ライフサイエンスコーパス: P. carinii

1 P. carinii aggregation was reduced by maltose, mannose,

2 P. carinii DNA has been detected in respiratory specimen

3 P. carinii free of SP-A and alveolar macrophages were is

4 P. carinii incubated with natural SP-D (10 micro g/ml) c

5 P. carinii organisms were first stripped with glutathion

6 P. carinii STE20 (PCSTE20), a gene participating in mati

7 P. carinii-infected mice were treated with local instill

8 P. carinii-infected, CD4(+)-depleted mice had elevated l

9 ation structure occurred in rats given 10(4) P. carinii organisms, suggesting that a small fraction o

10 efined as the ratio IC(50)(rat liver)/IC(50)(P. carinii), was 8-fold higher than that of 1 and >10(4)

11 ad structure 3a (ratio rat liver DHFR IC(50)/P. carinii DHFR IC(50): 114).

12 in selectivity (ratio rat liver DHFR IC(50)/P. carinii DHFR IC(50): 5.36) compared to the original l

13 dition, we found that inoculation with 10(7) P. carinii organisms from a population highly heterogene

14 All inoculated animals had a P. carinii-specific PCR product after infection.

15 We have previously identified a P. carinii MAPK, PCM, which has significant homology to

16 In a P. carinii cell culture study, analogue 8 exhibited 88%

17 acilitate the Pneumocystis genome project, a P. carinii f. sp. carinii genomic cosmid library and an

18 a pattern associated with naturally acquired P. carinii infection.

19 different kinetics of NF-kappaB activation, P. carinii beta-glucan and LPS also utilize different re

20 ar lavage (BAL) fluids of humans with active P. carinii pneumonia.

21 exposed to immunosuppressed mice with active P. carinii pneumonia.

22 CD8+ T cells are recruited to the lung after P. carinii infection and have been associated with both

23 The activity of 13 against P. carinii DHFR was 20 000 times greater than that of TM

24 The potency of 13 against P. carinii DHFR was 20-fold greater than that of PTX (IC

25 tes with potential clinical activity against P. carinii and other opportunistic pathogens in patients

26 HIV drugs have little or no activity against P. carinii in these in vitro and in vivo systems.

27 at B cells also mediate host defense against P. carinii by facilitating CD4(+) T cell activation or e

28 at SP-D plays a role in host defense against P. carinii in vivo by modulating clearance of organisms,

29 s, SP-A plays a role in host defense against P. carinii in vivo, perhaps by functioning as a nonimmun

30 or molecule in the lung host defense against P. carinii in vivo.

31 these cells are required for defense against P. carinii infection is unknown.

32 delta-TCR(+) T cells in host defense against P. carinii pneumonia.

33 t, but not critical, role in defense against P. carinii.

34 17 axis participates in host defense against P. carinii.

35 zed by this antibody in immunization against P. carinii.

36 he most potent of the new inhibitors against P. carinii DHFR was the naphthylmethyl-substituted triaz

37 13), with an IC(50) value of 0.65 nM against P. carinii DHFR, 0.57 nM against M. avium DHFR, and 55 n

38 mong the pteridines, the most potent against P. carinii DHFR and M. avium DHFR was the 2'-(5-carboxy-

39 es more potent against rat DHFR than against P. carinii or T. gondii DHFR and that the selectivity in

40 As in C. albicans, P. carinii PHR1 expression was repressed under acidic co

41 of DHFR and DHPS sequences revealed that all P. carinii strains were confined within a distinct group

42 differences in the DHFR and DHPS genes among P. carinii from different host species has important imp

43 e b gene mutations in patients with AIDS and P. carinii pneumonia (PCP) are associated with atovaquon

44 FN-gamma, lipopolysaccharide, Poly(I:C), and P. carinii in vitro, and results revealed that these sti

45 chially with macaque-derived P. carinii, and P. carinii-specific polymerase chain reaction (PCR) and

46 ect subtle differences between the human and P. carinii forms, which identify species-specific, high-

47 hin Pneumocystis species, with P. murina and P. carinii being more closely related to each other than

48 e mtDNA terminal structures of P. murina and P. carinii suggest a unique replication mechanism for li

49 marneffei, S. schenckii, C. neoformans, and P. carinii hybridized with homologous but not heterologo

50 In the setting of immune reconstitution and P. carinii pneumonia, pretreatment with the viral IL-10

51 ment of both the crude BAL fluid samples and P. carinii lysate and the 200 mM methylmannose eluate wi

52 eads, the inhibitor in BAL fluid samples and P. carinii lysate could be eluted with 200 mM methylmann

53 cytokines (IFN-gamma) and pathogens (SIV and P. carinii) as contributors to increased expression of p

54 T cells in lung lavage samples from SIV- and P. carinii-coinfected animals increased to >90% of total

55 dinavir and saquinavir exhibited slight anti-P. carinii activity at concentrations above those that c

56 immunodeficiency syndrome (AIDS)-associated P. carinii pneumonia (PCP), SIV-infected macaques were i

57 ogue 21, with SI values of >100 against both P. carinii and M. avium DHFR relative to rat DHFR.

58 macrophages were unable to phagocytose both P. carinii organisms and fluorescein isothiocyanate (FIT

59 We demonstrate that both P. carinii Asf1 (PcAsf1) and PcVps75 can bind histones.

60 .7 macrophages overexpressing Dectin-1 bound P. carinii at a higher level than control RAW cells.

61 vitro and in vivo The M1 response induced by P. carinii was plastic in nature and reversible with app

62 natively, the rats may have been infected by P. carinii organisms that were already different at the

63 ptor is not sufficient to allow infection by P. carinii in otherwise immunocompetent mice.

64 developed for the human form of P. carinii (P. carinii f sp hominis) that is applicable to both clin

65 an opportunistic fungal pathogen that causes P. carinii pneumonia (PCP) in the immunocompromised host

66 ted FcgammaRKO mice were still able to clear P. carinii.

67 -deficient (SRAKO) mice consistently cleared P. carinii faster than did wild-type control mice.

68 At about 4 weeks of cohousing, P. carinii f. sp. muris was readily detectable in the lu

69 mice cohoused for only 1 week also contained P. carinii f. sp. muris cysts detectable by silver stain

70 of a reliable method to isolate and culture P. carinii from environmental samples, it has not been p

71 Thus, human-derived P. carinii regulates MSG expression in a manner similar

72 d to ascomycete fungi and that human-derived P. carinii was most closely related to monkey-derived P.

73 study, the UCS of the MSG from human-derived P. carinii was obtained using an RNA ligase-mediated rap

74 ts a hierarchy of evolution of human-derived P. carinii.

75 ulated intrabronchially with macaque-derived P. carinii, and P. carinii-specific polymerase chain rea

76 i was most closely related to monkey-derived P. carinii.

77 termed 4F11 generated against mouse-derived P. carinii was shown by indirect immunofluorescence assa

78 family; in two specific forms of rat-derived P. carinii, regulation of MSG expression uses a single e

79 tive touchdown (QTD) PCR assay for detecting P. carinii f. sp. carinii, the subspecies of P. carinii

80 lecules CD2 and CD28 spontaneously developed P. carinii pneumonia.

81 learance of Pneumocystis In addition, during P. carinii infection the expression of Dectin-1, a criti

82 D (SP-D) accumulate in the airspaces during P. carinii pneumonia and are particularly abundant in ag

83 mannose receptor is not downregulated during P. carinii infection in wild-type mice.

84 the GATA-2 transcription factor gene during P. carinii infection, alveolar macrophages from dexameth

85 R(+) T cells infiltrate into the lung during P. carinii pneumonia.

86 phagocytosis in alveolar macrophages during P. carinii infection.

87 t was not potent or selective against either P. carinii or T. gondii DHFR.

88 ly transferred to SCID mice with established P. carinii infections.

89 oints, mice were sacrificed and analyzed for P. carinii burden, T-cell subsets, and cytokine levels i

90 and reproducible quantitative PCR assay for P. carinii f. sp. carinii has been developed and is appl

91 infection intensity, as measured by PCR for P. carinii rRNA, was unchanged between the IL-10 and luc

92 d clearance of infection measured by PCR for P. carinii rRNA.

93 Upon receipt, 64% of rats were positive for P. carinii f. sp. carinii-specific antibodies, while P.

94 e further show that Dectin-1 is required for P. carinii-induced macrophage inflammatory protein 2 pro

95 etermine whether this defect is specific for P. carinii organisms.

96 orted in vitro axenic cultivation system for P. carinii and confirmed our microscopy findings that no

97 owever, when CD4(+) cells were depleted from P. carinii-infected IL-10 KO mice, the ability to enhanc

98 R was performed with total RNA isolated from P. carinii f. sp. carinii.

99 in phagocytosis in alveolar macrophages from P. carinii-infected hosts can be corrected by overexpres

100 s, indicating that alveolar macrophages from P. carinii-infected hosts have a general defect in phago

101 as introduced into alveolar macrophages from P. carinii-infected rats.

102 ssive activity of the BAL fluid samples from P. carinii-infected rats on phagocytosis was retained wh

103 nchoalveolar lavage (BAL) fluid samples from P. carinii-infected rats.

104 facilitated characterization of a functional P. carinii kre6 (Pckre6) beta-1,6 glucan synthase in Pne

105 Here, we demonstrate that both genes, P. carinii asf1 (Pcasf1) and Pcvps75, function in a fash

106 PS) mutations in patients with AIDS who have P. carinii pneumonia compares the change in the prevalen

107 dies to an epitope shared by mouse and human P. carinii organisms reduced organism numbers by more th

108 initiation of antibiotic treatment for human P. carinii pneumonia and to immune reconstitution syndro

109 f the spread and persistence of viable human P. carinii in the environment.

110 polymorphism technique was used to identify P. carinii DHPS mutations in 107 patients with acquired

111 is QTD PCR assay can be used to determine if P. carinii is present in respiratory samples and to dist

112 odes a protein containing 786 amino acids in P. carinii and P. murina, and 788 amino acids in P. jiro

113 STE11 is associated with the MAPK cascade in P. carinii.

114 ve families (not previously characterized in P. carinii) were found to be similar to families encodin

115 ve families were previously characterized in P. carinii, namely the major surface glycoproteins (MSGs

116 .8S, and 26S rDNA genes being single copy in P. carinii.

117 nalyzed, QTD PCR assays showed a decrease in P. carinii DNA that exceeded the expected decrease due t

118 The multicopy trr1 gene fragments in P. carinii are not transcribed or expressed.

119 eumocystis carinii strains, these 2 genes in P. carinii obtained from 7 different host species were s

120 kinase, we have cloned a STE11 homologue in P. carinii.

121 arity to the MAb 4F11 epitopes identified in P. carinii.

122 g revealed specific beta-1,6 localization in P. carinii cyst walls.

123 ate this issue, we examined the UCS locus in P. carinii from rats that had been exposed to few of the

124 56 and in DNA damage response are present in P. carinii DNA and cell cycle progression.

125 air fragment of the trr1 gene are present in P. carinii, but not in P. jiroveci.

126 defect is due to a certain factor present in P. carinii-infected lungs, alveolar macrophages from uni

127 he first characterization of any proteins in P. carinii involved in meiosis and indicate the presence

128 action, the in vivo role of this receptor in P. carinii clearance in unclear.

129 d 85 and 99.88% reductions, respectively, in P. carinii cysts at sacrifice 21 days later; P. carinii

130 mediating beta-glucan cell wall synthesis in P. carinii.

131 enic variation are functioning inadequately, P. carinii can express a broad repertoire of MSG variant

132 Interestingly, P. carinii PHR1 DNA successfully restored proliferation

133 These observations provide new insights into P. carinii signaling induced by interactions of this imp

134 agocytic activity of alveolar macrophages is P. carinii major surface glycoprotein or one or more of

135 ctive hybridization was performed to isolate P. carinii genes expressed following binding to mammalia

136 inhibitors decreased the ability of isolated P. carinii preparations to generate beta-1,6 carbohydrat

137 concerning the ability of CD8+ cells to kill P. carinii.

138 h the mitogen-activated protein (MAP) kinase P. carinii Ste20 (PcSte20) and the cell wall-remodeling

139 P. carinii cysts at sacrifice 21 days later; P. carinii nuclei were reduced by 91.2 and >99.99%, resp

140 duced by bacterial lipopolysaccharide (LPS), P. carinii beta-glucan-induced macrophage NF-kappaB acti

141 2-thioredoxin had significantly reduced lung P. carinii burdens after CD4+ T-cell depletion and chall

142 By comparison of anti-mouse P. carinii immunoglobulin G1 monoclonal antibody (MAb) 4

143 Immune sera raised against intact mouse P. carinii recognized native antigens affinity purified

144 ognized by MAb 4F11 in two recombinant mouse P. carinii antigens.

145 the occurrence of coinfection with multiple P. carinii strains.

146 ite emergence of antibiotic-resistant mutant P. carinii strains.

147 found and splicing preference was observed: P. carinii isolated from infected rat lung contained pri

148 dose-dependent increase of the adherence of P. carinii to the macrophages.

149 Aggregation of P. carinii by SP-D was shown to be responsible for the i

150 y was developed to assess the aggregation of P. carinii in vitro by SP-D.

151 Thus, SP-D-mediated aggregation of P. carinii may represent one means by which the organism

152 eric subunits-mediate optimal aggregation of P. carinii.

153 Analysis of P. carinii burden showed a more rapid and complete resol

154 ence assay (IFA) to bind surface antigens of P. carinii derived from multiple host species, including

155 The binding of P. carinii to alveolar epithelial cells and extracellula

156 he best outcomes with efficient clearance of P. carinii and reduced inflammation.

157 gM is not sufficient to mediate clearance of P. carinii from the lungs since CD40-deficient mice prod

158 (CD40KO chimeras) we found that clearance of P. carinii infection is delayed compared with wild-type

159 migration into the lungs or of clearance of P. carinii organisms when SCID mice were reconstituted w

160 Similarly, clearance of P. carinii was delayed in mice deficient in FcgammaRI an

161 to be a vital host cell in the clearance of P. carinii, and the mechanisms of this interaction have

162 sed by alveolar macrophages for clearance of P. carinii, mice deficient in the expression of scavenge

163 al receptor for recognition and clearance of P. carinii, was upregulated in macrophages of IC animals

164 ially mediates opsonization and clearance of P. carinii.

165 ture determination of the ternary complex of P. carinii DHFR--NADPH bound to TAB, predicted that modi

166 patients contained a lower concentration of P. carinii DNA than samples from PCP patients: lower res

167 ed by alveolar macrophages in the context of P. carinii infection.

168 ed fungi to address functional correlates of P. carinii-encoded proteins.

169 vivo effect of these cells on the course of P. carinii infection.

170 Most proposed life cycles of P. carinii include both asexual and sexual replicative c

171 he assay to a series of 10-fold dilutions of P. carinii organisms isolated from rat lung demonstrated

172 process rather than being a direct effect of P. carinii.

173 h other methods to study the epidemiology of P. carinii.

174 successfully used heterologous expression of P. carinii genes in related fungi to address functional

175 fungal genes, the pH-dependent expression of P. carinii PHR1 was examined.

176 ty assay was developed for the human form of P. carinii (P. carinii f sp hominis) that is applicable

177 he full length, catalytically active form of P. carinii IMPDH.

178 dy against the major surface glycoprotein of P. carinii eliminated their suppressive activity.

179 experiments using intratracheal injection of P. carinii organisms to induce infection, the loss of CD

180 Inoculation of P. carinii into normal mice evoked a brisk release of IL

181 The frequency and intensity of P. carinii infection were significantly greater in the S

182 sonic phagocytosis and subsequent killing of P. carinii by alveolar macrophages is dependent upon rec

183 inhibited binding and concomitant killing of P. carinii by alveolar macrophages.

184 d in alveolar macrophage-mediated killing of P. carinii.

185 The clearance kinetics of P. carinii from IL-10 KO mice was significantly enhanced

186 40KO chimeric mice produced normal levels of P. carinii-specific IgM, but did not produce class-switc

187 nd IFN-gamma mRNA expression in the lungs of P. carinii-infected neonates was significantly lower tha

188 f Pneumocystis carinii in research models of P. carinii pneumonia (PCP) that is more convenient and r

189 The major surface glycoprotein (MSG) of P. carinii f. sp. carinii is a family of proteins encode

190 ution did not result in increased numbers of P. carinii cysts compared to the numbers of cysts in mic

191 opy, we show that nonopsonic phagocytosis of P. carinii by alveolar macrophages is mediated by the De

192 d to have a 46% reduction in phagocytosis of P. carinii organisms and a 65% reduction in phagocytosis

193 hagocytic activity by 66% in phagocytosis of P. carinii organisms and by 280% in phagocytosis of FITC

194 involved in the binding and phagocytosis of P. carinii.

195 Pretreatment of P. carinii with human SP-A resulted in a significant dos

196 The prevalence of P. carinii DHPS mutations has markedly increased in the

197 eptor may be important in the recognition of P. carinii, in vivo, this mechanism may be redundant, an

198 m 10-day-old mice would effect resolution of P. carinii if harbored in an adult lung environment, cel

199 Therefore, the potential role of P. carinii PHR1 in cell wall integrity was examined by a

200 the prevalence and clinical significance of P. carinii DHPS mutations in Italian patients.

201 P. carinii f. sp. carinii, the subspecies of P. carinii commonly used in research models of PCP.

202 M2 cells significantly improved survival of P. carinii-infected IS hosts.

203 nterpreting reports of the susceptibility of P. carinii to anti-HIV drugs on the basis of in vitro te

204 alues (4.0 +/- 0.9 mN/m) similar to those of P. carinii-free control mice.

205 ct each other, and that the doubling time of P. carinii in vivo is approximately 3 days.

206 educe the organism count in the treatment of P. carinii pneumonia in immunosuppressed mice.

207 Opsonized P. carinii could also be efficiently killed in the prese

208 e of Dectin-1 blockage, killing of opsonized P. carinii could be restored through FcgammaRII/III rece

209 er the mice were reconstituted with naive or P. carinii-sensitized lymphocytes.

210 Some of the rats with bottlenecks produced P. carinii populations in which a single MSG sequence re

211 fer frequent frameshift mutations, providing P. carinii with another mechanism to generate antigen va

212 Purified P. carinii beta-glucans predictably induce both cytokine

213 brane extracts derived from freshly purified P. carinii incorporate uridine 5'-diphosphoglucose into

214 ivity, suggesting that the previous putative P. carinii IMPDH might not represent full length, functi

215 were analyzed for their effects against rat P. carinii by an ATP cytotoxicity assay.

216 pitopes may explain its ability to recognize P. carinii derived from multiple hosts and will permit t

217 veloped an antibody response that recognized P. carinii antigens, as determined by Western blotting a

218 The expression of PCSTE20 and a related P. carinii mitogen-activated protein kinase (MAPK) kinas

219 eonatal lymphocytes are competent to resolve P. carinii infection when harbored in an adult lung envi

220 em PCR analysis of individual lungs revealed P. carinii f. sp. carinii DNA in all rat lungs, illustra

221 ion compared to that of glutathione-stripped P. carinii.

222 amino acid sequence of this new gene, termed P. carinii PHR1, exhibited 38% homology to Saccharomyces

223 These data demonstrate that P. carinii beta-glucan acts as potent inducer of macroph

224 Herein, we demonstrate that P. carinii beta-glucan-induced macrophage stimulation re

225 Herein, we demonstrate that P. carinii binding to lung cells specifically alters the

226 We found that P. carinii f. sp. muris was detectable in the lungs of c

227 We tested the hypothesis that P. carinii stimulates the early release of IL-23, leadin

228 These results indicate that P. carinii PHR1 encodes a protein responsive to environm

229 Together these data indicate that P. carinii-specific IgG plays an important, but not crit

230 ammaRI and III (FcgammaRKO), indicating that P. carinii-specific IgG partially mediates opsonization

231 We show that P. carinii-specific IgM is not sufficient to mediate cle

232 Previous studies showed that P. carinii populations from individual rats exhibited hi

233 in 80 to 90% of the organisms, showing that P. carinii can proliferate within a rat without generati

234 Our study shows that P. carinii and P. murina mtDNA share a nearly identical

235 The P. carinii expressed sequence tag (EST) database contain

236 The P. carinii genome contains much of the genetic machinery

237 ate that beta-1,6 glucans are present in the P. carinii cell wall and contribute to lung cell inflamm

238 ot analysis demonstrated its presence in the P. carinii genome.

239 acquired immune response was initiated, the P. carinii f. sp. muris organisms were quickly eliminate

240 ally interacts with a specific region of the P. carinii cell wall biosynthesis kinase, PcCbk1, a down

241 Portions of the P. carinii cytochrome b genes that were obtained from 60

242 After an in silico search of the P. carinii genomic sequencing project identified a 329-b

243 nce was found to be a unique property of the P. carinii SAM:SMT.

244 Unlike SAM:SMT from other organisms, the P. carinii enzyme had higher affinities for lanosterol a

245 Shortly after this immune response, the P. carinii f. sp. muris organisms were cleared from the

246 We also found that the P. carinii f. sp. muris organisms grew to greater number

247 Thus, the P. carinii SAM:SMT catalysed the transfer of both the fi

248 ractions with amino acid Phe69 unique to the P. carinii enzyme.

249 -1 beta-glucan receptor colocalized with the P. carinii cyst wall.

250 Also at this time, P. carinii f. sp. muris-specific immunoglobulin G was fo

251 ice that had seroconverted after exposure to P. carinii-infected SCID mice were more resistant to inf

252 The lack of response of pup mice to P. carinii f. sp. muris may reflect protective mechanism

253 o address the role of IL-23 in resistance to P. carinii, IL-23p19-/- and wild-type control C57BL/6 mi

254 the T cells, is ineffective at responding to P. carinii infection.

255 Macrophage activation in response to P. carinii beta-glucan was also substantially inhibited

256 ificant (though partial) blunted response to P. carinii beta-glucan.

257 e in vitro but less TNF-alpha in response to P. carinii in vitro.

258 IL-10 down-regulates the immune response to P. carinii in WT mice; however, in the absence of CD4(+)

259 rleukin 12 (IL-12), and IL-18 in response to P. carinii infection than did wild-type mice.

260 ant for activation of T cells in response to P. carinii.

261 Examination of inflammatory responses to P. carinii revealed that mice deficient in both CD2 and

262 ulates MSG expression in a manner similar to P. carinii f. sp. carinii and, in immunosuppressed patie

263 (+) T cells modulates host susceptibility to P. carinii pneumonia through interactions with pulmonary

264 more, when mice were rendered susceptible to P. carinii by CD4(+) depletion, mannose receptor knockou

265 es and rendered HuCD4/Tg mice susceptible to P. carinii, a CD4-dependent pathogen, but did not compro

266 pup alveolar macrophages are unresponsive to P. carinii f. sp. muris organisms, they are capable of a

267 We sought to determine whether P. carinii f. sp. muris could be transmitted between nor

268 ii f. sp. carinii-specific antibodies, while P. carinii f. sp. carinii DNA was amplified from 98% of

269 emonstrated that PcSte20 obtained from whole P. carinii lysates has the ability to phosphorylate PcCb

270 rotection against an airborne challenge with P. carinii by intranasal administration of antibody.

271 ter CD4+ T-cell depletion and challenge with P. carinii.

272 able to be infected by brief cohousing with P. carinii-infected SCID mice.

273 ted period of asymptomatic colonization with P. carinii before progression to PCP.

274 Although difficulties with P. carinii culture and transformation have traditionally

275 ing antibody to wild-type mice infected with P. carinii also caused increases in fungal burdens.

276 ory cells, SP-A-deficient mice infected with P. carinii exhibit an enhanced susceptibility to the org

277 unocompetent mice to SCID mice infected with P. carinii f. sp. muris by cohousing.

278 IL-10 knockout (KO)) mice were infected with P. carinii to determine whether the severity of pathogen

279 cavenger receptor A (SRA) were infected with P. carinii, and clearance of organisms was monitored ove

280 In IL-23p19-/- mice infected with P. carinii, there were fewer effector CD4(+) T cells in

281 part of the host response to infection with P. carinii and that gene therapy with viral IL-10 can le

282 d during the host response to infection with P. carinii and whether local delivery of the IL-10 gene

283 ompetent hosts develop a mild infection with P. carinii f. sp. muris which resolves in 5 to 6 weeks w

284 epleted models, 2 weeks after infection with P. carinii, SP-D KO mice developed increased intensity o

285 the initial susceptibility to infection with P. carinii.

286 tecting at-risk patients from infection with P. carinii.

287 f the normal host response to infection with P. carinii.

288 munodeficient scid mice were inoculated with P. carinii and were heavily infected after 4 weeks.

289 l and CD4-depleted mice were inoculated with P. carinii, and at serial intervals after inoculation, l

290 When inoculated with P. carinii, both wild-type (wt) and SP-D KO mice require

291 ts, beginning when rats were inoculated with P. carinii, caused 85 and 99.88% reductions, respectivel

292 luciferase gene followed by inoculation with P. carinii.

293 t) mice were inoculated intratracheally with P. carinii.

294 ro, stimulation of alveolar macrophages with P. carinii induced IL-23, and IL-23p19 mRNA was expresse

295 in respiratory specimens from patients with P. carinii pneumonia (PCP) and from patients without cli

296 fied from pulmonary samples of patients with P. carinii pneumonia demonstrated that multiple MSG gene

297 east fourfold in BAL fluids of patients with P. carinii pneumonia.

298 At 9 weeks postinfection with P. carinii, nonreconstituted SCID mice exhibited no sign

299 r necrosis factor alpha when stimulated with P. carinii beta-glucan.

300 Pneumocystis infection than CD4-depleted WT (P. carinii pneumonia [PCP] scores of 3 versus 2, respect