ライフサイエンスコーパス: alveolar macrophage

1 The initial target of C. burnetii is the alveolar macrophage.

2 cterium Francisella tularensis, that infects alveolar macrophages.

3 ecific signatures can be identified in human alveolar macrophages.

4 n of a viral pattern-recognition receptor in alveolar macrophages.

5 this protein being important for survival in alveolar macrophages.

6 le intermediate between monocyte-derived and alveolar macrophages.

7 ameter less than 6mum are rapidly cleared by alveolar macrophages.

8 ion of markers for alternative activation on alveolar macrophages.

9 came increasingly similar to tissue-resident alveolar macrophages.

10 artment or changes in the number of resident alveolar macrophages.

11 e the bacteria first encounter lung-resident alveolar macrophages.

12 rculosis in humans and predominantly infects alveolar macrophages.

13 aused proinflammatory cytokine production in alveolar macrophages.

14 uorescent particles showed reduced uptake by alveolar macrophages.

15 tiologic agent of TB, usually resides in the alveolar macrophages.

16 cally downregulates cell cycling pathways in alveolar macrophages.

17 sive genes in murine bone marrow-derived and alveolar macrophages.

18 is required for the perinatal development of alveolar macrophages.

19 ies promote opsonophagocytosis of bacilli by alveolar macrophages.

20 ition from prealveolar macrophages to mature alveolar macrophages.

21 the amount of cellular H2O2 in M2 polarized alveolar macrophages.

22 lung epithelial cells, dendritic cells, and alveolar macrophages.

23 C subset, but not other lung CD11b(+) DCs or alveolar macrophages.

24 r signaling in the pulmonary endothelium and alveolar macrophages.

25 gic airway inflammation through an action on alveolar macrophages.

26 ch provides a useful in vitro model to study alveolar macrophages.

27 matory cytokine responses of responder human alveolar macrophages.

28 and protected intracellular localization in alveolar macrophages.

29 s of myeloid regulatory cells, monocytes and alveolar macrophages.

30 ty to complement killing and phagocytosis by alveolar macrophages.

31 1 (MRC-1) in human dendritic cells and mouse alveolar macrophages.

32 tracellular phospholipid accumulation within alveolar macrophages.

33 earance, which was caused by IFNy priming of alveolar macrophages.

34 on of alveolar surfactant and dysfunction of alveolar macrophages.

35 a specific increase in intracellular TNF in alveolar macrophages.

36 istinct M2 state transcriptional patterns in alveolar macrophages.

37 ctor mechanisms, most likely in concert with alveolar macrophages.

38 mmation via increased apoptosis of recruited alveolar macrophages.

39 s sufficient to drive TGF-beta production by alveolar macrophages.

40 lungs and coincided with the accumulation of alveolar macrophages.

41 nsic recognition of Ag presented by infected alveolar macrophages.

42 Alveolar macrophages, a major host cell niche for M. tub

43 Selective depletion of alveolar macrophages abolished the PGD2-enhanced inflamm

44 pecific genetic deletion of monocyte-derived alveolar macrophages after their recruitment to the lung

45 s both DP1 and DP2 receptors were located on alveolar macrophages along with hematopoietic PGD syntha

46 We found that alveolar macrophages (AlvMs) were much less able to resp

47 GM-CSF is required for alveolar macrophage (AM) development shortly after birth

48 We hypothesized that normal alveolar macrophage (AM) functions, which are central to

49 sted the role of Stat5 in dendritic cell and alveolar macrophage (AM) homeostasis in the lung using C

50 The effect of COPD on alveolar macrophage (AM) microbicidal responses was inve

51 he lung cells, especially on the predominant alveolar macrophage (AM) population, is limited.Objectiv

52 Rationale: Serial measurements of alveolar macrophage (AM) transcriptional changes in pati

53 ution via accelerated apoptosis of recruited alveolar macrophage (AM).

54 rocytosis of apoptotic neutrophils (PMNs) by alveolar macrophages (AM s) is vital for resolution of i

55 controlling CXCL13 gene expression in human alveolar macrophages (AM) and monocyte-derived macrophag

56 Alveolar macrophages (AM) are at the center of the patho

57 Abnormal alveolar macrophages (AM) are found in chronic obstructi

58 Alveolar macrophages (AM) are lung-resident immune cells

59 Alveolar macrophages (AM) are the most prominent immune

60 formed unbiased gene expression profiling of alveolar macrophages (AM) obtained from RAGE null and C5

61 Alveolar macrophages (AM) play pivotal roles in modulati

62 ns of tissue resident macrophages, including alveolar macrophages (AM), in cancer were not well studi

63 part through frontline epithelial cells and alveolar macrophages (AM).

64 ghly efficient Cre-mediated recombination in alveolar macrophages (AMFs), bronchial epithelial cells

65 Alveolar macrophages (AMPhi) are innate immune cells str

66 Toll-like receptors in alveolar macrophages (AMPhi) recognize the molecular con

67 Alveolar macrophages (AMs) and epithelial cells (ECs) ar

68 onsible for activation of p38 in sarcoidosis alveolar macrophages (AMs) and PBMCs.

69 he impact of aging on the phenotype of mouse alveolar macrophages (AMs) and their response to Mycobac

70 Alveolar macrophages (AMs) are highly abundant lung cell

71 Alveolar macrophages (AMs) derived from embryonic precur

72 m but is limited by our understanding of how alveolar macrophages (AMs) kill bacteria.

73 Resident alveolar macrophages (AMs) suppress allergic inflammatio

74 tion due to a population of monocyte-derived alveolar macrophages (AMs) that produce increased interl

75 ized that S. aureus impairs efferocytosis by alveolar macrophages (AMs) through the activity of the s

76 ken to determine the susceptibility of human alveolar macrophages (AMs) to influenza A virus (IAV) in

77 he number of classical (SiglecFhighCD11bneg) alveolar macrophages (AMs) was reduced by approximately

78 Murine alveolar macrophages (AMs) were cultured ex vivo with/wi

79 ry microvascular endothelial cells (PMVECs), alveolar macrophages (AMs), and polymorphonuclear leukoc

80 s harvested by bronchoalveolar lavage (BAL), alveolar macrophages (AMs), are routinely used in studie

81 to invade due to virus-induced depletion of alveolar macrophages (AMs), but this is not the only con

82 damage and dysregulation of neutrophils and alveolar macrophages (AMs), have been suggested to contr

83 tion of transcriptomes and open chromatin of alveolar macrophages (AMs), interstitial macrophages (IM

84 Interestingly, alveoli outnumber alveolar macrophages (AMs), which favors alveoli devoid

85 tes such as aluminum salts and silica killed alveolar macrophages (AMs), which then released interleu

86 lveolar epithelial cells (AECs) and resident alveolar macrophages (AMs).

87 one marrow and an increase in ferroportin on alveolar macrophages (AMs).

88 e smoking synergize to alter the function of alveolar macrophages (AMs).

89 ulatory T cells but dependent on residential alveolar macrophages (AMs).

90 red IFN responses to rhinovirus by asthmatic alveolar macrophages (AMs); the molecular mechanisms und

91 SP-A affects IFN-gamma-induced activation of alveolar macrophages (aMvarphis) remains unknown.

92 Both in vivo and in cultured alveolar macrophages and BMDM, expression of several M1

93 ureus and B. anthracis compared with E. coli Alveolar macrophages and CD14(+) cells were overall more

94 P12 promotes the survival of tissue-resident alveolar macrophages and contributes to local production

95 ency in the AMPK catalytic alpha1 subunit in alveolar macrophages and conventional dendritic cells pr

96 ted a reduction in the accumulation of early alveolar macrophages and decreased Mtb control.

97 , R848 induced production of IL-27 by murine alveolar macrophages and dendritic cells and enhanced ex

98 n of innate immunity mediators, initiated by alveolar macrophages and dependent on transcription driv

99 atlas, we demonstrated heterogeneity within alveolar macrophages and epithelial cells from subjects

100 Mechanistically, OBKO alveolar macrophages and epithelial cells had increased

101 nicotine, altered lung lipid homeostasis in alveolar macrophages and epithelial cells.

102 (fl/fl)) exhibited significant reductions in alveolar macrophages and failed to effectively clear pul

103 the lungs revealed aberrant phospholipids in alveolar macrophages and increased surfactant-associated

104 hus, aging induces defective phagocytosis by alveolar macrophages and increases lung damage.

105 two macrophage populations, tissue-resident alveolar macrophages and interstitial macrophages, which

106 Legionella pneumophila infects human alveolar macrophages and is responsible for Legionnaire'

107 tif chemokine ligand 1 (CXCL1) in FABP4(-/-) alveolar macrophages and lower airway CXCL1 levels in FA

108 sis (PAP), we evaluated lipid composition in alveolar macrophages and lung surfactant, macrophage-med

109 entify TRIM29 as a key negative regulator of alveolar macrophages and might have important clinical i

110 cytosis and cytokine response to bacteria by alveolar macrophages and monocyte-derived macrophages (M

111 FN-gamma blocked EHV-1 replication in murine alveolar macrophages and mouse lungs and protected mice

112 infected, most prominently CD45(neg) cells, alveolar macrophages and neutrophils.

113 over lnc-IL7R levels were reduced in lavaged alveolar macrophages and primary human small airway epit

114 FN-gamma inhibited EHV-1 infection of murine alveolar macrophages and protected mice against lethal E

115 sion studies demonstrated robust recovery of alveolar macrophages and recruitment of CD4+ lymphocytes

116 where L. pneumophila can be phagocytosed by alveolar macrophages and replicate intracellularly.

117 by mediating both chemokine production from alveolar macrophages and T cell trafficking.

118 simultaneous uptake of silica and lipids in alveolar macrophages and that strategies aimed at blocki

119 human inhalation, C. burnetii is engulfed by alveolar macrophages and transits through the phagolysos

120 tron microscopy showed intact BaSO(4) NPs in alveolar macrophages and type II epithelial cells, and i

121 found principally in type I and II cells and alveolar macrophages and was also detected in vascular e

122 population shared many characteristics with alveolar macrophages and was retained in the alveolar sp

123 e production, reduced phagocytic function of alveolar macrophages, and consequently, increased pneumo

124 en genes, IgG4-rich immune complexes coating alveolar macrophages, and increased immunostaining for p

125 from cell-free bronchoalveolar lavage fluid, alveolar macrophages, and intrapulmonary lymphocytes.

126 e alpha7nAChR in granulocytes, monocytes and alveolar macrophages, and low expression levels of alpha

127 s and Main Results: Adding IFN-beta to MDMs, alveolar macrophages, and PBECs prior to, but not after,

128 such as alveolar epithelial cells (ECs) and alveolar macrophages, and plays an important role in inf

129 461630

130 mortality, bacterial burden, maintenance of alveolar macrophages, and reduced lung inflammation and

131 dulates inflammatory responses, and enhances alveolar macrophage antimicrobial activity.

132 Tissue-resident (TR) alveolar macrophages (APhi) are long-lived, self-renew a

133 that Akt1-mediated mitophagy contributes to alveolar macrophage apoptosis resistance and is required

134 Alveolar macrophages are among the first immune cells th

135 In summary, alveolar macrophages are critical regulators of Th2 immu

136 After injury, tissue-resident alveolar macrophages are depleted, and monocytes from th

137 Alveolar macrophages are found in the alveoli of the lun

138 ely, CD163(+)CD206(+) (double-positive [DP]) alveolar macrophages are long-lived, survive after SIV i

139 Alveolar macrophages are lung-resident sentinel cells th

140 mune cells present in the respiratory tract, alveolar macrophages are poised to defend against hantav

141 By contrast, alveolar macrophages are readily infected with PVM in vi

142 Alveolar macrophages are sentinels of the pulmonary muco

143 Alveolar macrophages are the first line of defense again

144 Although alveolar macrophages are the major infected cell for the

145 ite burden, and increased numbers of CD68(+) alveolar macrophages as well as apoptotic cells in the l

146 Alveolar macrophages at both day 4 and 14 and IMs at day

147 Perturbation of the bovine alveolar macrophage (bAM) transcriptome, due to Mycobact

148 LPS-induced inflammatory response in bovine alveolar macrophages (bAMs).

149 on or short hairpin RNA knockdown of Akt1 in alveolar macrophages blocked HC's effects on IAV growth

150 la facilitates type 3 secretion into primary alveolar macrophages but not into the commonly used THP-

151 Viral DNA isolated from blood monocytes and alveolar macrophages (but not T cells) of drug-suppresse

152 posomes resulted in significant reduction in alveolar macrophages, but depletion did not prevent path

153 o isoforms 5a and 5b) is highly expressed in alveolar macrophages, but its function there is unclear

154 el self-promoting mechanism of activation of alveolar macrophages by arachidonate 15-lipoxygenase-der

155 In human alveolar macrophages, C. burnetii uses a Dot/Icm type IV

156 n to humans, the bacteria proliferate within alveolar macrophages causing pneumonia.

157 llular bacterial pathogen that replicates in alveolar macrophages, causing a severe form of pneumonia

158 Small alveolar macrophage CD206 expression was lower in COPD p

159 Our results show that in an alveolar macrophage cell line, cellular ROS responses ar

160 Employing a rat alveolar macrophage cell line, we found that exposure to

161 led DK128 was correlated with an increase in alveolar macrophage cells in the lungs and airways, earl

162 single-cell metabolomic profiling using rat alveolar macrophage cells incubated with different conce

163 id not affect the viral replication in swine alveolar macrophage cells.

164 With aging, we found reduced numbers of alveolar macrophages, cells essential for lung homeostas

165 Alveolar macrophages clear bacteria from the lung and ma

166 intracellular depot of ciprofloxacin to the alveolar macrophage compartment that was sustained over

167 cation in MARC-145 cells and primary porcine alveolar macrophages could also be reversed by overexpre

168 Depletion of alveolar macrophages curtailed infection in mice infecte

169 ondiabetic recipients confirmed an intrinsic alveolar macrophage defect that hindered T-cell priming.

170 ue interstitial macrophages were elevated in alveolar macrophage-deficient mice identifying a new hom

171 the airways and expressed on the surface of alveolar macrophages, dendritic cells, innate lymphoid t

172 veolar macrophage-independent and 31 min for alveolar macrophage-dependent clearance of unencapsulate

173 nfection was exacerbated under conditions of alveolar macrophage depletion and in mice with a macroph

174 ated with global monocyte or tissue-resident alveolar macrophage depletion.

175 Alveolar macrophage-derived MVs were fully internalized

176 ntify a molecular pathway governing neonatal alveolar macrophage development and show that genetic di

177 We next identified the phase of alveolar macrophage development requiring LPL.

178 elopment and show that genetic disruption of alveolar macrophage development results in immunodeficie

179 Rgamma is known to promote M2-macrophage and alveolar macrophage development.

180 rated lung fibrosis, whereas tissue-resident alveolar macrophages did not contribute to fibrosis.

181 During the fibrotic phase, monocyte-derived alveolar macrophages differ significantly from tissue-re

182 flow-sorted cells, we found that monocyte to alveolar macrophage differentiation unfolds continuously

183 findings suggest that selectively targeting alveolar macrophage differentiation within the lung may

184 ic genes expressed by mouse monocyte-derived alveolar macrophages during fibrosis were up-regulated i

185 Our findings reveal that alveolar macrophages engage alveolar epithelial signals

186 reveal disease-related heterogeneity within alveolar macrophages, epithelial cells, or other cell ty

187 a distinct, novel population of profibrotic alveolar macrophages exclusively in patients with fibros

188 A majority of their alveolar macrophages exhibit lysosomal accumulations of

189 Diabetic alveolar macrophages exhibited reduced phagocytosis of M

190 eaction in mammalian macrophages (NR8383 rat alveolar macrophages) exposed to a centrifuge regime of

191 Alveolar macrophages express UDP-specific P2Y6 receptors

192 Alveolar macrophages from diabetic mice had reduced expr

193 Transfer of infected alveolar macrophages from diabetic mice into nondiabetic

194 We tested the capacity of alveolar macrophages from diabetic mice to phagocytose M

195 Alveolar macrophages from female mice exhibited greater

196 that IL-4-stimulated bone marrow-derived and alveolar macrophages from female mice exhibited greater

197 s during fibrosis were up-regulated in human alveolar macrophages from fibrotic compared with normal

198 ung histopathology characteristic of PAP; 2) alveolar macrophages from Rasgrp1-deficient mice are enl

199 Alveolar macrophages from toll-like receptor 3 (-/-) mic

200 ure increased mitochondrial Ca(2+) influx in alveolar macrophages from wild-type, but not MCU(+/-), m

201 R2 expression in a subset of mouse and human alveolar macrophages further highlights EGR2 as a conser

202 Molecular mechanisms controlling alveolar macrophage generation have not been fully defin

203 Moreover, IPF alveolar macrophages had evidence of increased mitophagy

204 Alveolar macrophages had similar numbers of small and la

205 Small alveolar macrophages had the highest phagocytic ability.

206 ammatory gene expression levels, while large alveolar macrophages had the lowest.

207 We recently characterized human alveolar macrophage (hAM) infection in vitro and found t

208 etii replicates efficiently in primary human alveolar macrophages (hAMs) in ex vivo human lung tissue

209 Additionally, primary human alveolar macrophages (hAMs) were infected with S. aureus

210 Alveolar macrophages have emerged as major mediators of

211 ed neutralization of GM-CSF thereby inhibits alveolar macrophage homeostasis and function, leading to

212 lammatory cytokine, plays a critical role in alveolar macrophage homeostasis, lung inflammation and i

213 ed metabolic and functional studies on human alveolar macrophages, human monocyte-derived macrophages

214 WTI induced a pronounced reduction of alveolar macrophages in both strains that recovered with

215 e airway immune cell repertoire shifted from alveolar macrophages in healthy control subjects to a pr

216 s not sufficiently upregulated in developing alveolar macrophages in LPL(-/-) pups, suggesting that p

217 abolism and accumulation of CD103(+) DCs and alveolar macrophages in lung.

218 We demonstrate that CLEC5A is expressed on alveolar macrophages in mice exposed long-term to cigare

219 es differ significantly from tissue-resident alveolar macrophages in their expression of profibrotic

220 hyperoxia caused a shift in the phenotype of alveolar macrophages, increasing proportion of cells wit

221 nisms, with reduced half-lives of 14 min for alveolar macrophage-independent and 31 min for alveolar

222 ressing pneumococci colocalize with MRC-1 in alveolar macrophages, induce lower pro-inflammatory cyto

223 Murine alveolar macrophages infected with DeltakatG display abn

224 Transplantation of infected Cftr-deficient alveolar macrophages into the lungs of noninfected CF mi

225 , although mitochondrial oxidative stress in alveolar macrophages is critical for fibrosis developmen

226 Mitochondrial oxidative stress in alveolar macrophages is directly linked to pulmonary fib

227 Alternative activation of alveolar macrophages is linked to fibrosis following exp

228 us, autophagy in myeloid cells, particularly alveolar macrophages, is critical for inhibiting spontan

229 nd impaired M1 polarization were observed in alveolar macrophages isolated from infected IL-36R(-/-)

230 of protective IL-12p40 and Th1 chemokines by alveolar macrophages, leading to activation of NK cells

231 MARC-145 cells and primary porcine pulmonary alveolar macrophages led to significant reduction of STA

232 that therapies that enhance the function of alveolar macrophages may improve outcomes in older peopl

233 These data demonstrate that alveolar macrophages may play a limited protective role

234 lso reveal the potential mechanisms by which alveolar macrophages mediate protection in vivo, namely

235 due to its intrinsic resistance to resident alveolar macrophage-mediated intracellular killing.

236 strategies aimed at blocking lipid uptake by alveolar macrophages might be effective in ameliorating

237 axis and differentiate into monocyte-derived alveolar macrophages (Mo-AMs), which is a cell populatio

238 by 23% in MDM (n = 37; P = 0.004) and 18% in alveolar macrophages (n = 20; P < 0.0001) in COPD.

239 Here, we examine the roles of alveolar macrophages, natural killer cells, and neutroph

240 hat, like in our prior T and B cell studies, alveolar macrophages neither prevent hantavirus infectio

241 More immune cells (including alveolar macrophages, neutrophils, eosinophils, and lymp

242 ion is characterized by increased numbers of alveolar macrophages, neutrophils, T lymphocytes (predom

243 g that immunodeficiency results from reduced alveolar macrophage numbers.

244 cells of patients with COPD and in isolated alveolar macrophages of patients with COPD or IPF.

245 wide variety of natural amoebal hosts and in alveolar macrophages of the human accidental host.

246 Here, we investigated the impact of alveolar macrophages on A. baumannii pneumonia using a m

247 CD163, C2+ and WSL, were compared to porcine alveolar macrophage (PAM) in terms of surface marker phe

248 In this study, we established the porcine alveolar macrophages (PAM) cells model co-infected with

249 Infection of primary pulmonary alveolar macrophages (PAMs) also induces interferons.

250 dy compared the interactions between porcine alveolar macrophages (PAMs) and wild-type A. pleuropneum

251 the miRNA-targeted transcriptome of porcine alveolar macrophages (PAMs) at early times after infecti

252 Immunophenotyping of porcine alveolar macrophages (PAMs) showed that pigs with the KO

253 A population of monocyte-derived alveolar macrophages persisted in the lung for one year

254 Moreover, aging decreases alveolar macrophage phagocytosis of apoptotic neutrophil

255 The diabetic alveolar macrophage phenotype depended in part on expres

256 This alveolar macrophage phenotype was absent in peritoneal a

257 d whether M2 signatures were associated with alveolar macrophage phenotypes in asthmatic patients.

258 We demonstrate that alveolar macrophages play a dominant role in conferring

259 To determine whether alveolar macrophages play a role in HPS pathogenesis, al

260 unications between lung epithelial cells and alveolar macrophages play an essential role in host defe

261 cesses essential for correct localization of alveolar macrophage precursors: (1) transmigration into

262 Human alveolar macrophages produced CCL2 in a PGL-dependent fa

263 ontributes to defective sentinel function of alveolar macrophages, promoting tuberculosis susceptibil

264 ught to address the contribution of resident alveolar macrophages (rAMs) to susceptibility to RSV inf

265 he transition from prealveolar macrophage to alveolar macrophage requires the upregulation of the tra

266 orne bacilli are inhaled and phagocytosed by alveolar macrophages, resulting in the formation of a gr

267 adily infected with PVM in vivo; ablation of alveolar macrophages results in prolonged survival in as

268 Large alveolar macrophages showed lower marker expression in C

269 Following lipopolysaccharide inhalation, alveolar macrophages strongly up-regulate cytokines for

270 d in the ATI-EVs are actively delivered into alveolar macrophages, subsequently promoting inflammasom

271 Aside from alveolar macrophages, subsets of Langerin(+), BDCA1(-)CD

272 Apoptotic cell uptake by lung alveolar macrophages suppressed HDM-driven allergic asth

273 rk between infected and noninfected AECs and alveolar macrophages that leads to decreased alveolar ep

274 differentiation, survival, and activation of alveolar macrophages, the cells responsible for surfacta

275 s a selective regulator of the activation of alveolar macrophages, the expression of type I interfero

276 h and was only found in lung parenchyma and alveolar macrophages thereafter.

277 lungs during a late fetal stage, maturing to alveolar macrophages through a prealveolar macrophage in

278 stimulates pathogen killing and clearance by alveolar macrophages through extracellular signal-regula

279 Th-17 lymphocytes and, conversely, a blunted alveolar macrophage TLR4 response.

280 Alveolar macrophage TNFalpha production was unaltered.

281 Aging impairs the ability of alveolar macrophages to limit lung damage during influen

282 localized in an intracellular compartment of alveolar macrophages together with SP-D.

283 n mouse models, depletion of tissue-resident alveolar macrophages (TRAMs) attenuated neutrophil recru

284 l (SAE) cell differential and transcriptome, alveolar macrophage transcriptome, and plasma apoptotic

285 bacterial pneumonia can be identified in the alveolar macrophage transcriptome.

286 d and basal cells, markedly abnormal SAE and alveolar macrophage transcriptomes, and elevated levels

287 Alveolar macrophages undergo productive infection and re

288 lease, and evaluated for in vivo absorption, alveolar macrophage uptake, and safety.

289 ) dendritic cells (DCs), but not PD-L1(high) alveolar macrophages, was dependent on IFNAR signaling.

290 In addition to a substantial population of alveolar macrophages, we identified subpopulations of mo

291 Additionally, alveolar macrophages were depleted and dysfunctional, re

292 macrophages play a role in HPS pathogenesis, alveolar macrophages were depleted in an adult rodent mo

293 Methods: Alveolar macrophages were obtained by bronchoscopy and M

294 nt mice reconstituted with Csf2ra-proficient alveolar macrophages were subjected to different models

295 ed GM-CSF-dependent cholesterol clearance in alveolar macrophages, which impairs alveolar surfactant

296 Aerosolized H5N1 exposure decimated alveolar macrophages, which were widely infected and cau

297 an primates, Siglec-1 is highly expressed by alveolar macrophages, whose abundance correlates with pa

298 phagocytic function respectively, and large alveolar macrophages with low pro-inflammatory and phago

299 subpopulations; Small interstitial and small alveolar macrophages with more pro-inflammatory and phag

300 alveolar epithelia (type I and II cells) and alveolar macrophages with similar trends in reactive mes