ライフサイエンスコーパス: M. pneumoniae

1 M. pneumoniae also bound lactose 3'-sulfate ligated to a

2 M. pneumoniae caused a community-wide outbreak of cough

3 M. pneumoniae HA mutant II-3 lacking P30 was nonmotile,

4 M. pneumoniae induced the generation of prostaglandins P

5 M. pneumoniae infection is associated with GBS, more fre

6 M. pneumoniae possesses a cytoskeleton-like structure re

7 M. pneumoniae recognizes sialylated and sulfated oligosa

8 M. pneumoniae significantly activated SHP-1 in airway ep

9 M. pneumoniae was associated with the increased synovial

10 M. pneumoniae was cultured directly from sibling 2 autop

11 M. pneumoniae was detected by PCR in 10 of 18 asthmatics

12 M. pneumoniae was detected by PCR in 10 students with pn

13 M. pneumoniae was detected by real-time PCR in 175 (5.8%

14 M. pneumoniae was detected in bronchoalveolar lavage flu

15 M. pneumoniae was present in the lower airways of chroni

16 M. pneumoniae-infected macrophages deficient for inflamm

17 M. pneumoniae-infected mice treated with IL-12 (MpIL12 m

18 A retrospective analysis of 154 M. pneumoniae clinical isolates collected over the last

19 We examined 199 M. pneumoniae-positive specimens collected during this t

20 er surfaces of both wild-type and mutant I-2 M. pneumoniae but to a considerably lesser extent in the

21 This assay correctly identified 36 M. pneumoniae reference strains and clinical isolates fr

22 cteristics of M. pneumoniae We collected 446 M. pneumoniae-positive specimens from 9 states between A

23 Furthermore, we screened over 3,500 M. pneumoniae transposon mutants individually to identif

24 glyA, atpA, arcC, and adk) and applied to 55 M. pneumoniae clinical isolates and the two type strains

25 l of 12 sequence types (STs) resulted for 57 M. pneumoniae isolates tested, with a discriminatory ind

26 Anti-TLR2 antibody completely abolished M. pneumoniae-induced AA release and TNFalpha secretion

27 s, SHP-1 plays a critical role in abrogating M. pneumoniae-induced IL-8 production in nonasthmatic ai

28 munologic and therapeutic responses to acute M. pneumoniae infection.

29 After M. pneumoniae lung infection, Muc18(-/-) mice exhibited

30 rts for analysis of serum antibodies against M. pneumoniae (n = 479) and GalC (n = 198).

31 determine the functions of ST2 during airway M. pneumoniae or HRV infection.

32 us automated PCR platform with its MGB Alert M. pneumoniae real-time PCR research use only reagents (

33 All M. pneumoniae specimens (n=12) and isolates (n=10) were

34 Although M. pneumoniae was detected in schools, its transmission

35 An M. pneumoniae mini-Tn4001-integrated, clpB-null mutant w

36 notypic consequences when introduced into an M. pneumoniae topJ mutant.

37 We recently reported that an M. pneumoniae-derived ADP-ribosylating and vacuolating t

38 underscoring the correlation between crl and M. pneumoniae cytadherence.

39 nia; 5 of these specimens were cultured, and M. pneumoniae was isolated in 4.

40 sed separately and in combination to ETS and M. pneumoniae for 16 weeks.

41 n combination to cigarette smoke extract and M. pneumoniae for 48 h had elevated apical levels of GSH

42 ctionally related genes in M. genitalium and M. pneumoniae are often preceded by promoters but rarely

43 /c mice were anesthetized with metofane, and M. pneumoniae was introduced intranasally on days 0, 1,

44 cobacterium tuberculosis, S. pneumoniae, and M. pneumoniae were the most common etiologic agents.

45 Anti-M. pneumoniae immunoglobulin (Ig) M antibodies were dete

46 mens (< 10 per batch) submitted for IgM anti-M. pneumoniae testing.

47 Serum anti-M. pneumoniae immunoglobulin G titers were positive in a

48 Serum anti-M. pneumoniae immunoglobulin G was detectable in all of

49 Anti-GalC antibodies correlated with anti-M. pneumoniae antibodies (p < 0.001) and cross-reacted w

50 viously, we reported that surface-associated M. pneumoniae elongation factor Tu (EF-Tu, also called M

51 cerevisiae chromosome III and IV, bacterium M. pneumoniae, human major histocompatibility complex se

52 were found to have significantly higher BAL M. pneumoniae concentrations than those of M. pneumoniae

53 e were found to have significantly lower BAL M. pneumoniae concentrations compared with M. pneumoniae

54 ed quantitative bronchoalveolar lavage (BAL) M. pneumoniae culture, lung histopathologic score (HPS),

55 ed quantitative bronchoalveolar lavage (BAL) M. pneumoniae culture, lung histopathologic scores (HPS)

56 this study we describe interactions between M. pneumoniae and human surfactant protein-A (hSP-A).

57 321Q and N323D substitutions, failed to bind M. pneumoniae lipids, directly implicating the carbohydr

58 2,3, but P1-specific antibodies that blocked M. pneumoniae hemadsorption (HA) and binding to the sial

59 l cells, and these increases were blocked by M. pneumoniae and were also associated with increased ce

60 roduced effects similar to those elicited by M. pneumoniae in macrophages by inducing the phosphoryla

61 mechanism of mucin overproduction induced by M. pneumoniae remains unclear.

62 In asthmatic airway epithelial cells, M. pneumoniae induced significant PI3K/Akt phosphorylati

63 nd polymerase chain reaction (PCR)-confirmed M. pneumoniae infection were eligible for inclusion.

64 By contrast, M. pneumoniae persisted in the respiratory tract for the

65 e represents a superior target for detecting M. pneumoniae DNA in clinical specimens, although use of

66 assay is a useful rapid method for detecting M. pneumoniae in clinical specimens.

67 (p < 0.001) and cross-reacted with different M. pneumoniae strains.

68 PCR assay successfully detected 31 distinct M. pneumoniae clinical isolates and reference strains, a

69 pneumonias are ineffective in distinguishing M. pneumoniae from viral pneumonia.

70 parison to the 20-mer containing 223K during M. pneumoniae infection.

71 cle, we show that the absence of SP-A during M. pneumoniae infection leads to increased numbers of ma

72 piratory specimens (n = 72) collected during M. pneumoniae outbreaks and sporadic cases occurring in

73 in maintenance of airway homeostasis during M. pneumoniae pulmonary infection by preventing an overz

74 ivity in reducing TNF-alpha induction during M. pneumoniae infection.

75 had an effect on p38 phosphorylation during M. pneumoniae infection, the 223Q-20mer peptide signific

76 is important for the immune response during M. pneumoniae acute infection.

77 lammation and BHR by reducing or eliminating M. pneumoniae in lungs.

78 As expected, M. pneumoniae bound to surfaces coated with sulfatide in

79 The lack of IL-12 in experimental M. pneumoniae pneumonia was associated with less severe

80 Treatment of experimental M. pneumoniae pneumonia with intranasal IL-12 was associ

81 xtension analysis with E. coli RNA from five M. pneumoniae clones and two M. genitalium clones indica

82 y of 0.006 CFU and a specificity of 100% for M. pneumoniae.

83 alactosylceramide) to provide a baseline for M. pneumoniae binding and gliding motility.

84 espiratory specimens previously cultured for M. pneumoniae, when real-time PCR with bidirectional seq

85 ELISA for serum IgM and immunoblots for M. pneumoniae antibody were positive in 21 (62%) of 34 a

86 imens submitted to clinical laboratories for M. pneumoniae serology.

87 of two separate pathogenetic mechanisms for M. pneumoniae-associated neurologic disease, one related

88 ltures, EIAs, and serology were negative for M. pneumoniae.

89 spiratory specimens that tested positive for M. pneumoniae and sent them to the University of Alabama

90 50% of whom are found to be PCR positive for M. pneumoniae.

91 212 were designated confirmed positives for M. pneumoniae The highest clinical sensitivities were fo

92 the first national surveillance program for M. pneumoniae in the United States.

93 lacks a systematic surveillance program for M. pneumoniae.

94 multilocus sequence typing (MLST) scheme for M. pneumoniae was developed based on the sequences of ei

95 because of the lack of a "gold standard" for M. pneumoniae serology.

96 a rapid, cost-efficient laboratory test for M. pneumoniae detection that is more widely available to

97 construction of a robust genetic toolkit for M. pneumoniae, and its successful deployment to engineer

98 tudies demonstrate that the AcpS enzyme from M. pneumoniae, like E. coli enzyme, exhibits a homodimer

99 ical studies show that the AcpS enzymes from M. pneumoniae and S. pneumoniae can utilize both short-

100 nsion reactions with total RNA isolated from M. pneumoniae or M. genitalium.

101 Membranes and lipoproteins from M. pneumoniae induced a 4-fold increase in arachidonic a

102 emophilus influenzae, Mycoplasma genitalium, M. pneumoniae, and Synechocystis PCC 6803, as well as on

103 A total of 365 children had M. pneumoniae detected in the cerebrospinal fluid (CSF)

104 6%) and 57 students (75%), respectively, had M. pneumoniae infection.

105 A HindIII M. pneumoniae fragment containing the lambda MP 5B52 ins

106 produce classical toxins, and precisely how M. pneumoniae injures the respiratory epithelium has rem

107 However, M. pneumoniae was detected in 2/4 synovial biopsy specim

108 ccording to strength of evidence implicating M. pneumoniae.

109 In M. pneumoniae, transcription of the six genes terminates

110 (WT) mice to determine the role of IL-12 in M. pneumoniae respiratory disease.

111 in gliding in other organisms are absent in M. pneumoniae, random transposon mutagenesis was employe

112 ranscription-PCR analysis of this cluster in M. pneumoniae shows that mRNA levels for all six genes v

113 expression of p30 and an hmw3-cat fusion in M. pneumoniae, while deletion of the promoter-like regio

114 the cytadherence-associated protein HMW1 in M. pneumoniae.

115 s cognate phosphatase gene (prpC; MPN247) in M. pneumoniae resulted in significant and contrasting ef

116 gnized unique RepMP1 sequences found only in M. pneumoniae.

117 rmed ORF1 and ORF2 herein) conserved only in M. pneumoniae.

118 est that PrkC and PrpC work in opposition in M. pneumoniae to influence gliding frequency.

119 and assembly of the attachment organelle in M. pneumoniae are poorly understood, and no counterparts

120 ype, indicating an important role for P30 in M. pneumoniae biology.

121 red CARDS toxin mRNA and protein profiles in M. pneumoniae during distinct in vitro growth phases.

122 y elevated airway methacholine reactivity in M. pneumoniae-inoculated mice compared with that in cont

123 proteins having direct or indirect roles in M. pneumoniae cytadherence have been previously localize

124 and translational analyses of heat shock in M. pneumoniae indicated that clpB is significantly upreg

125 e proposed pathogenic role of CARDS toxin in M. pneumoniae-mediated pathologies.

126 (2)alpha (cPLA(2)alpha) completely inhibited M. pneumoniae-induced AA release from macrophages.

127 from immune cells suggest that SP-A inhibits M. pneumoniae-induced DC maturation by regulating HMGB-1

128 Interestingly, M. pneumoniae ClpB does not use dual translational start

129 Consistent with its M. pneumoniae counterpart, MGA_1199 (renamed PlpA) was d

130 ce of numerous copies of four distinct large M. pneumoniae repetitive elements (RepMPs).

131 Evidence links M. pneumoniae respiratory disease severity with interleu

132 Evidence links M. pneumoniae respiratory disease severity with interleu

133 that surfactant protein-A (SP-A) binds live M. pneumoniae and mycoplasma membrane fractions (MMF) wi

134 We reported earlier that surface-localized M. pneumoniae elongation factor Tu (EF-Tu(Mp)) mediates

135 e genomes of Mycoplasma genitalium (0.6 Mb), M. pneumoniae (0.8 Mb) and M. mycoides subspecies capri

136 Murine M. pneumoniae respiratory infection can lead to chronic

137 genes was detected in M. genitalium but not M. pneumoniae.

138 tance was identified in approximately 10% of M. pneumoniae infections occurring during this time peri

139 R or both identified four episodes (0.8%) of M. pneumoniae-associated illness and no episodes of C. p

140 , antagonized the proinflammatory actions of M. pneumoniae, Pam3Cys, and MALP-2 by reducing the produ

141 Analysis of M. pneumoniae-infected mouse lung tissue revealed high e

142 present study, we determined that binding of M. pneumoniae EF-Tu to Fn is primarily mediated by the E

143 ram is necessary to understand the burden of M. pneumoniae disease in the United States, facilitate c

144 oculated once intranasally with 10(7) CFU of M. pneumoniae.

145 molecular epidemiological characteristics of M. pneumoniae We collected 446 M. pneumoniae-positive sp

146 xpand our understanding of the complexity of M. pneumoniae gliding and the identity of possible eleme

147 characterize the neurologic complications of M. pneumoniae in children using stringent diagnostic cri

148 , by its ability to reduce concentrations of M. pneumoniae in lung tissue.

149 The addition of SP-A to cultures of M. pneumoniae markedly attenuated the growth of the orga

150 e formation in detail in growing cultures of M. pneumoniae.

151 InGenius platform suitable for detection of M. pneumoniae directly from clinical specimens.

152 ay that enables rapid, low-cost detection of M. pneumoniae from nucleic acid extracts and directly fr

153 estations and IgM response, and detection of M. pneumoniae in the CSF, but not the respiratory tract.

154 sponse in peripheral blood, and detection of M. pneumoniae in the respiratory tract, but not the CSF,

155 commercial molecular assays for detection of M. pneumoniae in the United States and identified clear

156 PCR assay targeting repMp1 for detection of M. pneumoniae The ELITe InGenius PCR assay successfully

157 A postmortem diagnosis of M. pneumoniae infection was obtained for the first patie

158 Disruption of M. pneumoniae open reading frame MPN311 results in loss

159 ter insight into the genetic distribution of M. pneumoniae strains.

160 The strain diversity of M. pneumoniae associated with this outbreak setting was

161 current understanding of the epidemiology of M. pneumoniae and may ultimately lead to a more effectiv

162 xist in multiple copies within the genome of M. pneumoniae.

163 nd specific method for the identification of M. pneumoniae and was helpful for the detection and moni

164 ans to investigate the immunopathogenesis of M. pneumoniae infection and its possible role in reactiv

165 lammatory, and pulmonary function indices of M. pneumoniae pneumonia in IL-12 (p35) knockout (KO) mic

166 lammatory, and pulmonary function indices of M. pneumoniae pneumonia in mice.

167 nterface culture to study the interaction of M. pneumoniae with differentiated airway epithelium.

168 Libraries of M. pneumoniae and M. genitalium DNA constructed in pGFPU

169 to better understand the basic mechanisms of M. pneumoniae pathogenesis.

170 ease/asthma, a comprehensive murine model of M. pneumoniae lower respiratory infection was establishe

171 , we utilized in vitro and in vivo models of M. pneumoniae infection to characterize the role of the

172 Most non-cytadhering mutants of M. pneumoniae isolated to date exhibit defects in the ar

173 tion has yielded insights into the nature of M. pneumoniae cell division and the role of gliding moti

174 ast 50 years and a limited (n = 4) number of M. pneumoniae-positive primary specimens acquired by the

175 s undertaken during a very large outbreak of M. pneumoniae pneumonia at a facility for developmentall

176 s of cases, small clusters, and outbreaks of M. pneumoniae infections that were supported by the Cent

177 be useful during institutional outbreaks of M. pneumoniae pneumonia.

178 toxin as well as for the major adhesin P1 of M. pneumoniae.

179 lung epithelial cells in the pathogenesis of M. pneumoniae infection and provide a better understandi

180 ailed analysis of observed epidemic peaks of M. pneumoniae infection.

181 What emerges is a picture of M. pneumoniae cytadherence as a multifactorial process t

182 d to play a role in asthma, the potential of M. pneumoniae to establish chronic respiratory infection

183 ttractant IL-8 in the absence or presence of M. pneumoniae or HRV1B infection.

184 from sibling 2 demonstrated the presence of M. pneumoniae organisms and community-acquired respirato

185 ologic analysis to determine the presence of M. pneumoniae, Chlamydia pneumoniae, and seven respirato

186 response and influencing the progression of M. pneumoniae during acute infection.

187 The 65-kDa hSP-A binding protein of M. pneumoniae was identified by sequence analysis as a n

188 identified a 65-kDa hSP-A binding protein of M. pneumoniae.

189 Whole-cell radioimmunoprecipitation of M. pneumoniae with antibodies directed against the proli

190 es a powerful tool for greater resolution of M. pneumoniae strains and could be useful during outbrea

191 Students with positive results of M. pneumoniae IgM serologic testing and no alternative d

192 This case prompted us to unravel the role of M. pneumoniae in GBS in a case-control study.

193 However, the role of M. pneumoniae in the pathogenesis of chronic asthma has

194 ave been reported in some cases, the role of M. pneumoniae in the pathogenesis of GBS remains unclear

195 Although the entire genomic sequence of M. pneumoniae has been completed, the functions of many

196 s obtained from the whole genome sequence of M. pneumoniae.

197 t and NF-kappaB activation in the setting of M. pneumoniae infection in nonasthmatic cells, but it di

198 Here we analyzed a clinical strain of M. pneumoniae designated S1 isolated from a 1993 outbrea

199 L M. pneumoniae concentrations than those of M. pneumoniae-infected mice treated with placebo (MpP mi

200 an ADP-ribosylating and vacuolating toxin of M. pneumoniae, designated Community Acquired Respiratory

201 ays implicated the household transmission of M. pneumoniae among all 5 siblings and both parents.

202 Although two genetically distinct types of M. pneumoniae are known, variants of each also exist.

203 ection and provide a better understanding of M. pneumoniae pathology at the cellular level.

204 lcholines did not have significant effect on M. pneumoniae-induced AA release.

205 ay of asthma treatment, but their effects on M. pneumoniae and associated airway inflammation and BHR

206 adherence to host cells, but their impact on M. pneumoniae gliding has not been investigated.

207 mice received aerosolized sham solution plus M. pneumoniae, sham solution alone, or FP alone.

208 In addition, the ETS-plus-M. pneumoniae-exposed mice had elevated levels of oxidiz

209 ad evidence of infection with C. pneumoniae, M. pneumoniae, or both, there was no relationship betwee

210 ction and appropriate responses to potential M. pneumoniae outbreaks and clusters within the communit

211 No vaccine to prevent M. pneumoniae infection currently exists, since the mech

212 Biochemical characterization of purified M. pneumoniae recombinant ClpB revealed casein- and lysi

213 both recombinant EF-Tu(Mp) and radiolabeled M. pneumoniae cell binding to Fn.

214 FP reduced M. pneumoniae by up to 20-fold in lung tissue but not in

215 omes of M. genitalium and its close relative M. pneumoniae were determined by sequencing across the j

216 Macrolide-resistant M. pneumoniae (MRMp) was detected in 37 (8.3%) specimens

217 We report a cluster of macrolide-resistant M. pneumoniae cases among a mother and two daughters.

218 Isolates from several M. pneumoniae community outbreaks within the United Stat

219 2c was most common in macrolide-susceptible M. pneumoniae (67.5%).

220 MICs for macrolide-susceptible M. pneumoniae (MSMp) were <=0.008 mug/ml, whereas MICs f

221 These results demonstrate that M. pneumoniae EF-Tu and PDH-B, in addition to their majo

222 In this study, we demonstrate that M. pneumoniae infection also induces proinflammatory cyt

223 These findings demonstrate that M. pneumoniae is likely to be recognized by SP-D in the

224 Collectively, these data demonstrate that M. pneumoniae stimulates the production of eicosanoids f

225 We demonstrated that M. pneumoniae induced the expression of mucins MUC5AC an

226 ollectively, these studies demonstrated that M. pneumoniae induces airway mucus hypersecretion by mod

227 and antibody blocking methods, we found that M. pneumoniae cytoadherence is important for the inducti

228 It is possible that M. pneumoniae infection influences tic severity in CTD o

229 Evidence is provided that M. pneumoniae was readily transmitted to all members of

230 immunofluorescence microscopy revealed that M. pneumoniae readily expressed CARDS toxin during infec

231 Finally, our biochemical studies show that M. pneumoniae AcpS is kinetically a very sluggish enzyme

232 We show that M. pneumoniae MPN372 encodes a 68-kDa protein that posse

233 Further studies showed that M. pneumoniae exposure blocked ETS-induced increases in

234 Previous studies have shown that M. pneumoniae can induce proinflammatory cytokines in se

235 These studies suggest that M. pneumoniae infection synergizes with ETS and suppress

236 Consistent with this conclusion, the M. pneumoniae HA-negative mutant II-3 failed to bind to

237 inatory than both MLVA and P1 typing for the M. pneumoniae isolates examined, providing a method for

238 In the M. pneumoniae cytadherence mutant I-2, loss of HMW2 resu

239 of ELF GSH levels, which was blocked in the M. pneumoniae-exposed mice.

240 In the M. pneumoniae-infected mouse model, ST2 deficiency, in c

241 ls and ST2 sufficiency in mice increased the M. pneumoniae and HRV loads in cell supernatants and BAL

242 To investigate the M. pneumoniae genotype shift and its impact on clinical

243 The proteins of the M. pneumoniae AO share compositional features with prote

244 ew, I discuss recent work on the role of the M. pneumoniae attachment organelle (AO), a structure req

245 _0928, the M. gallisepticum homologue of the M. pneumoniae cytoskeletal protein HMW3, were identified

246 Analysis of the M. pneumoniae genome sequence indicated that this promot

247 Here we explored the molecular nature of the M. pneumoniae gliding machinery, utilizing fluorescent p

248 ing frames widely distributed throughout the M. pneumoniae genome; 30 of these were dispensable for c

249 rotein with 40.9 and 31.4% identity with the M. pneumoniae P30 and M. genitalium P32 cytadhesins, res

250 We here cultured, for the first time, M. pneumoniae from a GBS patient with antibodies against

251 detect immunoglobulin M (IgM) antibodies to M. pneumoniae.

252 whom had neurologic disease attributable to M. pneumoniae.

253 However, whether ST2 contributes to M. pneumoniae- and HRV-mediated airway inflammation is p

254 -13, increased dramatically upon exposure to M. pneumoniae.

255 ect role in antibody-independent immunity to M. pneumoniae by interacting with lipid ligands expresse

256 There was no discrete seasonality to M. pneumoniae infections.

257 We compared the ImmunoCard with two M. pneumoniae IgM-specific assays (immunofluorescence as

258 dified Tn4001 and transformed into wild-type M. pneumoniae and into a non-cytadhering mutant lacking

259 microscopy analyses of cores from wild-type M. pneumoniae and mutants producing HMW2 derivatives.

260 developing airway cells, comparing wild-type M. pneumoniae and mutants thereof with moderate to sever

261 EGFP) and expressed this fusion in wild-type M. pneumoniae and the hmw2- mutant I-2.

262 ts were morphologically similar to wild-type M. pneumoniae but failed to localize P1 to the attachmen

263 Wild-type M. pneumoniae cells are generally elongated, tapering to

264 Gliding ceases in wild-type M. pneumoniae during terminal organelle development, whi

265 a polar localization like that in wild-type M. pneumoniae in all mutants having normal levels of HMW

266 base of the terminal organelle in wild-type M. pneumoniae, functions in the late stages of assembly,

267 d gliding capacity quickly, unlike wild-type M. pneumoniae.

268 ssociated with the cell surface in wild-type M. pneumoniae.

269 idate in mice after challenge with wild-type M. pneumoniae.

270 Upon M. pneumoniae infection of mammalian cells, increased ex

271 moniae induces mucus hypersecretion by using M. pneumoniae infection of mouse lungs, human primary br

272 Adults admitted 2013-2017 with verified M. pneumoniae pneumonia and hypoxemia (SpO2 < 93% or oxy

273 Also, adherence of viable M. pneumoniae cells to hSP-A was inhibited by recombinan

274 Adherence of viable M. pneumoniae to immobilized Fn was inhibited by antirEF

275 Initially, we found that viable M. pneumoniae cells bound to immobilized hSP-A in a dose

276 ously ascribed to infection with WT virulent M. pneumoniae.

277 The present study examined whether M. pneumoniae infections synergize with environmental to

278 dy aimed to determine the mechanism by which M. pneumoniae induces mucus hypersecretion by using M. p

279 On the other hand, while M. pneumoniae protein synthesis and DNA synthesis do not

280 me to regression of hypoxemia in adults with M. pneumoniae pneumonia.

281 itis, also colonizes airway cells along with M. pneumoniae.

282 y and inflammatory responses associated with M. pneumoniae infection in humans and animals.

283 ar damage and other sequelae associated with M. pneumoniae infections in humans.

284 postinfectious autoimmunity associated with M. pneumoniae-mediated pathologies.

285 toxin per mycoplasma cell when compared with M. pneumoniae cells grown in SP-4 medium alone.

286 L M. pneumoniae concentrations compared with M. pneumoniae-infected WT mice.

287 The interaction of rat and human SP-D with M. pneumoniae was unaffected by the presence of surfacta

288 version to MPN372 in patients diagnosed with M. pneumoniae-associated pneumonia, indicating that this

289 Mice infected with M. pneumoniae (no FP) developed significant lung inflamm

290 gene expression in macrophages infected with M. pneumoniae C57BL/6 mice deficient for NLRP3 expressio

291 IL-12 (p35) KO mice infected with M. pneumoniae were found to have significantly lower BAL

292 iagnosis were considered to be infected with M. pneumoniae.

293 etectable in all of the mice inoculated with M. pneumoniae and was inversely correlated with HPS (r =

294 ys, however, 78% of the mice inoculated with M. pneumoniae demonstrated abnormal histopathology chara

295 BALB/c mice were inoculated with M. pneumoniae or SP4 broth.

296 mice were intranasally inoculated once with M. pneumoniae and examined at 109, 150, 245, 368, and 53

297 mice were intranasally inoculated once with M. pneumoniae and sacrificed at 0 to 42 days postinocula

298 ies were not only found in GBS patients with M. pneumoniae infection, but also in patients without ne

299 lium infection and children with and without M. pneumoniae infection, respectively.

300 ldren under 15 years of age with and without M. pneumoniae infection, who were unlikely to have been