ライフサイエンスコーパス: SP-A

1 SP-A alone had no effect upon inflammatory mediators in

2 SP-A also decreased TNF-alpha and CXCL10 secretion by ex

3 SP-A also reduces the phosphorylation of TLR signaling p

4 SP-A and SP-B(N) were able to interact in solution (Kd =

5 SP-A augmented CR3-mediated phagocytosis in a manner tha

6 SP-A can also bind the Mp membrane protein, MPN372.

7 SP-A decreases the phosphorylation of IkappaBalpha, a ke

8 SP-A functions as an important mediator in resolving tis

9 SP-A gene expression is developmentally regulated in fet

10 SP-A has a bacteriostatic effect on Mycoplasma pneumonia

11 SP-A has been proposed as a fetally produced signal for

12 SP-A inhibited LPS induced IkappaB-alpha degradation in

13 SP-A interaction with the EGFR signaling pathway appears

14 SP-A plays an important role in the lung during bacteria

15 SP-A prevented the invasion of AEC by alginate-producing

16 SP-A significantly suppressed TLR ligand-induced express

17 SP-A(-/-) alloBMT or SP-A-sufficient recipient mice that

18 SP-A(-/-) mice were challenged in allergen models, and e

19 SP-A(-/-)alloBMT mice also had increased colon expressio

20 SP-A, as well as the enzyme lysophosphatidylcholine acyl

21 SP-A-deficient mice are more susceptible than wild-type

22 SP-A/SP-B(N)-treated infected mice showed significant re

23 (3) SP-A WT and mutants enhanced phagocytosis of P. aerugino

24 In the lungs, surfactant protein A (SP-A) and SP-D contribute to immune defense by facilitat

25 surfactant-associated surfactant protein A (SP-A) and surfactant protein D (SP-D) to Mtb.

26 Mice lacking surfactant protein A (SP-A) are susceptible to bacterial infection associated

27 The identification of surfactant protein A (SP-A) as an important innate immune factor of the lungs,

28 In the lung, surfactant protein A (SP-A) enhanced interleukin-4 (IL-4)-dependent macrophage

29 rted that mice lacking surfactant protein A (SP-A) have increased airway hyperresponsiveness (AHR) du

30 vestigated the role of surfactant protein A (SP-A) in opsonization and clearance of S. aureus.

31 role for the collectin surfactant protein A (SP-A) in regulating the development of GVHD after alloge

32 studies reported that surfactant protein A (SP-A) inhibits lymphocyte proliferation.

33 Surfactant protein A (SP-A) is a hydrophilic glycoprotein of the collectin fam

34 Surfactant protein A (SP-A) is an immune modulator that increases pathogen upt

35 Surfactant protein A (SP-A) modulates host responses to infectious and environ

36 Surfactant protein A (SP-A) plays a critical role in the clearance of Pseudomo

37 Pulmonary surfactant protein A (SP-A) plays a key role in innate lung host defense, in s

38 Surfactant protein A (SP-A) plays a role in lung innate immunity and surfactan

39 Lung surfactant protein A (SP-A) plays an important function in modulating inflamma

40 Surfactant protein A (SP-A), a C-type lectin, plays an important role in innat

41 Pulmonary surfactant protein A (SP-A), a member of the collectin family, plays an import

42 The lung collectin, surfactant protein A (SP-A), has emerged as an important innate immune determi

43 We observed that surfactant protein A (SP-A)-deficient mice have impaired expression of Foxp3 a

44 presence or absence of surfactant protein A (SP-A).

45 l effects of pulmonary surfactant protein A (SP-A).

46 -1 and SRC-2) regulate surfactant protein-A (SP-A) and platelet-activating factor (PAF) expression, w

47 ports demonstrate that surfactant protein-A (SP-A) binds live M. pneumoniae and mycoplasma membrane f

48 Surfactant protein-A (SP-A) is an important antimicrobial protein that opsoniz

49 Surfactant protein-A (SP-A) is an important mediator of pulmonary immunity.

50 his defense mechanism, surfactant protein-A (SP-A), exerts multifunctional roles in mediating host re

51 -type lectins, such as surfactant protein-A (SP-A), SP-D, and mannose-binding lectin (MBL); phagocyte

52 Surfactant protein-A (SP-A), which is secreted by fetal lungs into amniotic fl

53 rophages, activated by surfactant protein-A (SP-A).

54 family in particular, surfactant protein-A (SP-A).

55 miting available molecular information about SP-A interactions with microbial surface components.

56 However, AF SP-A and fetal macrophages by themselves do not seem to

57 In humans, the concentration of AF SP-A decreases during labor, and no fetal macrophages ar

58 teins acted synergistically in vitro against SP-A- and SP-B(N)-resistant capsulated Klebsiella pneumo

59 Although SP-A is known to inhibit T cell proliferation under cert

60 Although SP-A was shown to inhibit maturation of DCs in vitro, th

61 We propose that an SP-A interaction among AF, placental amnion, and reflect

62 In this study, we report the basal and SP-A-induced transcriptional and posttranslational regul

63 trol of M. tuberculosis in SP-A-, SP-D-, and SP-A/-D-deficient mice.

64 owing aerosol challenge of SP-A-, SP-D-, and SP-A/-D-deficient mice.

65 he surfactant protein (SP)-B proprotein, and SP-A are lung anti-infective proteins.

66 These signal strength and SP-A-dependent effects are mediated by changes in intrac

67 C57BL/6 (H2b; WT) and SP-A-deficient mice on a C57BL/6 background (H2b; SP-A(-

68 tion of proinflammatory mediators as well as SP-A's ability to bind to IFN-gamma or IFN-gammaR1.

69 epithelial cells was sufficient to attenuate SP-A and eotaxin secretion.

70 When reared in the corn dust bedding, SP-A null pups had significant mortality (P < 0.001) com

71 examined the effect of interactions between SP-A and the pathogenic TLR agonists lipopolysaccharide

72 We characterized the interplay between SP-A and a collection of isogenic sequential isolates fr

73 mice that have undergone an allogeneic BMT [SP-A(-/-)alloBMT] or SP-A-sufficient recipient mice that

74 homeostasis, we generated mice lacking both SP-A and MCs (SP-A(-/-)Kit(W-sh/W-sh)) and infected them

75 While both SP-A- and SP-D-deficient mice exhibited evidence of immu

76 ly cleared in the lungs of wild-type mice by SP-A-mediated membrane permeabilization, and not by opso

77 tant was more susceptible to opsonization by SP-A and by other pulmonary and circulating opsonins, SP

78 Allergen-challenged SP-A(-/-) mice that received SP-A therapy had significan

79 hese structurally related defense collagens, SP-A and C1q, and the expression of their receptor, myos

80 Consequently, SP-A enhanced macrophage uptake of Eap-expressing (Eap(+

81 to review regulatory mechanisms that control SP-A expression in humans and other animal species.

82 Crystallographic SP-A.ligand complexes have not been reported to date, li

83 Surfactant proteins A and D (SP-A and -D) play a role in many acute bacterial, viral,

84 Viral clearance and SP-D/SP-A upregulation were unimpaired and so were early viru

85 ation of DCs in vitro, the consequence of DC/SP-A interactions in vivo has not been elucidated.

86 adequate amounts of exoproteases to degrade SP-A in vitro and in vivo, leading to its preferential c

87 Despite SP-A's ability to up-regulate TLR2 expression on human m

88 h could be reconciled by injection of either SP-A or PAF into the amnion.

89 es have a single SP-A gene, two genes encode SP-A in humans and primates (SFTPA1 and SFTPA2).

90 ressed H3K9 methylation and greatly enhanced SP-A expression.

91 human pregnancy and parturition by examining SP-A expression patterns in AF and amnion.

92 ly be restored after administering exogenous SP-A containing both SP-A1 and SP-A2 into the lungs of S

93 challenged in allergen models, and exogenous SP-A therapy was given after the last challenge.

94 The addition of exogenous SP-A completely reversed this phenotype.

95 an cells from asthma subjects when exogenous SP-A is added during IL-13 challenge.

96 Importantly, reconstitution with exogenous SP-A into the lungs of SP-A(-/-) mice stimulated with a

97 his capability was attenuated with exogenous SP-A treatment.

98 increase on extended culture with exogenous SP-A, providing a key mechanism for the maintenance and

99 SP-A variants than by insect-cell expressed SP-A variants.

100 nd/or more effectively by CHO cell-expressed SP-A variants than by insect-cell expressed SP-A variant

101 (iv) CHO cell-expressed SP-A was considerably more active than insect cell-expre

102 In a reciprocal fashion, SP-A failed to enhance uptake of Eap(+) S. aureus in per

103 ght, and 20 obese subjects were examined for SP-A.

104 ner that may have important implications for SP-A polymorphisms in human diseases.

105 membrane protein OprH as a novel ligand for SP-A on P. aeruginosa The last-available (late) isolates

106 These studies suggest a novel mechanism for SP-A in asthma as a modulator of IL-13-induced inflammat

107 We investigated a potential role for SP-A in human pregnancy and parturition by examining SP-

108 These findings suggest a protective role for SP-A in limiting MMF-stimulated mucin production that oc

109 ce, to our knowledge, of a critical role for SP-A in modulating GI GVHD.

110 These data identify a critical role for SP-A in modulating the lung inflammatory response by reg

111 opment of GI GVHD and establishes a role for SP-A in regulating the immune response in the GI tract.

112 ha by MCs, implicating a protective role for SP-A.

113 A univariable regression model found SP-A levels were significantly negatively correlated wit

114 icantly reduced in alveolar macrophages from SP-A(-/-) compared with SP-A(+/+) mice.

115 litates the escape of the microorganism from SP-A-mediated phagocytic killing.

116 actions to AHR in airways lacking functional SP-A during Mp infection.

117 elderly ALF was replenished with functional SP-A/SP-D.

118 ndergone an allogeneic BMT) or C57BL/6 (H2b; SP-A-deficient recipient mice that have undergone a syng

119 deficient mice on a C57BL/6 background (H2b; SP-A(-/-)) mice underwent allogeneic or syngeneic BMT wi

120 c BMT with cells from either C3HeB/FeJ (H2k; SP-A-deficient recipient mice that have undergone an all

121 y to undergo conformational changes may help SP-A adapt to different ligand classes, including microb

122 Hence, SP-A inhibited upregulation of IFN-gamma-inducible genes

123 elayed clearance, our goal was to define how SP-A mediates eosinophil resolution in allergic airways

124 To determine how SP-A interactions with MCs regulate airway homeostasis,

125 provides a signal for parturition; however, SP-A-deficient mice have only a relatively modest delay

126 cant differences in lung pathology; however, SP-A(-/-)alloBMT mice developed marked features of GI GV

127 se questions, we studied the effect of human SP-A on rat and human aMvarphis stimulated with IFN-gamm

128 y in human asthmatic patients and that human SP-A inhibits M pneumoniae-stimulated transcription and

129 r the multiple functions attributed to human SP-A, as well as the regulatory complexity of its expres

130 In vitro, human SP-A containing either the 223Q or the 223K allele was c

131 n an OVA model of allergic hypersensitivity, SP-A(-/-) mice had greater eosinophilia, Th2-associated

132 Mp infection were more severely affected in SP-A(-/-) mice.

133 ine the implications of these alterations in SP-A levels in asthmatic patients.

134 tivity of IL-13 is dramatically augmented in SP-A(-/-) mice, which have significantly increased neutr

135 introduced concurrently with MASP binding in SP-A but is uncontrolled and occurs even in the absence

136 th animal models sufficient and deficient in SP-A challenged with IL-13 and primary epithelial cells

137 udies, we demonstrate that mice deficient in SP-A that have undergone an allogeneic BMT have a greate

138 ry infection with Mp using mice deficient in SP-A.

139 Using an acute pneumonia model in SP-A+/+ versus SP-A-/- mice, the O-glycosylation-deficie

140 nhibited in mice, the phenotypes observed in SP-A(-/-) mice were significantly attenuated.

141 e responses to live Mycoplasma pneumoniae in SP-A knockout mice and RAW 264.7 cells.

142 nge dramatically reduced mucin production in SP-A(-/-) mice.

143 take or immune control of M. tuberculosis in SP-A-, SP-D-, and SP-A/-D-deficient mice.

144 tured HFL type II cells blocked cAMP-induced SP-A expression and accumulation of surfactant-containin

145 filtration, were much greater in Mp infected SP-A(-/-) mice than wild-type mice.

146 Additionally, M pneumoniae-infected SP-A(-/-)Kit(W-sh/W-sh) mice engrafted with TNF-alpha(-/

147 tory in the lung during bacterial infection, SP-A regulation of secretory leukoprotease inhibitor (SL

148 Administration of intratracheal SP-A to Sp-a(-/-) mice induced the translocation of CR3

149 Wild-type, SP-A knockout (SP-A KO) and humanized (SP-A2 223Q/Q, SP-A2 223K/K) C57B

150 Significantly less SP-A (P = .002) was detected in samples from OAs compare

151 om patients with CF bound significantly less SP-A than their respective first-available (early) isola

152 and type II alveolar epithelial cells marker SP-A, indicating the potential importance of CDC42 in th

153 ting showed a binding of high molecular mass SP-A in AF to amnion.

154 we generated mice lacking both SP-A and MCs (SP-A(-/-)Kit(W-sh/W-sh)) and infected them with M pneumo

155 Moribund SP-A null newborn mice exhibited Bacillus sp. and Entero

156 al adsorption than surfactants containing no SP-A or only SP-A2.

157 in domain, was shown to alter the ability of SP-A to inhibit eosinophil degranulation.

158 n production to MMF occurs in the absence of SP-A and is not dependent upon neutrophil recruitment.

159 In this article, we show that the absence of SP-A during M. pneumoniae infection leads to increased n

160 livery model, intrauterine administration of SP-A significantly inhibited preterm delivery, suppresse

161 Intratracheal administration of SP-A to SP-A(-/-) mice enhanced SLPI protein expression

162 inflammatory agents and that the binding of SP-A to IFN-gamma abrogates IFN-gamma effects on human m

163 Binding of SP-A to OprH promoted phagocytic killing; thus, late CF

164 h endoglycosidase H abrogates the binding of SP-A, indicating that the high mannose structures on gp1

165 sis infection following aerosol challenge of SP-A-, SP-D-, and SP-A/-D-deficient mice.

166 urse of evolution, the genetic complexity of SP-A has increased, particularly in the regulatory regio

167 ies set out to determine the contribution of SP-A to the response of a key effector cytokine in asthm

168 n described to play a role in the control of SP-A expression.

169 that SP-R210 mediates binding and control of SP-A-opsonized S. aureus by macrophages.

170 on of exoproteases and limits degradation of SP-A, thereby conferring susceptibility to this major pu

171 neck and carbohydrate recognition domain of SP-A with d-mannose, D-alpha-methylmannose, and glycerol

172 Mapping of the domains of SP-A that were required for optimal binding to CR3 revea

173 ophils were isolated to assess the effect of SP-A genetic variation on apoptosis and chemotaxis.

174 th of signal (SoS) and functional effects of SP-A interactions.

175 The effects of SP-A on macrophage and neutrophil CR3 redistribution bet

176 ity were reduced in bronchoalveolar fluid of SP-A(-/-) compared with SP-A(+/+) mice.

177 Cyclic AMP (cAMP) induction of SP-A expression in human fetal lung type II cells is O(2

178 cAMP induction of SP-A expression is repressed by transforming growth fact

179 cAMP induction of SP-A promoter activity is mediated by increased phosphor

180 observed that the developmental induction of SP-A was associated with increased recruitment of TTF-1,

181 resulting in the developmental induction of SP-A.

182 mRNA levels declined with cAMP induction of SP-A.

183 -R210(L) mediates recognition and killing of SP-A-opsonized S. aureus in vivo, coordinating inflammat

184 is (IPF) often have elevated serum levels of SP-A and SP-D, although their role in the disease is not

185 by our group showed differences in levels of SP-A binding to non-live mycoplasma membrane fractions t

186 The levels of SP-A in lungs of two hTG lines used were comparable with

187 Decreased levels of SP-A in OAs, which could be due to increased local TNF-a

188 polysaccharide is surface-exposed, levels of SP-A may be crucial to modulate the interaction of P. ae

189 ial to ensure proper physiological levels of SP-A under different conditions.

190 ining both SP-A1 and SP-A2 into the lungs of SP-A knock-out mice.

191 o its preferential clearance in the lungs of SP-A(+/+) mice.

192 tution with exogenous SP-A into the lungs of SP-A(-/-) mice stimulated with a strong signal also resu

193 anded to the greatest extent in the lungs of SP-A(-/-) OVA mice.

194 family members as TTF-1-driven mediators of SP-A expression and type II cell differentiation through

195 proliferation is enhanced in the presence of SP-A at low SoS imparted by exogenous mitogens, specific

196 re and that SRC-1/-2-dependent production of SP-A and PAF is crucial for this process.

197 The collagen-like region of SP-A conferred protection of SLPI against MMP mediated c

198 significant complexity of the regulation of SP-A expression at different levels, including transcrip

199 However, the exact role of SP-A and the mechanism by which SP-A affects IFN-gamma-i

200 In this study, we investigated the role of SP-A during acute phase pulmonary infection with Mp usin

201 In this study, we examined the role of SP-A in modulating complement receptor-mediated phagocyt

202 Here we report the roles of SP-A and SP-D in M. tuberculosis infection following aer

203 Significant sources of SP-A likely to protect a newborn include the neonatal lu

204 hypoxia, which inhibits cAMP stimulation of SP-A, markedly increased Suv39h1 and Suv39h2 binding to

205 d by N-glycanase or collagenase treatment of SP-A, implicating the N-linked sugar and collagen-like d

206 lated with the developmental upregulation of SP-A.

207 ire of single-amino acid genetic variants of SP-A that may be associated with lung disease, and our f

208 High molecular mass (>250 kDa) oligomeric SP-A was increased in AF with advancing gestation.

209 In C57BL/6 mice, oligomeric SP-A was also readily detected in AF from E15 onwards, b

210 SP-A(-/-) alloBMT or SP-A-sufficient recipient mice that have undergone an al

211 gone an allogeneic BMT [SP-A(-/-)alloBMT] or SP-A-sufficient recipient mice that have undergone an al

212 mice that have undergone a syngeneic BMT or SP-A-sufficient recipient mice that have undergone a syn

213 Injection of PAF or SP-A into AF at 17.5 days post coitum enhanced uterine N

214 Five days postchallenge, SP-A KO and humanized SP-A2 223K/K mice had persistent e

215 lonal antibodies to CKAP4/P63, the principal SP-A-binding receptor on AEC, or inhibition of its expre

216 binding into a pulmonary surfactant protein (SP-A), which has the same domain structure and architect

217 expression of the major surfactant protein, SP-A, in mid-gestation human fetal lung (HFL) are induce

218 FTPA) encoding the major surfactant protein, SP-A, in midgestation human fetal lung (HFL) is dramatic

219 rgen-challenged SP-A(-/-) mice that received SP-A therapy had significantly less tissue eosinophilia

220 Alginate binding to AEC reduced SP-A release by these cells.

221 e does not involve an overt lack of secreted SP-A but instead involves an increase in ER stress of re

222 timulated with LPS and IFN-gamma separately, SP-A inhibited both LPS-induced signaling and IFN-gamma-

223 iously been associated with STAT6 signaling, SP-A inhibited IL-13-induced STAT3 phosphorylation in mi

224 Although most species have a single SP-A gene, two genes encode SP-A in humans and primates

225 ox-1 (HMGB-1) abrogated this effect and that SP-A inhibits HMGB-1 release from immune cells suggest t

226 We conclude that SP-A acts via TLR2 to suppress TLR ligand-induced preter

227 We conclude that SP-A inhibition of (IFN-gamma + LPS) stimulation is due

228 We conclude that SP-A modulates the cell surface expression of CR3 on alv

229 Our data demonstrate that SP-A binds to HIV in a calcium-dependent manner that is

230 with dendritic cells (DCs) demonstrate that SP-A enhances the binding of gp120 to DCs, the uptake of

231 kinetic suppression assays demonstrate that SP-A enhances the frequency of functional Foxp3(+) Tregs

232 Our findings demonstrate that SP-A is vital to preserving lung homeostasis and host de

233 he results of these studies demonstrate that SP-A protects against the development of GI GVHD and est

234 We determined that SP-A binds S. aureus through the extracellular adhesin E

235 In addition, we found that SP-A bound to human IFN-gamma (KD = 11 +/- 0.5 nM) in a

236 We found that SP-A inhibited (IFN-gamma + LPS)-induced TNF-alpha, iNOS

237 , these findings support the hypothesis that SP-A affects T cell immune function by the induction of

238 We hypothesized that SP-A modulates the phenotype and prevalence of dendritic

239 We hypothesized that SP-A-mediated modulation of T cell activation depends up

240 Together, these data indicate that SP-A and SP-D are dispensable for immune control of M. t

241 Infectivity studies reveal that SP-A inhibits the infection of CD4+ T cells by two strai

242 capture of the HIV viral lysate reveals that SP-A targets the envelope glycoprotein of HIV (gp120), w

243 We show that SP-A(-/-) mice are more susceptible to MMF exposure and

244 Previous studies showed that SP-A mediates phagocytosis via the SP-A receptor 210 (SP

245 However, previous studies have shown that SP-A also aids in the formation and biophysical properti

246 Recent publications have shown that SP-A binds to and is bacteriostatic for Mycoplasma pneum

247 Collectively, these results suggest that SP-A acts as a dual modulator of HIV infection by protec

248 Our results suggest that SP-A aids in the resolution of allergic airway inflammat

249 with CD4 and mAbs F105 and b12 suggest that SP-A inhibits infectivity by occlusion of the CD4-bindin

250 MGB-1 release from immune cells suggest that SP-A inhibits M. pneumoniae-induced DC maturation by reg

251 findings in this study strongly suggest that SP-A signals amniotic anti-inflammatory response via AF

252 Taken together, our data suggested that SP-A influences the prevalence, types, and functions of

253 Finally, we report for the first time that SP-A decreases the phosphorylation of Akt, a major cell

254 PPI1 was overexpressed in the cytosol of the SP A. annua variety.

255 The SP-A cDNA in experimental constructs was driven by the 3

256 (+) DCs and Foxp3(+) T regulatory cells, the SP-A(-/-) mice had elevated proportions of CD4(+) activa

257 cell pools demonstrated that cells from the SP-A(-/-) OVA mice had the greatest proliferative and IL

258 The mortality of the SP-A null pups was associated with significant gastroint

259 ult of the conformational change is that the SP-A lectin site and the surrounding loop region become

260 These results indicate that the SP-A variant/mutant with Arg85 exhibits a higher ability

261 owed that SP-A mediates phagocytosis via the SP-A receptor 210 (SP-R210).

262 Thus, SP-A appears to integrate signal thresholds to control T

263 Intratracheal administration of SP-A to SP-A(-/-) mice enhanced SLPI protein expression and anti

264 The binding of CR3 to SP-A was calcium dependent and mediated by the I-domain

265 n of (IFN-gamma + LPS) stimulation is due to SP-A attenuation of both inflammatory agents and that th

266 ted mechanism of P. aeruginosa resistance to SP-A.

267 that several microorganisms are resistant to SP-A and SP-B(N).

268 lates were at least 2-fold more resistant to SP-A-mediated killing by human macrophages than their re

269 lux and mucin production that are similar to SP-A(-/-) mice.

270 ins showed equal levels of susceptibility to SP-A-mediated membrane permeability.

271 G231V mutation have similar levels of total SP-A as normal family members, which suggests that the m

272 ared with only a 50% increase in LPS-treated SP-A(-/-) mice 8 d after exposure.

273 not secreted into the medium with wild-type SP-A isoforms, form fewer intracellular dimer and trimer

274 Wild-type, SP-A knockout (SP-A KO) and humanized (SP-A2 223Q/Q, SP-

275 The Glu-202 side chain of unliganded SP-A extends out into the solvent and away from the calc

276 rison of these complexes with the unliganded SP-A neck and carbohydrate recognition domain revealed a

277 1 and 2 (SRC-1 and SRC-2), which upregulate SP-A transcription, to the parturition process.

278 Using SP-A(-/-)Kit(W-sh/W-sh) mice engrafted with TNF-alpha(-/

279 g an acute pneumonia model in SP-A+/+ versus SP-A-/- mice, the O-glycosylation-deficient DeltatfpO mu

280 In vitro, SP-A enhanced SLPI production by macrophage THP-1 cells

281 In vivo, SP-A aids in maintenance of airway homeostasis during M.

282 Epithelial alveolar type II cells were SP-A-positive, and Clara cells were negative by immunohi

283 ented AHR during M pneumoniae infection when SP-A is absent.

284 ent in the lungs of MMF-challenged mice when SP-A was absent.

285 We sought to determine whether SP-A levels are altered in OAs compared with a control g

286 Therefore, we examined whether SP-A could bind to HIV and also had any effect on viral

287 xact role of SP-A and the mechanism by which SP-A affects IFN-gamma-induced activation of alveolar ma

288 To determine mechanisms by which SP-A is antiinflammatory in the lung during bacterial in

289 enabled their binding to bacteria with which SP-A or SP-B(N) alone could not interact.

290 Treatment of AEC with SP-A, monoclonal antibodies to CKAP4/P63, or CKAP4/P63-s

291 Positive hTG mice were bred with SP-A knock-out mice to generate F8 offspring for study.

292 choalveolar fluid of SP-A(-/-) compared with SP-A(+/+) mice.

293 lar macrophages from SP-A(-/-) compared with SP-A(+/+) mice.

294 lungs when challenged with MMF compared with SP-A(-/-) mice.

295 ysis of human amnion explants incubated with SP-A revealed a molecular signature of inhibited cytokin

296 se (MMP)-12 cleaved SLPI and incubation with SP-A reduced MMP-12-mediated SLPI cleavage.

297 reatment of K. pneumoniae-infected mice with SP-A and SP-B(N) conferred more protection against K. pn

298 ith asthma that are exogenously treated with SP-A in the context of IL-13 challenge.

299 ly, we found that therapeutic treatment with SP-A and SP-B(N) 6 or 24 h after bacterial challenge con

300 with pathogenic TLR agonists with or without SP-A.