ライフサイエンスコーパス: granuloma

1 hage phagosome and later within the necrotic granuloma.

2 phage recruitment to the forming tuberculous granuloma.

3 pact that this has on the progression of the granuloma.

4 y was observed in macrophages throughout the granuloma.

5 Predictors of PTT, ECA, and granuloma.

6 etween abnormal Paneth cells and presence of granuloma.

7 nted of the growth and death of bacilli in a granuloma.

8 ignals are physically segregated within each granuloma.

9 ages undergoing apoptosis in the tuberculous granuloma.

10 atory pathways during the development of the granuloma.

11 bers and reduced CD4(+) T-cell counts within granulomas.

12 nt for long-term M. tuberculosis survival in granulomas.

13 lular response, and cytokine presence within granulomas.

14 nd monocytes, resulting in reduced number of granulomas.

15 rization, function, and bacterial control in granulomas.

16 developed, with foreign-body giant cells and granulomas.

17 vestigated vessel normalization in rabbit TB granulomas.

18 ribing mean polarization measures for entire granulomas.

19 age in both human and experimental rabbit TB granulomas.

20 i.e., IFNAR1(-/-)) also developed intestinal granulomas.

21 the formation of foamy macrophages (FMs) and granulomas.

22 Biopsy in all cases showed foreign body-type granulomas.

23 f inflammatory cells forming nodules, called granulomas.

24 lated with host defense in macaque and human granulomas.

25 and T cells drive [(64)Cu]-LLP2A avidity in granulomas.

26 rculosis is the formation of macrophage-rich granulomas.

27 mycobacteria trigger formation of organized granulomas.

28 he HIV infection progressively changes these granulomas.

29 n source are unable to sustain infections in granulomas.

30 pulate Mycobacterium tuberculosis-associated granulomas.

31 e generated detailed molecular maps of human granulomas.

32 population dynamics and heterogeneity within granulomas.

33 Consistent with the altered granulomas, 1,25(OH)2D3-treated mice also exhibited sign

34 everal novel roles for IL-10 in tuberculosis granulomas: 1) decreased levels of IL-10 lead to increas

35 ia (3 cases), trichiasis (2 cases), pyogenic granuloma (2 cases), eyelid margin nodule (1 case), lowe

36 ne findings were presence of >/=1 peripheral granulomas (57.1%), vasculitis (57.1%), vitreoretinal tr

37 Poorly formed granulomas (96%), neutrophils (75%), and necrosis (79%)

38 The site of infection in TB is the granuloma, a collection of immune cells and bacteria tha

39 that granuloma-up-regulated factors increase granuloma access to secondary lymph organs by lymphangio

40 Pyogenic granulomas, acquired vascular lesions, form on the ocula

41 model in mice, which develops necrotic lung granulomas after infection with Mycobacterium tuberculos

42 d to prevent host-induced tissue damage in a granuloma, an aggregate of cells that forms in response

43 d the causes of an inflammatory disease with granuloma and autoimmunity associated with decreasing T-

44 The diverse immunopathology of granulomas and cavities generates a plethora of microenv

45 p75-/- mice developed effective bactericidal granulomas and demonstrated increased pulmonary recruitm

46 macrophages in the lung, which formed type 2 granulomas and exacerbated inflammation in Mtb-infected

47 This response leads to the development of granulomas and fibrosis, with eosinophils, neutrophils,

48 periportal infiltrations, bile duct damage, granulomas and fibrosis.

49 es are among the most abundant cell types in granulomas and have been shown to serve as both critical

50 of latent infection, in which yeasts within granulomas and host macrophages emerge to cause disease.

51 was associated with reduced hypoxia in lung granulomas and induction of matrix metalloproteinases an

52 haracterized by the presence of noncaseating granulomas and is usually treated successfully with immu

53 ncreased PD-L1 expression within sarcoidosis granulomas and lung malignancy, but this was absent in h

54 on of NPC2 was lower in caseous tuberculosis granulomas and M. tuberculosis-infected monocytes compar

55 Granulomas and mediastinal lymph nodes from active-disea

56 f E-cadherin in macrophages disorganized the granulomas and protected the fish, introducing new ideas

57 Here, we demonstrate CD1b expression in TB granulomas and reveal a central role for meromycolate ch

58 Over the course of infection, granulomas and thoracic lymph nodes experienced dynamic

59 py in both C3HeB/FeJ (which produce necrotic granulomas) and the wild-type background C3H/HeJ mouse s

60 e and included tearing, discomfort, pyogenic granuloma, and dacryocystitis.

61 alled integrin alpha4beta1) binding cells in granulomas, and compared [(64)Cu]-LLP2A with [(18)F]-FDG

62 or host survival, containment of bacteria in granulomas, and control of bacterial burdens in vivo.

63 consequences of angiogenesis in tuberculous granulomas, and data that balanced inflammation in human

64 cruitment and enhanced T-cell recruitment in granulomas, and decreased the bacterial load.

65 reflecting the compartments of macrophages, granulomas, and open cavities as well as parameterizing

66 ctional characteristics, accumulated in lung granulomas, and protected against Mtb infection.

67 Enteropathy, autoimmunity, granulomas, and splenomegaly formed a set of interrelate

68 erin- and Mycobacterium tuberculosis-induced granulomas, and that infection results in lymph vessel s

69 a expression was observed in CBA splenic and granuloma APC subpopulations, but only DCs induced Th17

70 infected with S. mansoni had disrupted liver granuloma architecture and increased mortality, which in

71 to increased lung bacillary load, disrupted granuloma architecture with expanded necrotic foci and r

72 ulosis infected mice led to a change in lung granuloma architecture, characterized by a marked decrea

73 i- and Schistosoma japonicum-induced hepatic granuloma are also discussed.

74 While some features such as granuloma are typical signs of OT, atypical features can

75 Granulomas are a hallmark of tuberculosis.

76 Granulomas are complex lung lesions that are the hallmar

77 Granulomas are formed around the eggs to protect the org

78 Granulomas are immune cell aggregates formed in response

79 Granulomas are morphologically similar to solid cancerou

80 ediated antileishmanial mechanism, and (iii) granulomas are not necessarily hallmarks of protective a

81 ize that (i) recruited mononuclear cells and granulomas are not required to control infection or resp

82 Despite this protection, TB granulomas are often hypoxic, and bacterial killing via

83 Granulomas are the hallmark of Mycobacterium tuberculosi

84 Granulomas are the pathological hallmark of tuberculosis

85 nce in mycobacteria-which models tuberculous granulomas-are partly determined by a mechanism of tRNA

86 developed substantial numbers of intestinal granulomas around the site of infection, which were not

87 monstrated hepato-splenomegaly with multiple granulomas as well as ascites and a left-sided pleural e

88 ble knockout [DKO] mice) showed both delayed granuloma assembly and initially impaired control of par

89 oles in (i) mononuclear cell recruitment and granuloma assembly and maturation, (ii) initial control

90 ol of liver infection, parasite killing, and granuloma assembly were accelerated and chemotherapy's e

91 CCL2, CCL5) or downregulate (CXCL9) initial granuloma assembly, (iii) may enhance (CCL2, CCL5) or hi

92 nfection or respond to Sb chemotherapy, (ii) granuloma assembly, control of infection, and Sb's effic

93 i, CD8(+) T cell mechanisms are required for granuloma assembly, macrophage activation, intracellular

94 ) mice also presented with smaller liver egg granulomas associated with increased collagen deposition

95 al inhibition of the Vegf pathway suppresses granuloma-associated angiogenesis, reduces infection bur

96 Our data indicate that mycobacteria induce granuloma-associated angiogenesis, which promotes mycoba

97 Granuloma-associated vessels are morphologically and spa

98 In tuberculosis, some macrophages in granulomas assume an epitheloid appearance.

99 Finally, we find that on an individual granuloma basis, pre-treatment infection severity (inclu

100 -FDG, may be a useful tool for understanding granuloma biology in TB.

101 rophages undergo secondary necrosis, causing granuloma breakdown and increased mycobacterial growth.

102 e CLEAR group had a significant reduction in granuloma burden and experienced a mean (SD) decline of

103 y metabolically active inflammatory cells in granulomas, but lacks specificity for particular cell ty

104 increased host survival, suggesting that the granuloma can also serve a bacteria-protective role.

105 e generation of systemic T-cell responses to granuloma-contained antigens.

106 hallmark of pathogenesis is the formation of granulomas containing multinucleated giant cells (MNGCs)

107 fic polarization and plasticity, or why some granulomas control bacteria and others permit bacterial

108 erstanding M. tuberculosis metabolism within granulomas could contribute to reducing the lengthy trea

109 ed a large in silico repository of in silico granulomas coupled to lymph node and blood dynamics and

110 duction, and other phenotypic changes within granulomas, demonstrating the HIV infection progressivel

111 We found that noncaseating granulomas develop rapidly and eventually eradicate infe

112 Lung granulomas develop upon Mycobacterium tuberculosis (Mtb)

113 be, Pagan et al. (2015) reveal that necrotic granulomas develop when macrophage supply is insufficien

114 IKKalpha and IKKbeta have effects on hepatic granuloma development.

115 erentiation or recruitment occurs throughout granuloma development.

116 s of mycobacterial infection, thus impairing granuloma development.

117 ed a previously unappreciated level of inter-granuloma diversity in terms of the development of anti-

118 n spleen, liver, and lungs and smaller liver granulomas during 60 d of infection compared with wild-t

119 n malignant and benign SPNs in patients from granuloma-endemic regions.

120 We sought to determine temporal patterns of granuloma evolution that distinguished active-disease an

121 s to control the bacteria, the center of the granuloma exhibits necrosis resulting from the dying of

122 The 14-year-old patient, who had liver granuloma, extranodal marginal zone B-cell lymphoma, and

123 o 60s, who developed open [corrected] facial granulomas following microneedle therapy for skin rejuve

124 Here we integrate our computational model of granuloma formation and function with models for plasma

125 ent-based computational model that simulates granuloma formation and function, FQ plasma and tissue p

126 aptive immune determinants mediating leprosy granuloma formation and function.

127 bout the complex in vivo events that lead to granuloma formation and other pathological changes durin

128 l to this oxygenated MA induction of FMs and granuloma formation as evaluated by in vitro and in vivo

129 nuated IL-33-induced type 2 immunity and egg granuloma formation during S. japonicum infection.

130 he type 1 helper T (T(H)1) cell in sarcoidal granuloma formation has been well documented, and the T(

131 The precise chain of events driving lesional granuloma formation has remained elusive for many years.

132 The abolition of granuloma formation in embryos infected with the dehydra

133 vivo cytokine production, gross pathology or granuloma formation in lungs from M.tb DK9897 infected a

134 , we present a multiscale in silico model of granuloma formation in tuberculosis.

135 tor signaling may provide pathways to impede granuloma formation in vivo, but additional MyD88-mediat

136 hy and proliferation, resulting in excessive granuloma formation in vivo.

137 m marinum model, we found that mycobacterial granuloma formation is accompanied by macrophage inducti

138 lomas in the mouse model and have shown that granuloma formation is dependent upon the enzyme sphingo

139 e transparent larval zebrafish, we show that granuloma formation is intimately associated with angiog

140 Multicellular granuloma formation is the pathological hallmark of Myco

141 quent decreased NO expression and/or by poor granuloma formation with consequent decreased hypoxic st

142 une deficiency to delayed-onset disease with granuloma formation, autoimmunity, or both.

143 f E-cadherin function resulted in disordered granuloma formation, enhanced immune cell access, decrea

144 T cell-derived IL-4/IL-13 was essential for granuloma formation, IgE production, basophilia, differe

145 mensional cell culture model of tuberculosis granuloma formation, using bioelectrospray technology.

146 ge activation, and the Th2 response promotes granuloma formation.

147 ntribute to the fundamental understanding of granuloma formation.

148 8; 95% CI, 1.37-6.94; P = 0.007) resulted in granuloma formation.

149 e exacerbated lung inflammation and enhanced granuloma formation.

150 s evaluated by in vitro and in vivo model of granuloma formation.

151 FN-gamma-mediated immunity, and disorganized granuloma formation.

152 inct disease phenotypes such as necrosis and granuloma formation.

153 hat can establish the environment for mature granuloma formation.

154 and extracellular matrix in a 3D model of TB granuloma formation.

155 reign body particles in the bulla stimulates granuloma formation.

156 1R-MyD88 pathway is implicated in inhibiting granuloma formation; however, protective immunity in MyD

157 7 and decreased IL-6 and IL-10 levels within granulomas from B cell-depleted animals.

158 anulomas in TB, we analyzed the proteomes of granulomas from subjects with tuberculosis in an unbiase

159 We devise an overall measure of granuloma function based on three metrics - total bacter

160 In macaques, granulomas had higher [(64)Cu]-LLP2A uptake than uninfec

161 Macaque granulomas had upregulated inducible and endothelial NO

162 d a role for PknG in the formation of stable granuloma, hallmark structures of latent tuberculosis.

163 ppressive cytokine IL-10 at the level of the granuloma has proven difficult because of lesional heter

164 Understanding the pathogenesis of leprosy granulomas has been hindered by a paucity of tractable e

165 We found that the centers of granulomas have a pro-inflammatory environment that is c

166 ogether, these data support the concept that granulomas have organized microenvironments that balance

167 We highlight granuloma heterogeneity that emerges in the context of i

168 guinea pigs, which develop hypoxic, necrotic granulomas histologically resembling those in humans and

169 : 1) I-RL (n = 14), 2) peri-implant pyogenic granuloma (I-PG) (n = 5), 3) peri-implant peripheral gia

170 = 5), 3) peri-implant peripheral giant cell granuloma (I-PGCG) (n = 9), 4) T-RL (n = 44), 5) tooth-a

171 accine has been associated with chronic skin granuloma in 3 children with primary immunodeficiency.

172 T), eyelid contour abnormalities (ECAs), and granuloma in the 2 most common TT surgery procedures: po

173 tion in the Evicel group, 1 case of pyogenic granuloma in the Tisseel group, and no complications in

174 uences of vascularization of the tuberculous granuloma in the zebrafish-Mycobacterium marinum infecti

175 The effects of B cell depletion varied among granulomas in an individual animal, as well as among ani

176 TB granulomas in CD4-depleted macaques contained fewer IL-2

177 th increased collagen deposition compared to granulomas in infected wt mice.

178 ty of mice and during the formation of liver granulomas in mice infected with Schistosoma mansoni.

179 C1 induced apoptosis and completely resolved granulomas in myeloid TSC2-deficient mice.

180 l immunologic characteristics of tuberculous granulomas in nonhuman primates.

181 To understand the role of granulomas in TB, we analyzed the proteomes of granuloma

182 ns Deltagcs1) which can be contained in lung granulomas in the mouse model and have shown that granul

183 , CD68-positive and CD1a-negative palisading granulomas in widened interlobular fibrous septa were de

184 munity in MyD88-deficient mice appears to be granuloma independent.

185 oma maturation (CCL2, CCL5), (v) may exert a granuloma-independent action that enables self-cure (CCL

186 Histological analysis of these granulomas indicated infiltration of a diverse cadre of

187 hereby a few infected macrophages within the granuloma induce sustained cellular accumulation.

188 t response to Histoplasma capsulatum because granulomas induced by this pathogenic fungus develop hyp

189 Targeting granuloma-induced vascular permeability via vascular end

190 ) LC treatment resulted in fewer bladder egg granuloma-infiltrating macrophages, eosinophils, and T a

191 wever, macrophage-intrinsic pathways driving granuloma initiation and maintenance remain elusive.

192 le control of pulmonary bacterial burden and granuloma integrity, whereas TLR2 signaling on nonhemato

193 Groesser et al. demonstrate that pyogenic granuloma is a RAS pathway-driven tumor.

194 Conjunctival actinic granuloma is an underrecognized entity.

195 The granuloma is treated with isoniazid (INH), a drug that i

196 Central necrosis of granulomas is linked to progression of major diseases, i

197 suggest that penetration of drugs throughout granulomas is problematic.

198 Tissue verification of noncaseating granulomas is recommended for the diagnosis of sarcoidos

199 all to medium intraparenchymal, noncaseating granulomas lacking multinucleated giant cells and, in 1

200 uently below effective concentrations inside granulomas, leading to bacterial growth between doses an

201 ics and developed an in silico tool to scale granuloma level results to a full host scale to identify

202 the efficacy of MXF, LVX and GFX at a single granuloma level, we integrate computational modeling wit

203 Coalescing and mostly perivascular granuloma-like accumulations of storage-laden CD68(+) mi

204 Moreover, a chronic toxicity manifested as granuloma-like formation in spleen, liver, and lymph nod

205 controls, M. canettii-infected mice yielded granuloma-like lesions for 4/4 lungs at days 14 and 28 p

206 supply below a critical threshold decreases granuloma macrophage replenishment to the point where ap

207 Granuloma macrophage subsets are diverse and carry varyi

208 Thus, during mycobacterial infection, granuloma macrophages are broadly reprogrammed by epithe

209 Granuloma macrophages can then necrose, releasing mycoba

210 The production of NO by granuloma macrophages expressing nitric oxide synthase-2

211 Granuloma macrophages in humans with tuberculosis were s

212 sh model, Cronan et al. (2016) now show that granuloma macrophages undergo reprograming events involv

213 10) early parasite control, (iv) may promote granuloma maturation (CCL2, CCL5), (v) may exert a granu

214 As granulomas mature, they induce angiogenesis and vascular

215 egions of TB granulomas, we used a TB murine granuloma model in which NOS2 is absent.

216 Using an in vivo Matrigel granuloma model, the presence and activity of MMP-9 were

217 nt exhibits impaired survival in an in vitro granuloma model.

218 dormancy including a three-dimensional human granuloma model.

219 e to pulmonary Mtb, leading to poorly formed granulomas, more severe lung pathology, and increased my

220 In human TB granulomas, MT1-MMP immunoreactivity was observed in mac

221 , and the least common diagnosis was orbital granuloma (n = 28; 2.2% of ocular inflammation).

222 y to mycobacterial infection by accelerating granuloma necrosis.

223 This genotype displayed heightened granuloma numbers compared with wild-type mice, but with

224 Such granulomas occur in the lung and the mediastinal lymph n

225 wever, in other infectious diseases in which granulomas occur, such as leishmaniasis and schistosomia

226 ression is not induced in the lungs and lung granulomas of animals exhibiting latent tuberculosis inf

227 Granulomas of bacillus Calmette-Guerin-infected humanize

228 ells were significantly higher in spleen and granulomas of CBA mice, compared with C57BL/6 mice.

229 e recurrence after LT and presence of active granulomas on explant is associated with subsequent recu

230 Presence of granulomas on explanted lungs was the only predictor of

231 t imaging, and poorly formed non-necrotizing granulomas on pathology.

232 enocarcinomas) from benign fungal infection (granulomas) on 120 non-contrast CT studies.

233 nuloma polarization ratios are predictive of granuloma outcome.

234 in this setting resulted in exacerbated lung granuloma pathology and bacterial burden.

235 le of IL-33 and its receptor ST2L in hepatic granuloma pathology induced by Schistosoma japonicum inf

236 emonstrate that IL-33 contributes to hepatic granuloma pathology through induction of M2 macrophages

237 hage ratio to the tissue scale and define a "granuloma polarization ratio" describing mean polarizati

238 First, the temporal dynamics of granuloma polarization ratios are predictive of granulom

239 infection, while their presence in the lung granuloma protects against excessive inflammation.

240 Arg1 expression in hypoxic granuloma regions correlated with decreased T-cell proli

241 In human tuberculosis granulomas, regions of extracellular matrix destruction

242 itiated carcinogenesis instruct a long-lived granuloma-resident macrophage differentiation program th

243 Polyploid granuloma-resident macrophages formed via modified cell

244 g samples were positive for live bacilli and granulomas, respectively.

245 ldren, suggests that ocular surface pyogenic granulomas respond to topical timolol treatment, which h

246 ues in acute infection, analyzing individual granulomas revealed that B cell depletion resulted in al

247 proach, suggest that IL-10 at the individual granuloma scale is a critical regulator of lesion outcom

248 e site of infection (e.g., lung) at a single granuloma scale with blood level readouts that can be tr

249 metabolite- and gene-scale perturbations to granuloma-scale outcomes and predicting mechanisms of st

250 To explore how these adaptations influence granuloma-scale outcomes in vivo, we present a multiscal

251 ns are dominant within the inflammatory lung granulomas seen during active TB.

252 anisms involved in formation of inflammatory granulomas seen during active TB.

253 an 200 cells per muL) detection of choroidal granulomas should be accepted as evidence of disseminate

254 MXF and LVX have higher granuloma sterilization rates compared to GFX; and MXF p

255 rved increased mycobacterial burden, loss of granuloma structure, and increased progression of TB dis

256 t of tuberculosis (TB), induces formation of granulomas, structures in which immune cells and bacteri

257 T-RL (n = 44), 5) tooth-associated pyogenic granuloma (T-PG) (n = 21), and 6) tooth-associated perip

258 nd 6) tooth-associated peripheral giant cell granuloma (T-PGCG) (n = 23).

259 macrophages, resulting in the formation of a granuloma that ruptures into the airways to reinitiate t

260 mation of complex cellular aggregates called granulomas that are the hallmark of tuberculosis.

261 eral CD4(+) T-cell depletion correlated with granulomas that contained fewer CD4(+) and CD8(+) T cell

262 ronments, such as the macrophage or necrotic granuloma, that are acidic and rich in cholesterol and f

263 composition and dynamics of the tuberculous granuloma, the central host structure in mycobacterial i

264 Inside granulomas, the pathogen Mycobacterium tuberculosis may

265 After the histopathologic diagnosis of granulomas, the patient was treated with clobetasol oint

266 fection induces arginase-1-expressing type 2 granulomas, thereby increasing inflammation and TB disea

267 lecule delivery, and decreases hypoxia in TB granulomas, thereby providing a potential avenue to impr

268 Although basophils were recruited into liver granulomas, they appeared to be dispensable as a source

269 d experimental data from nonhuman primate TB granulomas to our computational model, and we predict tw

270 ildren with acquired ocular surface pyogenic granulomas treated at Boston Children's Hospital from 20

271 Finally, macaques develop the spectrum of granuloma types seen in humans, providing a unique oppor

272 Together, our data show that granuloma-up-regulated factors increase granuloma access

273 Granuloma was found in 50% of the 44 histological analys

274 Granuloma was less common in the TT clamp arm than in th

275 in whom tissue confirmation of noncaseating granulomas was indicated.

276 The percentage of natural killer cells in granulomas was significantly decreased in brain-injured

277 m similar functions in hypoxic regions of TB granulomas, we used a TB murine granuloma model in which

278 mong other findings, whereas eosinophils and granulomas were found more often in those with milder in

279 Because no granulomas were observed and only single lesional eosino

280 rly as 3 weeks postinfection, more pulmonary granulomas were observed in animals that would later dev

281 As a result, hypoxic fractions of these granulomas were reduced and small molecule tracer delive

282 mice there were less organ parasites and the granulomas were well defined.

283 ause of poor penetration of antibiotics into granulomas where the bacilli reside.

284 oupled with ill-defined and immature hepatic granulomas, whereas in WT mice there were less organ par

285 into polarization of single macrophages in a granuloma, which in turn modulates cellular functions, i

286 is infection in humans triggers formation of granulomas, which are tightly organized immune cell aggr

287 taining formulation resulted in formation of granulomas, which resolved by 28 weeks.

288 nderstanding antibiotic dynamics within lung granulomas will be vital to improving and shortening the

289 confirmed the presence of a 3.8 mm parietal granuloma with a few calcifications in the left eye.

290 active TB in humans a spectrum of pulmonary granulomas with central necrosis and hypoxia exists.

291 tissues, and immunohistochemical analysis of granulomas with known [(64)Cu]-LLP2A uptake identified s

292 Second, stable necrotic granulomas with low CFU counts and limited inflammation

293 n model, which is characterized by organized granulomas with necrotic cores that bear striking resemb

294 We treat in silico granulomas with recommended daily doses of each FQ and c

295 ich lack lymphocytes, also form noncaseating granulomas with similar kinetics, but these control infe

296 of biliary tree from mass effect of sarcoid granulomas with superimposed biliary sepsis is rare.

297 al to Mtb infection control, within a single granuloma, with minimal host-induced tissue damage.

298 tibiotic concentration gradients form within granulomas, with lower concentrations toward their cente

299 ated with the formation of mature protective granulomas within the lung.

300 erentiation of different cell populations in granulomas would be a useful research tool and could imp