ライフサイエンスコーパス: H. influenzae

1 H. influenzae associated with exacerbations caused more

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

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

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

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

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

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

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

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

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

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

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

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

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

20 prim/sulfamethoxazole and azithromycin among H. influenzae.

21 cal reactions that are known to differ among H. influenzae strains.

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

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

24 ucture where the C terminus is similar to an H. influenzae phage HP1 tail protein implicating this op

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

26 t response, we used acute infections with an H. influenzae strain expressing a mutation in the htrB g

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

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

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

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

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

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

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

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

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

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

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

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

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

40 6.6%) fewer meningococcal, pneumococcal, and H. influenzae meningitis patients were economically self

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 r-alpha inhibited IL-8 expression induced by H. influenzae and RV39.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 ore closely resembling those of encapsulated H. influenzae.

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

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

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

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

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

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

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

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

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

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

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

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

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

94 dditional nutritional role of sialic acid in H. influenzae physiology.

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

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

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

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

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

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

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

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

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

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

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

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

107 -related tetranucleotide repeat sequences in H. influenzae, were used to probe a collection of 25 gen

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

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

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

111 Invasive H. influenzae disease confirmed by positive culture from

112 44 years with laboratory-confirmed invasive H. influenzae disease during 2009-2012, encompassing 45,

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

114 171 women had laboratory-confirmed invasive H. influenzae infection, which included 144 (84.2%; 95%

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

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

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

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

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

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

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

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

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

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

125 similar to the less virulent nonencapsulated H. influenzae.

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

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

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

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

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

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

132 t insight into disease caused by nontypeable H. influenzae, as serotype d strains are not pathogens.

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

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

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

136 a potential virulence factor in nontypeable H. influenzae.

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

138 individual infectious strains of nontypeable H. influenzae (NTHi).

139 In contrast, strains of nontypeable H. influenzae are the primary pathogens of chronic and r

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

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

142 extends the ongoing analysis of nontypeable H. influenzae virulence determinants.

143 nto the pathogenic mechanisms of nontypeable H. influenzae.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

160 or variations in serum resistance between NT H. influenzae strains, which in turn may impact their vi

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

162 entary approach to MLST, particularly for NT H. influenzae isolates, and is potentially useful for ou

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

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

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

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

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

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

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

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

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

172 ize the lack of clonality of nontypable (NT) H. influenzae isolates.

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

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

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

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

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

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

179 useful in understanding the basic biology of H. influenzae, these data have not provided significant

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

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

182 insight into the structural determinants of H. influenzae type b adherence.

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

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

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

186 nsporter also results in decreased growth of H. influenzae in a chemically defined medium containing

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

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

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

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

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

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

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

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

195 , a major component of the outer membrane of H. influenzae, play an important role in microbial virul

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

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

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

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

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

201 Overexpression of H. influenzae ybaK decreased the in vivo ratio of Cys-tR

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

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

204 pithelial cells, facilitating persistence of H. influenzae.

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

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

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

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

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

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

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

212 .91 (95% CI, 2.13-3.88) for all serotypes of H. influenzae and 2.90 (95% CI, 2.11-3.89) for unencapsu

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

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

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

216 Approximately one-third of 297 strains of H. influenzae of diverse clinical and geographic origin

217 te aerosol exposures to wild-type strains of H. influenzae showed that TLR4 function was essential fo

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

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

220 equences among well-characterized strains of H. influenzae, 59 exacerbation strains and 73 asymptomat

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

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

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

224 ly profoundly influence our understanding of H. influenzae-induced diseases of the respiratory tract

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

226 , was associated with increased virulence of H. influenzae in vivo.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

242 m led us to examine the role of the putative H. influenzae homologue of csrA, a regulator of glycolys

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

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

245 of previous studies showing that serotypable H. influenzae isolates behave as highly clonal populatio

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

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

248 The results indicate that H. influenzae strains isolated from patients during COPD

249 The effect is that H. influenzae populations can readily adapt to environme

250 The recognition that H. influenzae possesses a mechanism for twitching motili

251 The H. influenzae glycosyltransferase LpsA is responsible fo

252 The H. influenzae Hap autotransporter protein mediates adher

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

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

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

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

257 We show that disease initiation by the H. influenzae mimic is prevented by tolerance to the sel

258 fection of SJL mice with TMEV expressing the H. influenzae mimic can exacerbate a previously establis

259 By contrast, expression from the H. influenzae napF-lacZ operon fusion in E. coli was sti

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

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

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

263 Overall, the H. influenzae napF operon control region provides a rela

264 We show that the H. influenzae mimic epitope only induces an immunopathol

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

266 % of these clones were novel compared to the H. influenzae Rd KW20 genome, and most of them did not m

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

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

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

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

271 4,378-bp island is inserted, in reference to H. influenzae Rd KW20, within a choline transport gene a

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

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

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

275 ium, that was present in all 25 non-typeable H. influenzae, 19 of which contained multiple copies of

276 miologically diverse strains of non-typeable H. influenzae.

277 ains were genetically different from typical H. influenzae.

278 or subunit of the heretofore uncharacterized H. influenzae-expressed type IV pilus, a gene with homol

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