H. influenzae (1545 isolates), and M. catarrhalis (456 i

140 vestigated host factors involved in limiting H. influenzae colonization in BALB/c mice, as colonizati

141 zae cases were confirmed and N. meningitidis/H. influenzae were serogrouped/serotyped by real-time po

142 ependent transcription factor that modulates H. influenzae response to formaldehyde, with two cystein

143 ource of antibody and complement in multiple H. influenzae isolates.

144 similar to the less virulent nonencapsulated H. influenzae.

145 In approximately 80% of nontypable H. influenzae isolates, the major adhesins are related p

146 Nontypeable H. influenzae (NTHi) isolates were probed with Hib cap-g

147 CXCL2 appeared to function as a nontypeable H. influenzae-responsive element, and the proximal AP-1

148 both H. influenzae strain Rd and nontypeable H. influenzae (NTHi) clinical isolate NT127.

149 b, Haemophilus haemolyticus, and nontypeable H. influenzae (NTHi) isolates.

150 ative organism was identified as nontypeable H. influenzae, biotype III.

151 In the postvaccine era, nontypeable H. influenzae emerged as the most dominant group causing

152 ignaling pathway is required for nontypeable H. influenzae-induced CXCL2 upregulation in the rat spir

153 smic solute receptor (SiaP) from nontypeable H. influenzae strain 2019.

154 molecular mechanism involved in nontypeable H. influenzae-induced cochlear infiltration of polymorph

155 a potential virulence factor in nontypeable H. influenzae.

156 We show that ArcA of nontypeable H. influenzae (NTHI) activates expression of a glycosylt

157 The outer membrane of nontypeable H. influenzae is dominated by lipooligosaccharides (LOS)

158 Approximately 20 percent of nontypeable H. influenzae strains contain copies of losA and losB in

159 ns are classified as typeable or nontypeable H. influenzae (NTHI) based upon the presence or absence

160 . influenzae PE knockout strain (nontypeable H. influenzae 3655Deltape) bound plasminogen with approx

161 owever, unencapsulated strains - nontypeable H. influenzae (NTHi) - remain important as causes of res

162 to release CXCL2 in response to nontypeable H. influenzae via activation of c-Jun, leading to the re

163 ave a higher binding affinity to nontypeable H. influenzae-activated c-Jun than that of the distal on

164 ere predominantly colonized with nontypeable H. influenzae, carrier C predominantly with b(-) H. infl

165 NT H. influenzae and H. haemolyticus are often misidentifie

166 sulated strains, while sodC genes from 13 NT H. influenzae strains were almost 95% identical to sodC

167 The sodC genes from 2/15 NT H. influenzae strains were similarly more closely relate

168 s sequence analysis confirmed that the 21 NT H. influenzae strains were H. influenzae and not H. haem

169 species and found that 21 of 169 (12.4%) NT H. influenzae strains and all 110 (100%) H. haemolyticus

170 plement in innate immune defenses against NT H. influenzae infections and specifically EOM.

171 a key arm of host innate immunity against NT H. influenzae-induced EOM.

172 the discrimination of H. haemolyticus and NT H. influenzae, a testing scheme combining two targets (H

173 e genomic analysis of H. haemolyticus and NT H. influenzae, we identified genes unique to H. haemolyt

174 and disease caused by H. haemolyticus and NT H. influenzae.

175 ndicated that 6 of the 21 sodC-containing NT H. influenzae strains in our study were likely capsule-d

176 ies exist as to the prevalence of sodC in NT H. influenzae.

177 ed to nontypeable Haemophilus influenzae (NT H. influenzae).

178 Neither NT H. influenzae strain tested bound factor H (alternative

179 The genome of NT H. influenzae middle ear strain G622 was subtracted from

180 r strain G622 was subtracted from that of NT H. influenzae throat strain 23221, and the resultant gen

181 We have shown previously that NT H. influenzae mutants defective in their ability to sial

182 C is not completely absent (9.2%) in true NT H. influenzae strains.

183 lic2B and hmwA, that are associated with NT H. influenzae strains isolated from the middle ears of c

184 is media but that are not associated with NT H. influenzae strains isolated from the throats of healt

185 enes from a nontypeable strain (86-028NP) of H. influenzae attenuated virulence in the chinchilla oti

186 The decreased ability of H. influenzae to import sialic acid had negative effects

187 her pathway decreased the limited ability of H. influenzae to initiate and sustain bacteremia in wean

188 tained in this work highlight the ability of H. influenzae to utilize a single protein to perform mul

189 ion of genes of the respiratory chain and of H. influenzae's partial tricarboxylic acid cycle, and de

190 tes revealed fitness phenotypes of a bank of H. influenzae mutants in viral coinfection in comparison

191 Of 9 cases of H. influenzae, 8 were type b (Hib) and 1 was type f.

192 and molecular traits between collections of H. influenzae and H. haemolyticus strains separated with

193 Higher densities of H. influenzae were observed in both microbiologically co

194 A key virulence determinant of H. influenzae is the polysaccharide capsule, of which si

195 e exacerbations and promoted displacement of H. influenzae by more macrolide-tolerant pathogens inclu

196 Emergence of H. influenzae nontypeable meningitis was observed after

197 growing interest in genomic epidemiology of H. influenzae Here we present hicap, a software tool for

198 We report that fnr of H. influenzae is required for anaerobic defense against

199 were high inoculum and pH 5.5 (no growth of H. influenzae and S. pneumoniae by BMD).

200 ance of exogenous heme for aerobic growth of H. influenzae.

201 d 100% specificity for the identification of H. influenzae, respectively.

202 solates before and after the introduction of H. influenzae serotype b (Hib) conjugate vaccines.

203 e (GF) conditions showed increased levels of H. influenzae colonization that were not limited by adap

204 note, the LOS genes licA, lic2A, and lgtC of H. influenzae were approximately 2, 6, and 54 times, res

205 no effect on outer membrane localization of H. influenzae P5 or IgA1 protease or levels of p5 or iga

206 The lipopolysaccharide (LPS) of H. influenzae is highly variable.

207 The majority of H. influenzae respiratory isolates lack the genes for ca

208 e periplasm and across the inner membrane of H. influenzae.

209 ion-selective pores in the outer membrane of H. influenzae.

210 h characterized functions in other models of H. influenzae pathogenesis and genes not previously impl

211 Mutants of H. influenzae Rd and type b strain Eagan having nonpolar

212 A, meningococcal PilQ and PorA, and OmpP2 of H. influenzae.

213 essential early step in the pathogenesis of H. influenzae disease.

214 a critical early step in the pathogenesis of H. influenzae disease.

215 pithelial cells, facilitating persistence of H. influenzae.

216 : HRV significantly impaired phagocytosis of H. influenzae by 23% in MDM (n = 37; P = 0.004) and 18%

217 Phagocytosis of H. influenzae was also impaired by poly I:C but not IFN-

218 ined bacterial meningitis as the presence of H. influenzae, Streptococcus pneumoniae, GBS, Listeria m

219 n in vitro by pneumococci in the presence of H. influenzae.

220 ene encoding an immunoglobulin A protease of H. influenzae, clustered apart from strains that did not

221 yticus, the closest phylogenetic relative of H. influenzae, is arguably a strict pharyngeal commensal

222 te a critical role for ytfE in resistance of H. influenzae to reactive nitrogen species and the antib

223 mmensal or virulent growth, respectively, of H. influenzae.

224 ene was designed to detect all serogroups of H. influenzae.

225 .91 (95% CI, 2.13-3.88) for all serotypes of H. influenzae and 2.90 (95% CI, 2.11-3.89) for unencapsu

226 ion of IgA proteases in clinical settings of H. influenzae infection.

227 nonpilus adhesin in encapsulated strains of H. influenzae and belongs to the trimeric autotransporte

228 ro and in vivo in 169 independent strains of H. influenzae collected longitudinally over 10 years fro

229 re associated with the ability of strains of H. influenzae to cause exacerbations of COPD, supporting

230 hereas 45% of acquisitions of new strains of H. influenzae were associated with exacerbations.

231 ria and is highly conserved among strains of H. influenzae.

232 Microarray studies of H. influenzae strain Rd KW20 identified 162 iron/heme-re

233 the importance of continued surveillance of H. influenzae colonization and disease patterns.

234 nce factor important for zinc utilization of H. influenzae under conditions where zinc is limiting.

235 ndent factors are important for virulence of H. influenzae.

236 433; 56%), S. pneumoniae (n = 1758; 40%), or H. influenzae (n = 180; 4%).

237 ffect on nasopharyngeal NTHi colonization or H. influenzae density in healthy Dutch children up to 2

238 S. agalactiae, E. coli, N. meningitidis, or H. influenzae in combination with cefotaxime or ceftriax

239 nd reduced IgG responses to S. pneumoniae or H. influenzae after colonization and after AOM; this imm

240 NP colonization with either S. pneumoniae or H. influenzae.

241 to inhibit the migration of S. pneumoniae or H. influenzae.

242 between groups in either NTHi prevalence or H. influenzae density were detected.

243 ng an interaction between the human pathogen H. influenzae and FH.

244 ic machinery from the opportunistic pathogen H. influenzae (and the homologous enzymes from A. pleuro

245 of pathogenic bacteria including Y. pestis, H. influenzae, and Proteus that cause plague, meningitis

246 The fact that S. pneumoniae, H. influenzae, and S. aureus polymicrobial carriage patt

247 opharynx with M. catarrhalis, S. pneumoniae, H. influenzae, and Staphylococcus aureus was assessed si

248 neonates were colonized with S. pneumoniae, H. influenzae, and/or M. catarrhalis at 4 weeks of age.

249 atal airway colonization with S. pneumoniae, H. influenzae, or M. catarrhalis is associated with incr

250 t influence total carriage of S. pneumoniae, H. influenzae, or S. aureus.

251 versity and distribution in 691 high-quality H. influenzae genomes from GenBank.

252 Polymerase chain reaction assays quantified H. influenzae and S. pneumoniae and confirmed H. influen

253 The development of a rapid H. influenzae diagnostic assay that would allow for the

254 demonstrated that the sodC genes of the six H. influenzae capsule-deficient mutants were, on average

255 We conclude that H. influenzae infection increases airway epithelial cell

256 The H. influenzae glycosyltransferase LpsA is responsible fo

257 The H. influenzae Hap autotransporter protein mediates adher

258 The H. influenzae HMW1 and HMW2 adhesins are homologous prot

259 The H. influenzae pangenome has 2 alleles of IgA protease ge

260 The H. influenzae PE knockout strain (nontypeable H. influen

261 ubstrate bicarbonate that occurs in both the H. influenzae and E. coli enzymes.

262 he proposed active and inactive forms of the H. influenzae and E. coli enzymes.

263 genome-scale study to identify genes of the H. influenzae ArcA regulon.

264 We conducted genome-wide profiling of the H. influenzae genes that promote its fitness in a murine

265 Hib caused 67% (2/3) of the H. influenzae meningitis isolates serotyped.

266 teins: the aforementioned KLH and rTTHC; the H. influenzae protein D (HiD); and the cross-reactive ma

267 These data demonstrate that the H. influenzae strain 2019 FirRS is a two-component regul

268 tein, a TpsB protein that interacts with the H. influenzae HMW1 adhesin.

269 To achieve this, H. influenzae utilizes a tripartite ATP-independent peri

270 oop compared to the remaining strains and to H. influenzae P2.

271 om GF mice exhibited less surface binding to H. influenzae, suggesting that natural antibody, induced

272 Incidence of invasive disease due to H. influenzae serotype a (Hia) increased an average of 1

273 The IL-10 response to H. influenzae was significantly impaired by poly I:C, IF

274 significantly reduced cytokine responses to H. influenzae.

275 antially strengthens the association of true H. influenzae with clinical infection.

276 al otitis media virulence genes revealed two H. influenzae pathotypes associated with otitis media.

277 matory milieu during infection, non-typeable H. influenzae must resist the antimicrobial activity of

278 ains were genetically different from typical H. influenzae.

279 Unencapsulated H. influenzae infection during the first 24 weeks of pre

280 Unencapsulated H. influenzae infection during the second half of pregna

281 2.90 (95% CI, 2.11-3.89) for unencapsulated H. influenzae compared with the background rate for preg

282 he incidence rate of invasive unencapsulated H. influenzae disease was 17.2 (95% CI, 12.2-24.1; P < .

283 ed susceptibility to invasive unencapsulated H. influenzae disease.

284 ly healthy and presented with unencapsulated H. influenzae bacteremia.

285 ly expressed in nontypeable (unencapsulated) H. influenzae, which did not bind FH, an increased FH af

286 This need arises because, unlike H. influenzae type B, high NTHi exposure diminishes cumu

287 To survive and propagate in vivo, H. influenzae has evolved mechanisms for subverting this

288 The primary outcome was H. influenzae infection and the secondary outcomes were

289 f iga in 412 of the isolates, 346 (84%) were H. influenzae, 47 (11%) were H. haemolyticus, 18 (4%) we

290 ed that the 21 NT H. influenzae strains were H. influenzae and not H. haemolyticus.

291 e data provide a cellular mechanism by which H. influenzae infection may increase the susceptibility

292 pitalization were positively associated with H. influenzae and Streptococcus and negatively associate

293 omatic colonization of patients with CF with H. influenzae.

294 of H. parainfluenzae during coinfection with H. influenzae are topics for future work.

295 hese data, we conclude that coinfection with H. influenzae facilitates pneumococcal biofilm formation

296 The results showed that coinfection with H. influenzae promoted clearance of H. parainfluenzae fr

297 umoniae will prevail during competition with H. influenzae, even if production of a capsule is otherw

298 o severe illness on secondary infection with H. influenzae by a mechanism that involves innate immuni

299 hes to block Hap activity and interfere with H. influenzae colonization.

300 ary-differentiated cells, preincubation with H. influenzae enhanced RV serotype 39-induced protein ex