ライフサイエンスコーパス: B. pertussis

1 B. pertussis also requires a relatively expensive growth

2 B. pertussis and B. bronchiseptica core OS were bound to

3 B. pertussis blocked migration of neutrophils and inhibi

4 B. pertussis does not express the O antigen, while B. pa

5 B. pertussis encodes many uncharacterized transcription

6 B. pertussis grew efficiently and caused moderate pathol

7 B. pertussis LPS has a branched core structure with a no

8 B. pertussis uses pertussis toxin (PT) and adenylate cyc

9 B. pertussis was confirmed in all cases.

10 B. pertussis-induced histamine sensitization (Bphs) is a

11 B. pertussis-infected pendrin knockout (KO) mice had hig

12 B. pertussis-stimulated dendritic cells from IL-1R(-/-)

13 el of conservation of gene content among 137 B. pertussis strains with different geographical, tempor

14 Only 16 (38%) B. pertussis-associated hospitalizations fulfilled the C

15 Sixty of 72 B. pertussis isolates were viable for analysis.

16 measure of in vivo fitness, the ability of a B. pertussis heme utilization mutant to colonize and per

17 nce of functional adenylate cyclase toxin, a B. pertussis toxin that has been shown to depress neutro

18 P phosphatase activity by NSC87877 abrogated B. pertussis survival inside murine macrophages.

19 Acellular B. pertussis vaccines were not efficiently protective ag

20 these are novel for responses to penta-acyl B. pertussis LPS, and their mutation does not affect the

21 suggests that recognition of penta-acylated B. pertussis lipid A is dependent on uncharged amino aci

22 However, antibodies affected B. pertussis after a delay of at least a week by a mecha

23 e-induced antisera were bactericidal against B. pertussis, and the titers correlated with ELISA-measu

24 a saline solution, were bactericidal against B. pertussis, and their titers correlated with their ELI

25 ter vaccinations were more effective against B. pertussis than B. holmesii (effectiveness: 67% and 36

26 ively and actively acquired immunity against B. pertussis.

27 ion in adaptive immunological memory against B. pertussis.

28 ntigens, confer efficient protection against B. pertussis but not against B. parapertussis.

29 ines were not efficiently protective against B. pertussis in IL-1R(-/-) mice.

30 and suppress innate immune responses against B. pertussis infection.

31 ophil recruitment, which consequently allows B. pertussis to avoid rapid antibody-mediated clearance

32 Although B. pertussis infection of monocytes induced rapid and ro

33 ussis and Bordetella bronchiseptica Although B. pertussis represents a pathogen strictly adapted to t

34 the in vivo fitness of B. bronchiseptica and B. pertussis.

35 protects against both pertussis disease and B. pertussis infection.

36 Symptoms were similar among B. holmesii- and B. pertussis-infected patients.

37 on systems in mice, sera from uninfected and B. pertussis-infected human donors were screened for ant

38 The two conjugates induced similar anti-B. pertussis LPS IgG levels in mice.

39 Molecular characterization of archived B. pertussis isolates (collected January 2007 to March 2

40 of other Bordetella species misidentified as B. pertussis during a period of increased pertussis inci

41 ti-inflammatory properties of the attenuated B. pertussis BPZE1 vaccine candidate and supports its de

42 ectrum antibiotic treatment delivered before B. pertussis inoculation reduced the infectious dose to

43 rences in low-temperature adaptation between B. pertussis and B. bronchiseptica may result from selec

44 PCR-based assay that can distinguish between B. pertussis and Bordetella holmesii.

45 e upregulated during iron starvation in both B. pertussis strain Tohama I and Bordetella bronchisepti

46 rdetella species (Bordetella bronchiseptica, B. pertussis, and B. parapertussis) and its role in thei

47 Alcaligin-mediated iron acquisition by B. pertussis may be critical for successful host coloniz

48 d by PRN(-) B. pertussis and cases caused by B. pertussis producing pertactin (PRN(+)) (P = .01).

49 Biofilm formation by B. pertussis plays an important role in pathogenesis.

50 ntly to the inflammatory response induced by B. pertussis infection by augmenting COX-2 expression an

51 However, immunity induced by B. pertussis infection prevented subsequent B. pertussis

52 is considerably larger than that induced by B. pertussis or B. parapertussis.

53 Ptx contributes to IL-1beta induction by B. pertussis, which is involved in IL-10 induction throu

54 ment enhanced respiratory tract infection by B. pertussis, even though it also induced a rapid influx

55 ntities that are comparable to those made by B. pertussis.

56 was induced in the lungs of C57BL/6 mice by B. pertussis.

57 ssis toxin (Ptx), which is expressed only by B. pertussis.

58 ourse and were less efficiently protected by B. pertussis vaccination than wild-type mice.

59 early infection of the respiratory tract by B. pertussis.

60 control infection but did not rapidly clear B. pertussis from the lungs.

61 We characterized 703 clinical B. pertussis isolates collected in the United Kingdom be

62 Under iron starvation stress conditions, B. pertussis produces the siderophore alcaligin.

63 ay is useful as a diagnostic tool to confirm B. pertussis infections and to rapidly identify other Bo

64 pertactin-producing and pertactin-deficient B. pertussis infections.

65 An isogenic Ptx-deficient B. pertussis strain had only a modest phenotype in wild-

66 ith wild-type (WT) or PT-deficient (DeltaPT) B. pertussis.

67 ped a multitarget PCR assay to differentiate B. pertussis, B. holmesii, and B. parapertussis and prov

68 Of the USPHLs that differentiated B. pertussis and B. holmesii, sensitivity was 96% and sp

69 tively, 72% and 79% of USPHLs differentiated B. pertussis and B. holmesii and 68% and 72% identified

70 t lower levels of IL-10 were detected during B. pertussis infection in IL-1R(-/-) mice.

71 ls deregulate immune system functions during B. pertussis infection.

72 gly, we found no role for neutrophils during B. pertussis infection in naive mice.

73 er neutrophils play a protective role during B. pertussis infection in mice.

74 jacking of SHP-1 by CyaA action then enables B. pertussis to evade NO-mediated killing in sentinel ce

75 CyaA-produced signaling of cAMP thus enables B. pertussis to evade the key innate host defense mechan

76 o the circulation, significantly exacerbated B. pertussis infection.

77 sted at two U.S. commercial laboratories for B. pertussis and B. parapertussis detection.

78 Our data reveal a biofilm lifestyle for B. pertussis in the nose and the requirement of Bps in t

79 A total of 171 patients tested positive for B. pertussis from 1 March to 31 October 2010 by polymera

80 As shown previously for B. pertussis, bfrD expression in B. bronchiseptica was a

81 hough BrkA has been shown to be required for B. pertussis to resist complement-mediated killing in vi

82 uence 481 (IS481), which is not specific for B. pertussis; therefore, the relative contribution of ot

83 t the time of illness visits were tested for B. pertussis by polymerase chain reaction (PCR).

84 teria of respiratory illness were tested for B. pertussis infection by PCR on paired NPSs and NPAs; o

85 tics of nucleic acid amplification tests for B. pertussis.

86 PAs), and induced sputum, have been used for B. pertussis detection, although there is limited head-t

87 rtance of alcaligin and haem utilization for B. pertussis in vivo growth and survival.

88 IS481 cycle threshold (CT) values for B. pertussis samples had coefficients of variation (CV)

89 u) most likely acquired its fhaS allele from B. pertussis horizontally, suggesting fhaS may contribut

90 pertussis to colonize mice convalescent from B. pertussis infection.

91 B. bronchiseptica strain expressing FHA from B. pertussis (FHA(Bp)) and compared it with wild-type B.

92 with illness, 0.7 percent to 5.7 percent had B. pertussis infection, and the percentage increased wit

93 Thus it is critical to understand how B. pertussis remains endemic even in highly vaccinated o

94 ronchiseptica) and whooping cough in humans (B. pertussis and B. parapertussis).

95 t appears that in adapting to infect humans, B. pertussis and B. parapertussis independently modified

96 In B. pertussis, BtrA retains activity as a BtrS antagonist

97 In B. pertussis, deletion of the rseA gene results in high

98 y is required for cytochrome c biogenesis in B. pertussis, a targeted knockout was made in dsbB.

99 Most importantly, deletion of btrA in B. pertussis revealed T3SS-mediated, BteA-dependent cyto

100 ted, inactivated, or unregulated by BvgAS in B. pertussis.

101 system; however, in contrast to the case in B. pertussis, the known modulators nicotinic acid and su

102 resent study examined genome-wide changes in B. pertussis gene transcript abundance in response to ir

103 All three genes are highly conserved in B. pertussis, B. parapertussis, and B. avium.

104 ernative mechanisms to oxidize disulfides in B. pertussis are analyzed and discussed.

105 pare in vivo and in vitro gene expression in B. pertussis, and that temporal regulation patterns prev

106 iplex assay include IS481, commonly found in B. pertussis and B. holmesii; IS1001 of B. parapertussis

107 he regulation of four bvg-repressed genes in B. pertussis.

108 d that localization of PtlH was perturbed in B. pertussis strains that were treated with carbonyl cya

109 indicating that gene acquisition is rare in B. pertussis.

110 Comparative analysis of Bvg regulation in B. pertussis and B. bronchiseptica revealed a relatively

111 iple aspects of adaptive immune responses in B. pertussis-infected IL-6(-/-) mice and suggest that IL

112 results indicate a role for S1P signaling in B. pertussis-mediated pathology and highlight the possib

113 r sphingosine-1-phosphate (S1P) signaling in B. pertussis-mediated pathology and highlight the possib

114 In contrast, bfeA transcription in B. pertussis and B. bronchiseptica bfeR mutants was comp

115 in vivo technology (RIVET) system for use in B. pertussis.

116 These heat-inactivated B. pertussis Ag/LPS-stimulated mast cells fail to promot

117 tella bronchiseptica cluster, which includes B. pertussis, B. parapertussis, and B. bronchiseptica.

118 2% (n = 99) were identified as indeterminate B. pertussis at CDC.

119 In immunocompetent individuals, B. pertussis infection elicits an effective adaptive imm

120 During infection, B. pertussis releases several toxins, including pertussi

121 Klebsiella species was sufficient to inhibit B. pertussis colonization of antibiotic-treated mice.

122 ablish that delivery of this toxin by intact B. pertussis is not dependent on the surface-associated

123 Interestingly, an isogenic B. pertussis strain lacking pertussis toxin did not indu

124 ce produced IL-17 in response to heat-killed B. pertussis in the presence of APC.

125 ting that interspecies competition may limit B. pertussis colonization of mice.

126 om the human lower respiratory tract limited B. pertussis growth in vitro, indicating that interspeci

127 However, live B. pertussis persists in the host for 3 to 4 weeks prior

128 enting apoptosis induced by exposure to live B. pertussis.

129 auses lethal disease in TLR4-deficient mice, B. pertussis and B. parapertussis do not.

130 W contained up to approximately 10(8) CFU/ml B. pertussis and 1 to 5 ng/ml ACT at the peak of infecti

131 e analyzed for changes in antibodies to nine B. pertussis antigens.

132 itical in limiting B. bronchiseptica but not B. pertussis or B. parapertussis bacterial numbers durin

133 Interestingly, B. parapertussis, but not B. pertussis, produces an O antigen, a factor shown in o

134 The incidence (per 1000) of B. pertussis-associated hospitalization was 2.9 (95% con

135 anges in genome-wide transcript abundance of B. pertussis as a function of growth phase and availabil

136 The adenylate cyclase toxin (ACT) of B. pertussis is a potent enzyme that converts cytosolic

137 In this study, transcriptional activation of B. pertussis bhu genes in response to heme compounds was

138 for calmodulin, the eukaryotic activator of B. pertussis ACT.

139 essory protein required for the acylation of B. pertussis ACT.

140 tica may result from selective adaptation of B. pertussis to the human host.

141 ions as an adhesin by promoting adherence of B. pertussis and Escherichia coli to human nasal but not

142 An exploratory analysis of B. pertussis culture was performed on induced sputum spe

143 ystem protein production by an assortment of B. pertussis laboratory-adapted and low-passage clinical

144 rable host microbiota, whereas 10 000 CFU of B. pertussis were required to colonize murine nasal cavi

145 sis antibodies and reduce the circulation of B. pertussis.

146 -type mice in their control and clearance of B. pertussis or B. parapertussis, suggesting that IgA is

147 required for antibody-mediated clearance of B. pertussis.

148 surveillance with laboratory confirmation of B. pertussis infection, we cannot definitively conclude

149 of pertussis toxin, allowing both control of B. pertussis numbers and regulation of the inflammation

150 e defect of IL-6(-/-) mice in the control of B. pertussis numbers.

151 were admitted to hospital within 21 days of B. pertussis detection, whereas none of the 20 cases >/=

152 tum performed similarly for the detection of B. pertussis infection in young infants by PCR.

153 assays to improve the molecular detection of B. pertussis.

154 283 and BP485, for the specific detection of B. pertussis.

155 heir coexistence and the limited efficacy of B. pertussis vaccines against B. parapertussis suggest a

156 arlier role than ACT in the establishment of B. pertussis infection.

157 variety of approaches to examine features of B. pertussis genetic variation.

158 ligin transport to the ecological fitness of B. pertussis may be important for adaptation to iron-res

159 of the enterobactin system to the fitness of B. pertussis was confirmed using wild-type and enterobac

160 ation, while knockout of the BpeGReg gene of B. pertussis results in decreased biofilm formation.

161 st to our previous report, the fhaB genes of B. pertussis and B. bronchiseptica are functionally inte

162 We also show that the cyaA genes of B. pertussis and B. bronchiseptica, which encode adenyla

163 evious studies showed that the fhaB genes of B. pertussis and B. bronchiseptica, which encode filamen

164 s complementation using cloned alcS genes of B. pertussis or B. bronchiseptica restored the wild-type

165 In this study, the bfrD and bfrE genes of B. pertussis were shown to be functional in B. bronchise

166 ntly specific for reliable identification of B. pertussis.

167 Imaging of B. pertussis-exposed neutrophils revealed that B. pertus

168 uld contribute to the increased incidence of B. pertussis infection since the transition to the use o

169 Isolation of B. pertussis in adults is difficult, resulting in a dela

170 both gene and protein levels in the lungs of B. pertussis-infected mice.

171 curated flux balance analysis-based model of B. pertussis metabolism.

172 t (PTx-dependent) mechanism; a PTx mutant of B. pertussis induced rapid neutrophil recruitment and wa

173 Adacel vaccines contain high copy numbers of B. pertussis DNA, which can be aerosolized, causing fals

174 eport the first documented mixed outbreak of B. pertussis and B. holmesii infections.

175 ilization contributes to the pathogenesis of B. pertussis in the mouse infection model and indicate t

176 central role of CyaA in the pathogenesis of B. pertussis.

177 of CR3, FHA, and ACT on the phagocytosis of B. pertussis by human neutrophils was examined.

178 enzymatic activity inhibits phagocytosis of B. pertussis in vitro.

179 We show that the Bps polysaccharide of B. pertussis is critical for initial colonization of the

180 duction requires growing large quantities of B. pertussis.

181 to investigate BvgAS-mediated regulation of B. pertussis virulence factors in vivo using the mouse a

182 n between neonatal mice, the first report of B. pertussis transmission in mice.

183 etics of BvgA phosphorylation after shift of B. pertussis cultures from non-permissive to permissive

184 In the virulent phase, the default state of B. pertussis, the cytoplasmic enzymatic moiety of BvgS a

185 ner membrane fractions of a mutant strain of B. pertussis that does not produce PT.

186 ately 10(8) CFU/ml of a laboratory strain of B. pertussis was cultured in vitro, ACT production was d

187 raction of the cell in a wild-type strain of B. pertussis.

188 We also engineered strains of B. pertussis by introducing multiple copies of the ptl g

189 bcellular localization of PtlH in strains of B. pertussis lacking PT, lacking other Ptl proteins, or

190 eting cellular ATP levels, and in strains of B. pertussis that produce an altered form of PtlH that l

191 We have previously shown that two strains of B. pertussis, BP338 (a Tohama I-derivative) and 18-323,

192 to how it localized in wild-type strains of B. pertussis, PtlH exhibited aberrant localization in st

193 rrelate to the in vivo expression studies of B. pertussis iron systems in mice, sera from uninfected

194 me utilization contributed to the success of B. pertussis as a pathogen.

195 tive results that can, given the tendency of B. pertussis to cause outbreaks, result in unnecessary a

196 is that is similar but distinct from that of B. pertussis.

197 h it is widely believed that transmission of B. pertussis occurs via aerosolized respiratory droplets

198 In addition, treatment of B. pertussis-infected mice with the carbonic anhydrase i

199 indicating that the particular virulence of B. pertussis in these mice requires Ptx.

200 tinct, and current vaccines, containing only B. pertussis-derived antigens, confer efficient protecti

201 heat-killed whole-cell B. bronchiseptica or B. pertussis inhibited shedding of B. bronchiseptica.

202 The overall B. pertussis PCR positivity was 2.3% (42/1839), of which

203 By comparing parental B. pertussis to an rseA gene deletion mutant (PM18), we

204 quired for persistence of the human pathogen B. pertussis in the murine LRT and we provide evidence t

205 xacerbated host airway responses during peak B. pertussis infection but also may inhibit host mechani

206 ed the ability of neutrophils to phagocytose B. pertussis, suggesting that elevated CR3 expression al

207 h can be aerosolized, causing false-positive B. pertussis PCR results.

208 eal that resident microorganisms can prevent B. pertussis colonization and influence host specificity

209 trategy in a setting such us ours to prevent B. pertussis-associated illness in women and their young

210 tion differed between cases caused by PRN(-) B. pertussis and cases caused by B. pertussis producing

211 cine dose had a higher odds of having PRN(-) B. pertussis compared with unvaccinated case-patients (a

212 rmining whether pertactin-deficient (PRN(-)) B. pertussis is evading vaccine-induced immunity or alte

213 pertactin-deficient and pertactin-producing B. pertussis infection in infants and describe correspon

214 deficient and those with pertactin-producing B. pertussis.

215 ile B. bronchiseptica has a wide host range, B. pertussis and B. parapertussis evolved separately fro

216 , though lower in titer, efficiently reduced B. pertussis numbers in IL-6-sufficient mice.

217 IL-10 treatment reduced B. pertussis numbers in IL-1R(-/-) mice, suggesting that

218 compared with B. bronchiseptica Remarkably, B. pertussis maintained the production of virulence fact

219 urse of gene expression in vivo for selected B. pertussis virulence factors (cya, fha, prn and ptx).

220 strain elicited greater responses to several B. pertussis antigens than did infection with the WT, de

221 als and wP-vaccinated animals possess strong B. pertussis-specific T helper 17 (Th17) memory and Th1

222 B. pertussis infection prevented subsequent B. pertussis infections but did not protect against B. p

223 ly conserved in the human-adapted subspecies B. pertussis and B. parapertussis.

224 In response to low temperatures, B. pertussis adapted its fatty acid composition and memb

225 stantially earlier in B. bronchiseptica than B. pertussis following a switch from Bvg(-) to Bvg(+) ph

226 vestigated because it is easier to grow than B. pertussis.

227 S) is 10- and 100-fold more stimulatory than B. pertussis or B. parapertussis LPS, respectively.

228 expression among Bordetella species and that B. pertussis is capable of expressing a full range of T3

229 Given that B. pertussis is thought to have derived from a Bordetell

230 tin and haem, supporting the hypothesis that B. pertussis is iron-starved and responds to the presenc

231 rtussis proteins support the hypothesis that B. pertussis perceives an iron starvation cue and expres

232 pertussis-exposed neutrophils revealed that B. pertussis lacking ACT induces formation of neutrophil

233 Here we show that B. pertussis and B. parapertussis are predominantly diff

234 e same time and vaccine studies showing that B. pertussis vaccines have little effect on B. parapertu

235 data suggest increasing selection among the B. pertussis population in Australia in favor of strains

236 . bronchiseptica bvgAS mutant expressing the B. pertussis bvgAS genes revealed that the interspecies

237 481, which is present in high numbers in the B. pertussis chromosome.

238 t IS481, present in 218 to 238 copies in the B. pertussis genome and 32 to 65 copies in B. holmesii.

239 mouse respiratory model, inactivation of the B. pertussis ferric alcaligin receptor protein was found

240 tenuation resulting from inactivation of the B. pertussis heme system was assessed using mixed infect

241 e propose that the reduced plasticity of the B. pertussis membranes ensures sustained production of v

242 al evidence of the in vivo importance of the B. pertussis receptors was obtained from serologic studi

243 des a predicted protein with homology to the B. pertussis FhaC outer membrane protein that is involve

244 pertussis patient serum reactivity with the B. pertussis BfrD and BfrE proteins.

245 infection model showed that several of these B. pertussis iron systems are required for colonization

246 d natural-host animal models should apply to B. pertussis FHA as well.

247 gAS alleles of B. bronchiseptica compared to B. pertussis, but appears to be species specific.

248 d capacity in B. bronchiseptica, compared to B. pertussis, for ex vivo adaptation.

249 sA regulon adds a new layer of complexity to B. pertussis virulence gene regulation.

250 In contrast to B. pertussis ACT, however, ACT from B. hinzii is less ex

251 r Toll-like receptor 4 (TLR4) in immunity to B. pertussis and B. bronchiseptica, while no role for TL

252 ugh the mechanisms of protective immunity to B. pertussis have been well studied, those of B. paraper

253 immunity to B. pertussis Natural immunity to B. pertussis induced by infection is considered long las

254 of respiratory CD4 TRM cells in immunity to B. pertussis Natural immunity to B. pertussis induced by

255 xamine the nature of sterilizing immunity to B. pertussis.

256 e immune response and restored resistance to B. pertussis infection.

257 nd T cell cytokine production in response to B. pertussis as well as the generation of effective vacc

258 needed to understand the immune response to B. pertussis infection in children vaccinated with aP va

259 ich reduces neutrophil influx in response to B. pertussis infection, potentially providing an advanta

260 rophages and other lung cells in response to B. pertussis infection.

261 nts impaired their innate immune response to B. pertussis infection.

262 flux to the lungs and airways in response to B. pertussis respiratory tract infection in mice.

263 Enhanced innate immune response to B. pertussis was characterized by increased production o

264 factor, in lung transcriptional responses to B. pertussis infection in mouse models.

265 ic or pulmonary T cell cytokine responses to B. pertussis, including Th1 and Th17 cytokine production

266 that controls differential susceptibility to B. pertussis PTX-induced HA sensitization (Bphs).

267 hown that newborn piglets are susceptible to B. pertussis.

268 r bfrE imparted catecholamine utilization to B. pertussis.

269 than naive animals, and readily transmitted B. pertussis to unvaccinated contacts.

270 ic phases, we isolated and characterized two B. pertussis mutants that were able to express Bvg- and

271 the attachment and phagocytosis of wild-type B. pertussis and FHA mutants.

272 xtracellular traps (NETs), whereas wild-type B. pertussis does not, suggesting that ACT suppresses NE

273 were efficiently phagocytosed, but wild-type B. pertussis or ACT mutants plus exogenous ACT resisted

274 ducing this mutation into multiple wild-type B. pertussis strains allowed us to confirm the in vitro

275 us macaques and olive baboons with wild-type B. pertussis strains and evaluated animals for clinical

276 bind, aggregate, nor permeabilize wild-type B. pertussis.

277 Unfortunately, B. pertussis has relatively slow growth in culture, with

278 Using B. pertussis cytochrome c4 as a reporter for cytochromes

279 Previous studies using B. pertussis and cultured mammalian cells identified sev

280 lenged with a high dose of a highly virulent B. pertussis isolate, they were fully protected against

281 ate or negative results, 46.1% (n = 53) were B. pertussis positive when tested by an alternate master

282 These CD4 TRM cells were B. pertussis specific and secreted IL-17 or IL-17 and IF

283 of ACT internalization all influence whether B. pertussis will be phagocytosed and ultimately killed

284 ient availability may serve as cues by which B. pertussis regulates virulence according to the stage

285 We encountered an adult patient in whom B. pertussis was isolated by culture who previously rece

286 cularly the infection of infant baboons with B. pertussis, are enabling longstanding questions about

287 eveloped severe disease when challenged with B. pertussis at 5 weeks of age.

288 pertussis (wP) vaccines and challenged with B. pertussis at 7 mo.

289 or intoxication of cells when incubated with B. pertussis, we characterized the requirements of intox

290 n to unvaccinated mothers were infected with B. pertussis at 5 weeks of age.

291 itical factor in establishing infection with B. pertussis and acts by specifically inhibiting the res

292 nteraction that is central to infection with B. pertussis and other Bordetella species.

293 expanded in the lungs during infection with B. pertussis and proliferated rapidly after rechallenge

294 d in the lungs of mice during infection with B. pertussis and significantly expanded through local pr

295 sponse was not observed after infection with B. pertussis mutant strains lacking filamentous hemagglu

296 and memory induced by natural infection with B. pertussis.

297 Following inoculation with B. pertussis, but not B. parapertussis, IL-1R(-/-) mice

298 ears, compared with 35% of 112 patients with B. pertussis infections (P = .001).

299 cells from the lungs of mice reinfected with B. pertussis produced significantly more IL-17 than gamm

300 By comparing a wild-type (WT) B. pertussis strain to a mutant strain with an in-frame