ライフサイエンスコーパス: amebic

1 encoded protein correlates with detection of amebic 170-kDa antigen in serum and feces.

2 Children with mucosal IgA antibodies to the amebic adherence lectin were found to be resistant to re

3 re-treated erythrocytes but had no effect on amebic adherence to or destruction of cell monolayers or

4 and required intact parasite, since blocking amebic adherence with galactose inhibited tyrosine depho

5 Moreover, disruption of amebic adherence with galactose promoted recovery of pho

6 stent with a primary defect in regulation of amebic adherence, EhMSP-1 silencing also resulted in red

7 ce metalloprotease involved in regulation of amebic adherence, with additional effects on cell motili

8 In contrast, amebic alcohol dehydrogenase 1 and ferredoxin, which are

9 dies to be identical to or an isoform of the amebic alcohol/aldehyde dehydrogenase (EhADH2).

10 ns (excluding the viral hepatitides) include amebic and pyogenic liver abscess and cholangitis.

11 All patients had 170-kDa amebic antigen in serum, compared with 1 of 50 cyst pass

12 ba histolytica protein (SREHP), a protective amebic antigen, fused to a maltose binding protein (MBP)

13 ik Chek assay developed by Techlab to detect amebic antigens in fecal samples collected from independ

14 lution, the role of lateral gene transfer in amebic biology and the adaptations required for eukaryot

15 of a C-terminal KDEL peptide, identified on amebic BiP, retained chitinase in a putative endoplasmic

16 amoeba histolytica requires adherence via an amebic cell surface lectin.

17 he molecule central to these processes is an amebic cell surface protein that recognizes the sugars g

18 In a mouse model of amebic colitis and a hamster model of amebic liver absce

19 ntamoeba histolytica, the causative agent of amebic colitis and liver abscess, would reduce childhood

20 istolytica is the cause of potentially fatal amebic colitis and liver abscesses.

21 Amebic colitis is an important worldwide parasitic disea

22 nowledge of host-parasite interaction during amebic colitis, and highlights a potential immunomodulat

23 In conclusion, in amebic colitis, development of humoral and mucosal IgA r

24 dying this early step in the pathogenesis of amebic colitis, we demonstrate that E. histolytica troph

25 utes to the tissue damage that occurs during amebic colitis, with tumor necrosis factor alpha (TNF-al

26 of amebic disease: amebic liver abscess and amebic colitis.

27 tor alpha (TNF-alpha) in the pathogenesis of amebic colitis.

28 kDa subunit were determined in patients with amebic colitis.

29 vanced by the use of a novel murine model of amebic colitis.

30 and contribute to the tissue damage seen in amebic colitis.

31 pithelial cell lines and in a mouse model of amebic colitis.

32 minish epithelial apoptosis may be useful in amebic colitis.

33 Entamoeba histolytica is the agent of amebic colitis.

34 lytica is the protozoan parasite that causes amebic colitis.

35 chanisms in amebic liver abscess compared to amebic colitis.

36 erythrocytes, suggesting the existence of an amebic coreceptor specific for PS.

37 We show that amebic CPs are required for amebic trogocytosis and cell

38 Interfering with amebic CPs decreased amebic trogocytosis and amebic cyto

39 These data suggest that amebic CPs play a distinct role in amebic trogocytosis a

40 Amebic cysteine proteases (CPs) were inhibited using an

41 7 and CRAMP were rapidly cleaved by released amebic cysteine proteases.

42 In contrast to the other amebic cysteine proteinases characterized so far, which

43 amebic CPs decreased amebic trogocytosis and amebic cytotoxicity but did not impair phagocytosis.

44 channels was highly effective in preventing amebic cytotoxicity in intestinal epithelial cells and m

45 ded that K(+) channels are host mediators of amebic cytotoxicity in multiple cells types and of infla

46 mice was found to increase susceptibility to amebic cytotoxicity in single cells.

47 signaling mutants showed that resistance to amebic cytotoxicity was dependent on activation of STAT3

48 n signaling increased cellular resistance to amebic cytotoxicity, including caspase-3 activation.

49 hozoites in models of the two major forms of amebic disease: amebic liver abscess and amebic colitis.

50 that the tetraplex real-time PCR can detect amebic DNA corresponding to as little as a 0.1 trophozoi

51 tozoan parasite Entamoeba histolytica causes amebic dysentery and amebic liver abscess, diseases asso

52 parasite Entamoeba histolytica, the cause of amebic dysentery and amebic liver abscess, is an obligat

53 Cholera therefore joins amebic dysentery and Clostridioides difficile colitis as

54 tamoeba histolytica, the protist that causes amebic dysentery and liver abscess, are of great interes

55 al ameba Entamoeba histolytica, which causes amebic dysentery and liver abscesses.

56 tolytica, the protozoan parasite that causes amebic dysentery, phagocytose bacteria in the colonic lu

57 Granulomatous amebic encephalitis (GAE), an infection of immunocomprom

58 soil sample associated with a fatal case of amebic encephalitis in a northern California child.

59 free-living ameba that causes granulomatous amebic encephalitis in both immunocompromised and immuno

60 alamuthia antibody-containing serum from the amebic encephalitis patient.

61 We report a unique case of granulomatous amebic encephalitis that was proven pathologically with

62 ual Balamuthia mandrillaris and Acanthamoeba amebic encephalitis with neurotoxoplasmosis coinfection.

63 and Balamuthia mandrillaris and Acanthamoeba amebic encephalitis with Toxoplasma gondii coinfection.

64 s, disseminated infection, and granulomatous amebic encephalitis, which is generally fatal.

65 ons of other organs, and fatal granulomatous amebic encephalitis.

66 Amebic erythrophagocytosis is characteristic of invasive

67 resent in over 75% of phagocytic cups during amebic erythrophagocytosis.

68 Interestingly, we found that the amebic EVs impacted intercellular communication between

69 s, including Argonaute, were also present in amebic EVs.

70 ecause of the critical role of EhADH2 in the amebic fermentation pathway and the lack of known eukary

71 tained mucosal IgA antibody responses to the amebic galactose-inhibitable lectin and a high level of

72 stinal and humoral antibody responses to the amebic galactose-inhibitable lectin and to determine whe

73 ing a mechanism that requires contact via an amebic galactose-specific lectin.

74 osis, and E. histolytica phagocytosis alters amebic gene expression in a feed-forward manner that res

75 gh it is not clear from which bacteria these amebic genes derive.

76 upport the idea of coincidental selection of amebic genes encoding proteins that mediate destruction

77 We used this approach to silence multiple amebic genes, including an E. histolytica Myb gene, whic

78 lture medium in quantities commensurate with amebic growth when studied in a novel culture system.

79 Like Hsp60 of mitochondria, amebic Hsp60 RNA and protein were both strongly induced

80 he possible function and localization of the amebic Hsp60 were explored here.

81 demonstrating the chaperonin function of the amebic Hsp60.

82 ulin A (IgA) monoclonal antibodies (MAbs) on amebic in vitro galactose-specific adherence.

83 A subjects demonstrated greater clearance of amebic infection after an anti-lectin IgA antibody peak

84 Amebic infection also induced an 18-fold increase in int

85 itor ZVAD decreased the rate and severity of amebic infection in CBA mice by all measures (cecal cult

86 These results indicate that amebic infection in the colon induces the expression of

87 cell apoptosis in the intestine facilitates amebic infection in this mouse model.

88 rotective role in the early host response to amebic infection of the liver.

89 al epithelial cell inflammatory responses to amebic infection were inhibited by the intraluminal admi

90 specimens from two individuals negative for amebic infection were spiked with Balamuthia amebas.

91 isms of MUC2 production by goblet cells upon amebic infection, regulation of antimicrobial peptide pr

92 educed inflammation and intestinal damage in amebic infection, while inhibition of IL-1 reduced cytok

93 e enhanced epithelial permeability seen with amebic infection.

94 ugh cyclooxygenase-2 to the host response to amebic infection.

95 ase in intestinal permeability observed with amebic infection.

96 y human intestinal xenografts in response to amebic infection.

97 on and intestinal epithelial apoptosis after amebic infection.

98 Amebic infections involving the central nervous system a

99 While no subsequent amebic infections occurred in the three organ recipients

100 earlier attention had focused on Giardia and amebic infections, the other "emerging" protozoan beside

101 eba histolytica trophozoites, and 12 h after amebic inoculation, reduced the mean liver abscess size

102 ies suggest that the acute host response and amebic invasion result from a complex interplay of paras

103 host factors that control susceptibility to amebic killing.

104 In support of this idea, the amebic lectin and pore-forming peptide are involved in b

105 l the extracellular adhesive activity of the amebic lectin and provide in vivo demonstration of the l

106 xenografts with a monoclonal antibody to the amebic lipophosphoglycan-peptidoglycan molecules can pre

107 We followed 93 subjects with amebic liver abscess (ALA) and 963 close associate contr

108 We monitored 93 subjects cured of amebic liver abscess (ALA) and 963 close associate contr

109 Durban, South Africa, were recently cured of amebic liver abscess (ALA) with or without concurrent En

110 ls of the two major forms of amebic disease: amebic liver abscess and amebic colitis.

111 The complications of amebic liver abscess are underappreciated in developed c

112 amage may proceed by different mechanisms in amebic liver abscess compared to amebic colitis.

113 mbined immunodeficient (SCID) mouse model of amebic liver abscess formation and compared liver damage

114 or their ability to delay the development of amebic liver abscess formation in an E. histolytica infe

115 s a significant but not an exclusive role in amebic liver abscess formation in the mouse model.

116 rominent role in the host cell death seen in amebic liver abscess in a mouse model of disease and sug

117 CID mice while NO is required for control of amebic liver abscess in immunocompetent mice.

118 oked at the effect of inhibiting caspases on amebic liver abscess in the mouse model of infection.

119 In most cases, amebic liver abscess is associated with an excellent pro

120 Amebic liver abscess is characterized by extensive areas

121 In the United States, amebic liver abscess occurs largely in individuals from

122 gamma plays a role in the innate immunity to amebic liver abscess seen in SCID mice while NO is requi

123 We next used a hamster model of amebic liver abscess to determine the effect of immuniza

124 Amebic liver abscess usually occurs in individuals from

125 An association of this allele with amebic liver abscess was also determined in an independe

126 or full virulence in the SCID mouse model of amebic liver abscess, but E. histolytica trophozoites th

127 oeba histolytica causes amebic dysentery and amebic liver abscess, diseases associated with significa

128 We report a 16-month-old male child with amebic liver abscess, initially misdiagnosed with pneumo

129 stolytica, the cause of amebic dysentery and amebic liver abscess, is an obligate anaerobe, and deriv

130 del of amebic colitis and a hamster model of amebic liver abscess, oral auranofin markedly decreased

131 In contrast to amebic liver abscess, pyogenic liver abscess is associat

132 typhimurium SREHP-MBP were protected against amebic liver abscess, the most common extraintestinal co

133 ddition to highlighting the complications of amebic liver abscess, this case demonstrates the value o

134 Patients with diagnoses of amebic liver abscess, traumatic liver abscess, post chol

135 mbined immunodeficient (SCID) mouse model of amebic liver abscess.

136 ) infection are at an increased incidence of amebic liver abscess.

137 ng added to the diagnostic armamentarium for amebic liver abscess.

138 l-depleted animals have significantly larger amebic liver abscesses at early stages of infection and

139 Diarrhea and amebic liver abscesses due to invasive Entamoeba histoly

140 on of hamsters reduced development of severe amebic liver abscesses following intrahepatic injection

141 the prominent inflammatory cell ring seen in amebic liver abscesses in control SCID mice.

142 ent amebae may exacerbate the damage seen in amebic liver abscesses.

143 use as a vaccine antigen to protect against amebic liver abscesses.

144 ose inhibited tyrosine dephosphorylation and amebic lysates had no effect on phosphotyrosine levels.

145 Amebic lysates have also been shown to activate the prec

146 contrast to the activation of proIL-1beta by amebic lysates, the purified proteinase cleaved proIL-18

147 E. histolytica trophozoites and accelerated amebic lysis via activation of the classical complement

148 n a previous study, we showed that acidified amebic lysosomes are required for both amebic trogocytos

149 tral nervous system infection called primary amebic meningoencephalitis (PAM) in healthy children and

150 Primary amebic meningoencephalitis (PAM) is a fulminant central

151 Primary amebic meningoencephalitis (PAM) is a rapidly progressiv

152 Primary amebic meningoencephalitis (PAM), caused by the free-liv

153 Primary amebic meningoencephalitis (PAM), which is almost univer

154 Primary amebic meningoencephalitis (PAM), which is almost univer

155 rtunistic pathogen that causes granulomatous amebic meningoencephalitis in animals, including humans.

156 amebas from brain tissue from cases in which amebic meningoencephalitis is a diagnostic possibility,

157 eria fowleri, the causative agent of primary amebic meningoencephalitis, is resistant to complement l

158 scription via nuclear run on analysis and an amebic nuclear protein was demonstrated to specifically

159 We demonstrate that amebic nuclear protein(s) bind specifically to four of t

160 r abscess is typically either of pyogenic or amebic origin.

161 Conditioned medium from amebic parasites contained particles consistent with the

162 a mammalian signaling pathway that restricts amebic pathogenesis and represents an important advance

163 an evolutionary dead end, it is likely that amebic pathogenicity is coincidentally selected, i.e., t

164 Here amebic phagocytosis of bacteria, RBC, and mucin-coated b

165 is, we used a flow cytometry-based assay for amebic phagocytosis, a method for making single-ligand p

166 he collectins alone were adequate to trigger amebic phagocytosis, because single-ligand particles coa

167 trometry analyses identified calreticulin in amebic phagosome preparations, and, in addition to its f

168 cA-V12) overexpression, wortmannin abolished amebic pinocytosis of dextrans but had no inhibitory eff

169 . histolytica trophozoites, one of the first amebic products to interact directly with components of

170 unction with published findings showing that amebic proteinases are responsible for the induction of

171 activated by caspase-1, we evaluated whether amebic proteinases had a similar effect.

172 The activity of amebic proteinases was examined by zymography.

173 e complex of surface-associated and released amebic proteinases.

174 raction F3, but not F1, F2, or F4, inhibited amebic proteinases.

175 ance between degradation of cathelicidins by amebic released cysteine proteinases and upregulation of

176 We conclude that the amebic secretory pathway is similar to those of other eu

177 ction of mucosal and immune responses to the amebic SREHP antigen is dependent on the level of SREHP-

178 When five of these genes were silenced, amebic strains with significant decreases in the ability

179 Interfering with amebic CPs decreased amebic trogocytosis and amebic cytotoxicity but did not

180 We show that amebic CPs are required for amebic trogocytosis and cell killing but not phagocytosi

181 gest that amebic CPs play a distinct role in amebic trogocytosis and cell killing.

182 ified amebic lysosomes are required for both amebic trogocytosis and phagocytosis, as well as cell ki

183 l the cell eventually dies, a process termed amebic trogocytosis.

184 o studying the specific interactions between amebic trophozoites and human intestine, we used a SCID

185 Extracellular cysteine proteinases from amebic trophozoites are key virulence factors and have a

186 appears to involve the initial attachment of amebic trophozoites to intestinal epithelial cells, foll

187 rine-rich E. histolytica protein (SREHP), an amebic vaccine candidate.

188 Inhibition of amebic vacuolar acidification by bafilomycin also decrea