ライフサイエンスコーパス: SP-D

1 SP-D agglutinated HIV and gp120 in a calcium dependent m

2 SP-D binding organisms are predominant in mucus in vivo

3 SP-D binding to cap59Delta mutant cells was approximatel

4 SP-D binding to clinical isolates was demonstrated by fl

5 SP-D binds to the enveloped viruses, influenza A virus a

6 SP-D deficiency also increased macrophage-dominant cell

7 SP-D enhanced the binding of HIV to immature monocyte de

8 SP-D enhanced the phagocytosis of cap59Delta cells by ap

9 SP-D has been shown to bind to HIV via the HIV envelope

10 SP-D inhibited the infectivity of HIV strains at both pH

11 SP-D mRNA and protein levels in the lung also increased

12 SP-D multimers lacking the collagenous sequence efficien

13 SP-D NCRD increased transcription of CTLA4, a negative r

14 SP-D NCRD no longer decreased lymphoproliferation and IL

15 SP-D was detected by anti-SP-D antibody on BALF-treated

16 SP-D-deficient animals displayed an inverse pattern of d

17 sCD14 was decreased in both MMP(9-/-)/SP-D-/- and MMP12(-/-)/SP-D-/- mice demonstrating MMP-9

18 agenous domain was evaluated by expressing a SP-D collagen deletion mutant protein (rSftpdCDM) in wil

19 ectins, such as surfactant protein-A (SP-A), SP-D, and mannose-binding lectin (MBL); phagocyte cytoki

20 We have recently shown that collectins SP-A, SP-D, and mannose binding lectin recognize DNA and RNA v

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

22 ection following aerosol challenge of SP-A-, SP-D-, and SP-A/-D-deficient mice.

23 Although HNPs did not alter SP-D-dependent uptake of IAV, they counteracted the abil

24 Although SP-D shows a preference for glucose/maltose, the protein

25 These data suggest that alveolar SP-D regulates numbers of macrophages and fibrocytes in

26 s when combined with SP-D in assays using an SP-D-sensitive IAV strain.

27 SP-A and SP-D also influence surfactant homeostasis, contributing

28 Rat SP-A and SP-D also permeabilized the J5-containing liposomes.

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

30 The significance of SP-A and SP-D as components of the neonatal immune system has not

31 nd opsonizing infectious pathogens, SP-A and SP-D bind to the surfaces of host defense cells, promoti

32 In contrast, SP-A and SP-D effects on bacterial adherence to SAEC differed bet

33 Here we report the roles of SP-A and SP-D in M. tuberculosis infection following aerosol chal

34 To determine the role of SP-A and SP-D in neonatal immunity, wild-type, SP-A null, and SP-

35 we conclude that collectins such as SP-A and SP-D reduce the generation of anti-DNA autoantibody, whi

36 often have elevated serum levels of SP-A and SP-D, although their role in the disease is not known.

37 s surfactant-associated protein A (SP-A) and SP-D are components of innate immunity that are present

38 n the lungs, surfactant protein A (SP-A) and SP-D contribute to immune defense by facilitating the ag

39 Additionally, both SP-A- and SP-D-deficient mice accumulate anti-DNA Abs in sera in a

40 While both SP-A- and SP-D-deficient mice exhibited evidence of immunopatholog

41 ce of their physiologic functions, SP-A- and SP-D-dependent pathways are targets for clinical therapi

42 (SP-D-/-) BALF, or a mixture of SP-A-/- and SP-D-/- BALF.

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

44 bacteria include EGTA-sensitive factors and SP-D.

45 otect two key components, the neutrophil and SP-D, from NSP damage during the host response to infect

46 neonatal immunity, wild-type, SP-A null, and SP-D null mice were bred in a bacterium-laden environmen

47 OSCAR and SP-D did not exclusively colocalize in lung, as they wer

48 Changes in IL-6, IL-8, TNF receptors, and SP-D over the first 3 days of ALI/ARDS are also associat

49 mutant protein (rSftpdCDM) in wild type and SP-D null mice (Sftpd(-/-)).

50 y (P < 0.001) compared to both wild-type and SP-D null pups exposed to the same environment.

51 the bronchoalveolar lavage fluid from WT and SP-D(-/-) mice after C. neoformans infection.

52 injury (API) with C57BL/6 Wild-type (WT) and SP-D knockout (KO) mice in cecal ligation and puncture (

53 SP-D was detected by anti-SP-D antibody on BALF-treated unwashed B. dermatitidis i

54 Immunomodulators such as SP-D and ST2 also contribute.

55 tidis may utilize BALF constituents, such as SP-D, to blunt the host defensive reaction; this effect

56 IGN was shown to inhibit the binding between SP-D and gp120.

57 d not interfere with the interaction between SP-D and gp120.

58 level information about interactions between SP-D and biological ligands under physiologically releva

59 characterize antiviral interactions between SP-D and HNPs.

60 IAV, and suggest a complex interplay between SP-D and HNPs at sites of active inflammation.

61 ntification of the immunoreceptors that bind SP-D is essential for understanding its contribution to

62 Eight-week old C57/BL6 SP-D-deficient (-/-) mice and syngeneic wild-type (WT) c

63 eneic wild-type (WT) controls or Swiss Black SP-D-overexpressing (SP-D OE) mice and littermate contro

64 HNP-1-3 and RCs bound SP-D with high affinity; however, unlike HNP-1 and HNP-2

65 ow that bacterial recognition and binding by SP-D is inversely related to LPS chain extent and comple

66 d in vitro inhibition of hemagglutination by SP-D.

67 4 expression and function were influenced by SP-D, the surface expression of CD14 was assessed on alv

68 r the recognition of diverse types of LPS by SP-D.

69 ulence, which is at least partly mediated by SP-D-induced clearance from the lung.

70 lishes a new paradigm for the role played by SP-D during host responses to C. neoformans and conseque

71 S suggests that efficient LPS recognition by SP-D requires multiple binding interactions utilizing th

72 ds and proteins, including SP-A, SP-B, SP-C, SP-D, ABCA3 (a lamellar body associated protein) and FAS

73 substantial increases in the lung collectin SP-D, including significant amounts of an S-nitrosylated

74 In conclusion, SP-D influences innate host defense, in part, by regulat

75 Our results confirm SP-D expression in pancreatic islets and intercalated du

76 protein/ml, P < 0.05 to 0.01); in contrast, SP-D-/- BALF did not significantly inhibit TNF-alpha pro

77 lectins--surfactant proteins A (SP-A) and D (SP-D)--play important roles in innate host defense by bi

78 lectins, surfactant proteins A (SP-A) and D (SP-D).

79 Surfactant protein D (SP-D) and CD14 are important innate immune defense molec

80 vels of the biomarkers surfactant protein D (SP-D) and soluble receptor for advanced glycation endpro

81 Lung surfactant protein D (SP-D) binds to Mycobacterium tuberculosis surface lipoar

82 host defense component surfactant protein D (SP-D) interacts with glycans on the hemagglutinin of IAV

83 Surfactant protein D (SP-D) is a member of the collectin family of innate defe

84 Surfactant protein D (SP-D) is an important effector of innate immunity.

85 Surfactant protein D (SP-D) is an important regulator of pulmonary immune resp

86 Surfactant protein D (SP-D) is an innate immune effector that contributes to a

87 Surfactant Protein D (SP-D) is an oligomerized C-type lectin molecule with imm

88 Surfactant protein D (SP-D) is critical for maintenance of lung homeostasis an

89 uenza A virus (IAV) by surfactant protein D (SP-D) is mediated by interactions between the SP-D carbo

90 us studies showed that surfactant protein D (SP-D) is present in human tear fluid and that it can pro

91 Innate immune molecule surfactant protein D (SP-D) plays a critical role in host defense and regulati

92 Surfactant protein D (SP-D) plays diverse and important roles in innate immuni

93 Surfactant protein D (SP-D) plays important roles in antiviral host defense.

94 Surfactant protein D (SP-D) plays important roles in innate host defense again

95 Surfactant protein D (SP-D) plays important roles in lung host defense.

96 Surfactant protein D (SP-D) plays important roles in the initial innate defens

97 menting that pulmonary surfactant protein D (SP-D) protects C. neoformans cells against macrophage-me

98 RDs) of lung collectin surfactant protein D (SP-D) recognize sugar patterns on the surface of lung pa

99 Surfactant protein D (SP-D) shows specific interactions with LPS, both in vitr

100 Surfactant protein D (SP-D), a component of innate immunity, is expressed in t

101 Pulmonary surfactant protein D (SP-D), a member of the collectin family, is an innate im

102 Polymorphisms of surfactant protein D (SP-D), an important molecule within lung innate immunity

103 ory protein (CC16) and surfactant protein D (SP-D), and five systemic inflammatory markers (C-reactiv

104 The roles of NK cells, surfactant protein D (SP-D), and IFN-gamma, as well as the effect of ozone (O3

105 eractions of HNPs with surfactant protein D (SP-D), another important effector of innate immunity and

106 Surfactant protein D (SP-D), shown to play a role in host defense, binds to th

107 The role of surfactant protein D (SP-D), which inhibits P. aeruginosa cell invasion in vit

108 Surfactant protein D (SP-D)-deficient (SP-D-/-) mice exhibit early development

109 e BALB/c, C57BL/6, and surfactant protein D (SP-D)-deficient mice.

110 enhanced expression of surfactant protein D (SP-D).

111 innate immune molecule surfactant protein-D (SP-D) plays an important regulatory role in the allergic

112 allenge with high-dose surfactant protein-D (SP-D)-sensitive influenza A/Philadelphia/82 (H3N2), serp

113 lysis of the collectin surfactant protein-D (SP-D).

114 Surfactant protein D (SP-D)-deficient (SP-D-/-) mice exhibit early development of emphysema.

115 (SP-A-/-) or surfactant protein D-deficient (SP-D-/-) BALF, or a mixture of SP-A-/- and SP-D-/- BALF.

116 Collectively, these results demonstrate SP-D plays protective roles by inhibiting apoptosis and

117 e receptor, was necessary for dose-dependent SP-D binding to NK cells in vitro and DC migration in vi

118 c neck and carbohydrate recognition domains (SP-D NCRD).

119 solated from BLM-treated iSP-D mice off Dox (SP-D off) expressed more of the profibrotic cytokine TGF

120 BLM-treated iSP-D mice off Dox (SP-D off) had increased lung fibrosis compared with mice

121 solated from BLM-treated iSP-D mice off Dox (SP-D off) secreted more TGF-beta1.

122 lungs of the BLM-treated iSP-D mice off Dox (SP-D off).

123 sed lung fibrosis compared with mice on Dox (SP-D on).

124 Phase variation to evade SP-D contributes to the persistence of this common gastr

125 Here, we show that H. pylori evades SP-D binding through phase variation in lipopolysacchari

126 potential mechanisms responsible for evading SP-D binding and establishing persistent infection.

127 Exogenous SP-D administered intratracheally attenuated BLM-induced

128 reversed by the administration of exogenous SP-D.

129 t purified elastase could degrade tear fluid SP-D in vivo.

130 No significant association was noted for SP-D variants of aa160.

131 Donor DNA was assayed by pyrosequencing for SP-D polymorphisms of two single-nucleotide variations a

132 vo evidence for an antiinflammatory role for SP-D in response to noninfectious, subacute lung injury

133 sed in the bronchoalveolar lavage fluid from SP-D-/- mice.

134 D14 was reduced on alveolar macrophages from SP-D-/- mice and was associated with reduced uptake of L

135 14 was assessed on alveolar macrophages from SP-D-/- mice.

136 previously reported for the lectin homologs SP-D and mannan-binding lectin.

137 at C. neoformans is capable of coopting host SP-D to increase host susceptibility to the yeast.

138 However, SP-D is not protective against C. neoformans.

139 recognition domains (NCRDs) of rat and human SP-D exhibited dose-dependent, calcium-dependent, and in

140 nt determinant of recognition of PI by human SP-D.

141 carbohydrate recognition domains from human SP-D (hNCRD) preferred alpha1-2-linked dimannose (DM) ov

142 t to comparable fragments derived from human SP-D.

143 Although native human SP-D shows potent antiviral and aggregating activity, tr

144 Likewise, recombinant human SP-D decreased IL-1beta and IL-6 in the lung and IL-8 in

145 Recombinant human SP-D did not alter pulmonary mechanics following endotox

146 ted whether treatment with recombinant human SP-D influenced the response of the lung and systemic ci

147 Intratracheal recombinant human SP-D prevented shock caused by endotoxin released from t

148 Recombinant human SP-D prevented systemic inflammation and decreased the e

149 Recombinant human SP-D was readily detected in the lung 5 h after intratra

150 st, all lambs treated with recombinant human SP-D were physiologically stable and survived.

151 prevented by intratracheal recombinant human SP-D.

152 Mass spectroscopy of HOCl-treated human SP-D demonstrated several modifications, but none involv

153 blotted corneas after EGTA treatment and in SP-D knockouts.

154 nking of SP-D, and a significant decrease in SP-D-dependent aggregating activity in the lavage of mic

155 AO1 (high protease producer), was delayed in SP-D gene-targeted (SP-D(-/-)) knockout mice.

156 that allergen exposure induces elevation in SP-D protein levels in an IL-4/IL-13-dependent manner, w

157 ally attenuated BLM-induced lung fibrosis in SP-D(-/-) mice.

158 PAO1, but this difference was negligible in SP-D(-/-) mice, which were less able to clear the protea

159 , plays important, if not critical, roles in SP-D function.

160 The increased sCD14 seen in SP-D-/- mice was dependent upon the activation of MMP-12

161 . neoformans cells in wild-type mice than in SP-D(-/-) mice was observed, consistent with in vitro da

162 double knockout mice that failed to increase SP-D production upon allergen challenge.

163 ecreased cross-linking of SP-D and increased SP-D-dependent aggregating activity in the pneumonia mod

164 rgillus fumigatus (Af) or OVA have increased SP-D levels in their lung.

165 Triple transgenic inducible SP-D mice (iSP-D mice), in which rat SP-D is expressed i

166 unlike HNP-1 and HNP-2, RCs did not inhibit SP-D antiviral activity.

167 Interestingly, SP-D protected C. neoformans cells against macrophage-me

168 To investigate SP-D binding in vivo, SP-D(-/-) mice were intranasally i

169 In this study we investigated SP-D functions in the acute pancreatic injury (API) with

170 At 8 d, ITB SP-D (-/-) mice had greater respiratory distress (freque

171 By 21 d, compared with all groups, ITB SP-D (-/-) survivors had increased Trichrome staining an

172 a dose-dependent decrease in survival in ITB SP-D (-/-) mice receiving 2 U/kg bleomycin, with a 14-d

173 Y) were increased to a greater extent in ITB SP-D (-/-) mice.

174 ell activation in vitro whereas mice lacking SP-D had increased numbers of CD4(+) cells with elevated

175 Postinfection, mice lacking SP-D have reduced eosinophil infiltration and interleuki

176 Here, we demonstrate that mice lacking SP-D were partially protected during C. neoformans infec

177 A full-length SP-D mutant lacking N-terminal cysteine residues and tru

178 estigated the association between donor lung SP-D polymorphisms and posttransplant CLAD and survival

179 sed in both MMP(9-/-)/SP-D-/- and MMP12(-/-)/SP-D-/- mice demonstrating MMP-9 and MMP-12 contribute t

180 which altered binding by a truncated mutant SP-D to IAV HA glycans facilitates viral aggregation, le

181 gion of recombinant SP-D and captured native SP-D from human bronchoalveolar lavage.

182 Incubation of native SP-D or trimeric SP-D lectin domains (NCRDs) with peroxy

183 ide I contour from X-ray coordinates of NCRD SP-D is applied and coupled to quantitative IRRAS equati

184 By native PAGE, formation of S-nitrosylated SP-D in vivo resulted in disruption of SP-D multimers.

185 f effector cells modulated by S-nitrosylated SP-D.

186 ize (>25 microm) within the BAL (62+/-10% of SP-D-/- control), and a percentage of BAL macrophages pr

187 ecreases in total BAL cell count (63+/-6% of SP-D-/- control), macrophage size (>25 microm) within th

188 L macrophages producing oxidants (76+/-9% of SP-D-/- control).

189 Here, the abilities of SP-D to bind to and facilitate the phagocytosis and surv

190 ake of IAV, they counteracted the ability of SP-D to increase IAV-induced neutrophil H2O2 generation.

191 er diseases involving tissue accumulation of SP-D, infiltration of inflammatory monocytes, and releas

192 s also did not inhibit antiviral activity of SP-D.

193 the hemagglutination-inhibiting activity of SP-D.

194 Administration of SP-D NCRD in vivo no longer decreased allergen induced r

195 mma) seen in bronchoalveolar lavage (BAL) of SP-D-/- mice.

196 incubated with BALF inhibited the binding of SP-D in BALF to B. dermatitidis as demonstrated by IFA.

197 The binding of SP-D to HIV particles and gp120 was inhibited by the pre

198 the carbohydrate recognition domain (CRD) of SP-D.

199 lated SP-D in vivo resulted in disruption of SP-D multimers.

200 indings indicate that the collagen domain of SP-D is not required for assembly of disulfide-stabilize

201 The collagen domain of SP-D is probably critical for its homeostatic functions

202 The collagen domain of SP-D is required for the regulation of pulmonary macroph

203 ck and/or carbohydrate recognition domain of SP-D.

204 Exposure of SP-D to the complete MPO-H(2)O(2)-halide system caused l

205 that porcine-specific structural features of SP-D contribute significantly to its distinct anti-IAV a

206 Recombinant and/or natural forms of SP-D and related collectins and HNPs were tested for ant

207 In this study, we used two forms of SP-D, a dodecamer and a shorter fragment containing the

208 anti-viral activity of multimerized forms of SP-D.

209 alterations in the structure and function of SP-D at sites of inflammation in vivo.

210 reactive species might alter the function of SP-D.

211 mutations on lectin activity, incubation of SP-D dodecamers or murine lavage with peroxynitrite decr

212 A biomarker index of SP-D, MMP-7, and osteopontin enhanced diagnostic accurac

213 hallenged with Af, and in vitro induction of SP-D mRNA and protein by IL-4 and IL-13, but not IFN-gam

214 Interactions of SP-D with microorganisms and organic antigens involve bi

215 To further explore the interplay of SP-D, eosinophils, and IL-5, mice expressing altered lev

216 Therefore, a lack of SP-D did not affect newborn survival, while SP-A produce

217 O3 exposure and lack of SP-D reduced NK cell IFN-gamma and lung tissue CCL21 mRN

218 cient mice showed decreased cross-linking of SP-D and increased SP-D-dependent aggregating activity i

219 We also observed nitration, cross-linking of SP-D, and a significant decrease in SP-D-dependent aggre

220 te MPO-H(2)O(2)-halide system caused loss of SP-D-dependent aggregating activity.

221 12 activities were increased in the lungs of SP-D-/- mice, the role of these metalloproteases in the

222 Thus, modification of SP-D by reactive oxygen-nitrogen species could contribut

223 erived oxidants can lead to modifications of SP-D structure with associated alterations in its charac

224 est this hypothesis, we examined the role of SP-D in response to C. neoformans using SP-D(-)/(-) mice

225 Furthermore, susceptibility of SP-D(-/-) mice to C. neoformans infection could be resto

226 y to 14.7+/-6.1% of saline-treated 10-wk-old SP-D-/- littermates.

227 by other pulmonary and circulating opsonins, SP-D and mannose binding lectin 2, respectively.

228 Several SNPs highly associated with CC16 or SP-D levels were nominally associated with COPD in a col

229 0% mortality for WT receiving 2 U/kg ITB or SP-D (-/-) mice given saline (p < 0.05).

230 Our results identify the OSCAR:SP-D interaction as a potential therapeutic target in ch

231 controls or Swiss Black SP-D-overexpressing (SP-D OE) mice and littermate controls received either IT

232 CLP decreased pancreatic SP-D levels and caused severe pancreatic injury with hig

233 the first to explore the role of pancreatic SP-D in sepsis.

234 ic neck lectin fragment derived from porcine SP-D (pSP-D) exhibits profound inhibitory activity again

235 HNPs precipitated SP-D from bronchoalveolar lavage fluid and reduced the a

236 As proof of principle, SP-D OE mice were highly resistant to bleomycin-induced

237 an be multitrimerized using the lung protein SP-D (surfactant protein D), enhancing immune responses.

238 Finally, pure SP-D added to SP-D-/- BALF inhibited TNF-alpha productio

239 the current studies, we used a panel of rat SP-D mutants lacking all or part of the collagen domain

240 ducible SP-D mice (iSP-D mice), in which rat SP-D is expressed in response to doxycycline (Dox) treat

241 und to the collagenous region of recombinant SP-D and captured native SP-D from human bronchoalveolar

242 Notably, addition of recombinant SP-D to naive mononuclear cells stimulated IFN-gamma rel

243 were noted in some instances when relatively SP-D-resistant strains were treated with SP-D and HNPs.

244 roducer), was delayed in SP-D gene-targeted (SP-D(-/-)) knockout mice.

245 es for these innate immune proteins and that SP-D enhances efficient pinocytosis and phagocytosis of

246 exhibit enhanced allergic responses and that SP-D induction requires lymphocytes.

247 r, these studies support the conclusion that SP-D increases susceptibility to C. neoformans infection

248 work from our laboratory demonstrating that SP-D-deficient mice infected with C. neoformans have a l

249 -infection model to test the hypothesis that SP-D contributes to the clearance of viable Pseudomonas

250 f this study was to test the hypothesis that SP-D plays an important role in lung fibrosis using a mo

251 We hypothesized that SP-D alters susceptibility to C. neoformans by dysregula

252 We hypothesized that SP-D modulates inflammation during noninfectious lung in

253 We hypothesized that SP-D plays a role in C. neoformans pathogenesis by bindi

254 Our results indicate that SP-D decreases allergen responses, an effect that may be

255 Thus, we postulated that SP-D may decrease adaptive allergic responses through in

256 ense mechanisms in vitro, we postulated that SP-D would facilitate fungal infection in vivo.

257 Here we show that SP-D binds to different strains of HIV (BaL and IIIB) an

258 Furthermore, we show that SP-D bound to the surface of the yeast cells and protect

259 Together, these data show that SP-D can contribute to the clearance of P. aeruginosa fr

260 Here we show that SP-D enhances the uptake of Cy3-labeled fragments of DNA

261 Here we show that SP-D limits the intracellular growth of bacilli in macro

262 We previously showed that SP-D-deficient mice exhibit enhanced allergic responses

263 We have previously shown that SP-D accumulates at sites of acute bacterial infection a

264 Previously we have shown that SP-D deficiency results in increased production and acti

265 olated mouse alveolar macrophages shows that SP-D, but not SP-A, deficiency results in reduced cleara

266 s of bronchoalveolar lavage fluid shows that SP-D- but not SP-A-deficient mice are defective in clear

267 and DC migration in vivo, we speculate that SP-D may constitutively stimulate IFN-gamma production b

268 These results suggest that SP-D can bind to and inhibit direct infection of T-cells

269 The data also suggest that SP-D degradation in vivo is a mechanism by which P. aeru

270 Our data suggest that SP-D in BALF binds beta-glucan on B. dermatitidis, block

271 in mucus in vivo (P = 0.02), suggesting that SP-D facilitates physical elimination.

272 P-D) is mediated by interactions between the SP-D carbohydrate recognition domains (CRD) and glycans

273 rine lavage with peroxynitrite decreased the SP-D-dependent aggregation of lipopolysaccharide-coated

274 ree major ligand-binding determinants in the SP-D binding pocket, with Ca-dependent binding of inner-

275 Polymorphisms in the SP-D-encoding gene SFTPD have been associated with chron

276 Lung allografts with the SP-D polymorphic variant Thr(11) Th of aa11 are associat

277 clast-associated receptor (OSCAR) within the SP-D collagenous domain.

278 Finally, pure SP-D added to SP-D-/- BALF inhibited TNF-alpha production by BAM-B. de

279 dent antiviral activity and their binding to SP-D.

280 esonance to evaluate binding of defensins to SP-D.

281 es, which secreted TNF-alpha when exposed to SP-D in an OSCAR-dependent fashion.

282 HBDs, HD6, and HNP-4 bound minimally to SP-D.

283 in the modulation of macrophage responses to SP-D-ligand complexes.

284 aggregate surfactant in a manner similar to SP-D, but rSftpdCDM did not correct the abnormal surfact

285 S) activity to 12.7+/-6.3% of saline-treated SP-D-/- mice.

286 sed only in aged, blotted, and EGTA-treated, SP-D knockout mice.

287 Incubation of native SP-D or trimeric SP-D lectin domains (NCRDs) with peroxynitrite resulted

288 f a biologically active recombinant trimeric SP-D CRD complexed with a delipidated Eagan 4A LPS sugge

289 e of SP-D in response to C. neoformans using SP-D(-)/(-) mice.

290 To investigate SP-D binding in vivo, SP-D(-/-) mice were intranasally inoculated with Alexa F

291 SP-A-/- BALF was mixed in equal amounts with SP-D-/- BALF, TNF-alpha production by BAM-B. dermatitidi

292 ad genome-wide significant associations with SP-D levels.

293 s and myeloperoxidase (MPO) colocalized with SP-D in a murine bacterial pneumonia model of acute infl

294 y had competitive effects when combined with SP-D in assays using an SP-D-sensitive IAV strain.

295 neutralizing activity and compatibility with SP-D, RCs may provide attractive prototypes for designin

296 y crossing the IL-5-overexpressing mice with SP-D(-/-) mice.

297 rtment of alveolar macrophages together with SP-D.

298 ely SP-D-resistant strains were treated with SP-D and HNPs.

299 attenuation of pulmonary inflammation within SP-D-/- mice as shown by decreases in total BAL cell cou

300 attenuate the inflammatory processes within SP-D deficiency.