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 to cap59Delta mutant cells was approximatel

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

4 SP-D deficiency also increased macrophage-dominant cell

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

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

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

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

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

10 SP-D multimers lacking the collagenous sequence efficien

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

12 SP-D NCRD no longer decreased lymphoproliferation and IL

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

14 SP-D was not active on LPAIV but was on H3 HAs.

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

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

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

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

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

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

21 rly ALF was replenished with functional SP-A/SP-D.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

42 in-injured lungs of mice, collectins MBL and SP-D were endocytosed and routed for lysosomal degradati

43 e uPARAP-mediated cellular uptake of MBL and SP-D.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 characterize antiviral interactions between SP-D and HNPs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 ular matrix components surfactant protein D (SP-D) and mucin 5b (Muc5b).

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

78 nding lectin (MBL) and surfactant protein D (SP-D) are regulated by tissue fibroblasts at extravascul

79 nding lectin (MBL) and surfactant protein D (SP-D) become temporarily deposited in extravascular comp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 t protein A (SP-A) and surfactant protein D (SP-D) to Mtb.

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

101 Lung surfactant protein D (SP-D), a key factor in first-line innate immunity defens

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

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

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

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

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

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

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

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

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

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

112 the lung by pulmonary surfactant protein D (SP-D).

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

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

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

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

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

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

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

120 head region high-mannose glycosites dictates SP-D activity, the ability to predict these glycosite gl

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

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

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

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

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

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

127 fic expression of uPARAP governed endogenous SP-D levels and overall survival after lung injury.

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

129 Exogenous SP-D administered intratracheally attenuated BLM-induced

130 reversed by the administration of exogenous SP-D.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 gate the activities of two recombinant human SP-D forms against representative LPAIV strains, includi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

192 the hemagglutination-inhibiting activity of SP-D.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

220 12 activities were increased in the lungs of SP-D-/- mice, the role of these metalloproteases in the

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

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

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

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

225 domain (CTLD2) is critical for the uptake of SP-D, but not MBL, indicating an additional level of com

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

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

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

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

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

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

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

243 Since SP-D affinity for influenza HA depends on the presence o

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 n the head region, our data demonstrate that SP-D may not protect against virus containing these HA s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

294 igh-mannose glycans and do not interact with SP-D, and that sequence analysis can predict glycan subt

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

296 rved in fibroblasts adjacent to regions with SP-D secretion.

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.