ライフサイエンスコーパス: helminth

1 injury after infection with a lung-migrating helminth.

2 on by bacteria, viruses, fungi and parasitic helminths.

3 uent to primary and secondary infection with helminths.

4 in understanding how RQ is made in parasitic helminths.

5 eradication of pathogens, such as parasitic helminths.

6 nd public health control of soil-transmitted helminths.

7 chronically infected with endemic parasitic helminths.

8 mune responses directed against allergens or helminths.

9 butions in reducing the global prevalence of helminths.

10 inophils are effectors of immunity to tissue helminths.

11 Helminths, allergens, and certain protists induce type 2

12 ing potential cost/benefit ratios of various helminths along with other factors, such as feasibility

13 fied in single infections, rabbits with both helminths also activate new pathways that asymmetrically

14 ent of other diseases that are not caused by helminth and insect parasites.

15 Helminth and protozoan infections affect more than 1 bil

16 sity infections; thus, a causal link between helminths and allergy outcomes cannot be discounted.

17 through which the immune system responds to helminths and an array of environmental substances such

18 omes, and observational associations between helminths and metabolic outcomes.

19 r small intestinal perturbation by migratory helminths and move to distant tissues to influence the l

20 Nitazoxanide (NTZ) is effective against helminths and numerous microorganisms, including bacteri

21 y against coinfections with soil-transmitted helminths and Opisthorchis viverrini were secondary outc

22 tissue remodeling in response to colonizing helminths and protists.

23 g their innate host defense function against helminths and snake envenomation.

24 associations between acute infections by GI helminths and the faecal microbial and metabolic profile

25 occurring between gastrointestinal parasitic helminths and the microbial flora (microbiota) inhabitin

26 Helminths and tuberculosis (TB) largely overlap at the p

27 d to zoonotic parasites, including protozoa, helminths, and arthropods, may represent a major threat

28 tion in innate immune responses to parasitic helminths, and emerging evidence also indicates these ce

29 RQ biosynthesis in animals such as parasitic helminths, and most details of this pathway have remaine

30 prominent cell type in the host response to helminths, and some evidence suggests that neutrophils m

31 imal DC phenotypic activation in response to helminth antigen (Ag), and efficient migration to, and l

32 d Strongyloides stercoralis soil-transmitted helminths ("ANTS" parasites) significantly co-occur, and

33 We conclude that helminths are a small but important and potentially seve

34 We hypothesised that helminths are protective and their treatment detrimental

35 , and adverse effects in children in endemic helminth areas.

36 g feature of infection with parasitic worms (helminths), as well as being responsible for widespread

37 risk of infection with the soil-transmitted helminths Ascaris lumbricoides, hookworm (Ancylostoma du

38 Current deworming programs might remove this helminth-associated protective effect.

39 ts with an effective immune response against helminths can be more susceptible to allergy.

40 Conversely, many helminths can cause allergic-type inflammation, includin

41 Certainly, gastrointestinal helminths can protect against gut and lung mucosa inflam

42 Helminths cause chronic infections and affect the immune

43 t is essential for intestinal remodeling and helminth clearance.

44 also observed in a model of gastrointestinal helminth clearance.

45 thesis attenuates type 2 immunity and delays helminth clearance.

46 cally within the small intestine caused by a helminth co-infection would influence oral prion disease

47 required to reverse the negative effects of helminth coinfection on the CD8 T cell response.

48 Parasitic helminths, common in these settings, may be protective.

49 Mass deworming for soil-transmitted helminths compared with controls led to little to no imp

50 hown to clear the transmissible stage of the helminth completely in treated individuals.

51 Protection against helminths consists of adaptive responses by TH2 cells an

52 bility of production, we argue that the four helminths currently in use for CIAD treatments in humans

53 ortance of neutrophil extracellular traps in helminth damage after primary infections.

54 broad family of heme-binding proteins (MF6p/helminth defense molecules (HDMs)).

55 by noncellular particulate materials both to helminth-derived materials and to flexible/soft material

56 s of helminth infection or administration of helminth-derived molecules on chronic inflammatory disea

57 ical symbiosis, intact helminths rather than helminth-derived products are likely to prove more usefu

58 achievement of immunological tolerance using helminth-derived products is also an exciting future pro

59 st that intentional exposure to helminths or helminth-derived products may hold promise for treating

60 d investigation of the potential benefits of helminth-derived therapies for the prevention or treatme

61 Elimination of the helminth disease, river blindness, remains challenging d

62 and Drug Administration (FDA)-approved anti-helminth drug nitazoxanide (NTZ) on mitochondrial respir

63 rom single to multiple infections and impact helminth dynamics remains largely unclear.

64 nied by an increase in multiple type 2 (anti-helminths) effectors, including interleukin-5 (IL-5), IL

65 nowledge of the impact that infections by GI helminths exert on the developing microbiota of juvenile

66 Zoonotic helminth exposure in Norway was less frequent in offspri

67 We aimed to assess how helminth exposure influences rural-urban differences in

68 en rural and urban communities in Uganda but helminth exposure is unlikely to be the sole mechanism o

69 Changes in response to helminth exposure may provide insights into the increase

70 It is proposed that helminth exposure protects against allergy-related disea

71 nearby mainland urban communities with lower helminth exposure, we assessed risk factors for atopy (a

72 ession and effector function associated with helminth expulsion during type 2 inflammation.

73 asite eggs identified by microscopy included helminth genera pathogenic for humans and animals: the w

74 pression system will fuel the development of helminth glycoproteins for pharmaceutical applications o

75 able variation in their capacity to suppress helminth growth by two orders of magnitude.

76 w, the first biomechanical factor capable of helminth guidance within the host.

77 Secondary outcomes included helminths, haemoglobin, and hepatosplenomegaly.

78 Helminths have been previously shown to suppress effecto

79 Although helminths have been used therapeutically to ameliorate i

80 (H)2 cell response in mice infected with the helminth Heligmosomoides polygyrus bakeri H. polygyrus e

81 During infection with the helminth Heligmosomoides polygyrus bakeri, Bhlhe40 was r

82 g1b(-/-) mice failed to expel the intestinal helminths Heligmosomoides polygyrus or Nippostrongylus b

83 e were divided into four groups: uninfected; helminth-Heligmosomoides polygyrus infected; Pseudomonas

84 nerated in the future to further investigate helminth-host interactions.

85 ungulates, pose two evolutionary puzzles as helminth hosts.

86 nisms and components are known for parasitic helminths, how these relationships change from single to

87 accelerate single-cell discoveries of local helminth immune responses that have previously been unfe

88 lease cysteinyl leukotrienes to amplify anti-helminth immunity in the small intestine.

89 n cytokine production and contribute to anti-helminth immunity, maintaining mucosal tissue integrity,

90 Conversely, TFF3 deficiency reduces helminth immunity.

91 ng a previously overlooked mechanism of anti-helminth immunity.

92 be prevented by prior infection of mice with helminths in an IgE-dependent manner.

93 ecdotal reports of the beneficial effects of helminths in CD patients.

94 e morbidity attributable to soil-transmitted helminths in children but do not interrupt transmission

95 y pressing questions concerning the study of helminths in livestock, to help guide research prioritie

96 Here, we show that infection with helminths in the intestine also induces an ILC2-driven,

97 2 Ags such as alum-precipitated proteins and helminths induce IgG1, whereas Th1 Ags, such as Salmonel

98 oinfected mice recapitulated the spectrum of helminth-induced effects on the polyclonal CD8 T respons

99 Here, we demonstrate that helminth-induced group 2 innate lymphoid cell (ILC2) res

100 tion with important clinical significance in helminth-induced immunomodulation and sepsis.

101 hRetn promoted helminth-induced immunomodulation, with increased surviv

102 s on the CD8 T cell response, we demonstrate helminth-induced suppression of IL-12-dependent differen

103 They play a crucial role during allergy and helminth-induced Th2 responses.

104 that infection by gastrointestinal-dwelling helminths induces a systemic innate mucin response that

105 First, why do some helminths infect intermediate hosts prior to infecting u

106 Parasitic helminths infect over a billion humans.

107 Single cell isolation from helminth-infected murine intestines has been notoriously

108 = .04) (P value for interaction = .01) among helminth-infected subjects as detected by microscopy.

109 In helminth-infected subjects, treatment significantly incr

110 med involving all subjects and ad hoc in the helminth-infected subjects.

111 Instead, helminth infection altered the metabolic profile of the

112 ate an additional 3-way interaction in which helminth infection alters the metabolic environment of t

113 study investigates the relationship between helminth infection and allergic sensitization by assessi

114 ne responses throughout the entire course of helminth infection and has the potential to accelerate s

115 e progression of a subsequent lung migratory helminth infection and limits its transit through the ai

116 The type 2 immune response controls helminth infection and maintains tissue homeostasis but

117 omes, and observational associations between helminth infection and metabolic outcomes.

118 l-derived protein that is highly elevated in helminth infection and sepsis.

119 is a negative association between a chronic helminth infection and skin prick test reactivity even i

120 immune responses to house dust mite (HDM) or helminth infection and to identify mechanisms and functi

121 host's immune response to a gastrointestinal helminth infection can alter susceptibility to co-infect

122 ese data demonstrate that a strictly enteric helminth infection can have remote protective antiviral

123 ponses in LTB, we postulated that coexistent helminth infection could modulate chemokine production i

124 the national prevalence of soil-transmitted helminth infection has continued to decline in Sri Lanka

125 In this review, we consider how studies of helminth infection have contributed toward our expanding

126 LC2s upon activation with IL-33 or following helminth infection in an IL-33-dependent manner.

127 differentiation and clearance of a parasitic helminth infection in mice, and also abrogates the abili

128 We show that an ongoing helminth infection increased colonization by Salmonella

129 Hence, coexistent helminth infection induces downmodulation of chemokine r

130 The type 2 immune response to helminth infection is critical in limiting worm-induced

131 Helminth infection may influence cardiometabolic risk th

132 a also reveal a different mechanism by which helminth infection modulates immune function in LTBI.

133 These results suggest that chronic helminth infection of the intestines can influence and e

134 It is interesting to note that secondary helminth infection on the basis of persistent (chronic)

135 have demonstrated the potential benefits of helminth infection or administration of helminth-derived

136 y and tissue repair genes in the lungs after helminth infection or in the gut after induction of coli

137 Concurrent helminth infection potently inhibits T cell immunity; ho

138 n the more traditional approach in which the helminth infection precedes the onset of allergy.

139 cuss the applicability of this technology to helminth infection research, including strategies of co-

140 he T(H)2 cell transcriptional program during helminth infection to support normal expression of Csf2,

141 We modelled the risk of soil-transmitted helminth infection using generalised linear mixed-effect

142 National prevalence of soil-transmitted helminth infection was 0.97% (95% CI 0.63-1.48) among pr

143 dramatic increases in tissue ILC2s following helminth infection were mediated through local expansion

144 investigated the effects of strictly enteric helminth infection with Heligmosomoides polygyrus on res

145 During helminth infection, ASC depletion impaired lung ILC2 and

146 n this study, we show that during intestinal helminth infection, IL-4 derived from Tfh cells is requi

147 pregulated in inflammatory bowel disease and helminth infection, induces intestinal goblet cells, but

148 hat accumulate in tissues during allergy and helminth infection, performing critical effector functio

149 particularly in humans and rodent models of helminth infection, points towards a multitude of intera

150 Upon helminth infection, recruited and BM-derived cells gener

151 cles can also be generated in the context of helminth infection, since these large pathogens often sh

152 n associated with diarrhea, soil-transmitted helminth infection, trachoma, environmental enteric dysf

153 4 and PD-1 in immune modulation in a chronic helminth infection.

154 during colitis and augments immunity against helminth infection.

155 ) producing type 2 cytokines and controlling helminth infection.

156 ene expression among lung lymphocytes during helminth infection.

157 ent strategies on community soil-transmitted helminth infection.

158 tivation status of these granulocytes during helminth infection.

159 ammatory ILC2s, which are elicited following helminth infection.

160 in the reactive lymph nodes during parasitic helminth infection.

161 may lead to dysregulated inflammation during helminth infection.

162 and IL-37 in immune modulation in a chronic helminth infection.

163 M) responses and increased susceptibility to helminth infection.

164 )- and IL-13-dependent host responses during helminth infection.

165 te type 2 immunity following chemosensing of helminth infection.

166 n impaired memory IgE response subsequent to helminth infection.

167 iduals were also tested for soil-transmitted helminth infections (ie, hookworm, Ascaris lumbricoides,

168 Diseases caused by helminth infections affect more than a quarter of the po

169 Whether helminth infections also modulate monocyte responses in

170 lopment of Notch pathway modulators to treat helminth infections and allergies.

171 typically associated with protection against helminth infections and also with harmful inflammation i

172 ate lymphoid cells (ILC2s) are implicated in helminth infections and asthma where they play a role in

173 Most studies on the relationship between helminth infections and atopic disorders have been condu

174 ments and are crucial for protection against helminth infections and for the maintenance of tissue ho

175 inct phenotypes associated with clearance of helminth infections and tissue repair, but the phenotype

176 rasitic drugs might induce diabetes, whereas helminth infections appear to afford some protection aga

177 Helminth infections are accompanied by eosinophilia in p

178 an and animal studies have demonstrated that helminth infections are associated with a decreased prev

179 Emerging evidence suggests that helminth infections are associated with lower insulin re

180 Chronic helminth infections are known to be associated with the

181 Helminth infections are known to influence T and B cell

182 Helminth infections are known to modulate cytokine respo

183 Coexistent helminth infections are known to modulate T cell and cyt

184 Mosquito-borne helminth infections are responsible for a significant wo

185 a, deworming programmes for soil-transmitted helminth infections became an integral part of school he

186 strong type 2 immune responses they induce, helminth infections can suppress allergy through regulat

187 Intestinal helminth infections elicit Th2-type immunity, which infl

188 Immunity to intestinal helminth infections has been well studied, but the mecha

189 tigate if existing gut-restricted intestinal helminth infections impact bacterial-induced acute airwa

190 Helminth infections improve lipid profiles and may lower

191 These data support the hypothesis that GI helminth infections in young livestock are associated wi

192 Whether helminth infections influence disease severity and bacte

193 Helminth infections inhibit host immunity against microb

194 populations at high risk of soil-transmitted helminth infections living in urban slums and in plantat

195 human studies indicate that definitive host helminth infections may confer protection from allergies

196 Helminth infections may modulate the inflammatory respon

197 Intestinal helminth infections occur predominantly in regions where

198 Immunity to intestinal helminth infections requires the rapid activation of T h

199 the national prevalence of soil-transmitted helminth infections to enable implementation of a more f

200 Gastro-intestinal helminth infections trigger the release of interleukin-3

201 Interleukin-4 (IL-4) is crucial in many helminth infections, but its role in urogenital schistos

202 able, the danger of transplantation-mediated helminth infections, exacerbated by coincident immunosup

203 nce of preexisting allergy on the outcome of helminth infections, rather than the more traditional ap

204 for protection against subsequent secondary helminth infections.

205 type 2 immunity and tissue repair following helminth infections.

206 ere Schistosoma-specific antibody levels and helminth infections.

207 quently in countries with high prevalence of helminth infections.

208 the anti-inflammatory effector cells during helminth infections.

209 ance and disease-tolerance mechanisms during helminth infections.

210 ettings, including allergic inflammation and helminth infections.

211 ntial insights to the understanding of multi-helminth infections.

212 ifferent cell types respond to bacterial and helminth infections: Salmonella infection caused an incr

213 ies with sewage-contaminated water supplies, helminth infestations, bare footedness, and poor housing

214 Because RQ is absent in mammalian hosts of helminths, inhibition of RQ biosynthesis may have potent

215 tial to improve our current understanding of helminth interactions with their hosts and to replace or

216 or more sensitive diagnostics for intestinal helminths is well known, the cost of developing and impl

217 has been well studied, but the mechanism of helminth killing prior to expulsion remains unclear.

218 as a role in constraining lung neutrophilia, helminth killing, and type 2 immune responses in an infl

219 -derived Pla2g1b as an essential mediator of helminth killing, highlighting a previously overlooked m

220 that CD4+ Th2-mediated eosinophil-dependent helminth larval killing in the lung tissue occurs.

221 We comprehensively surveyed helminth life cycles and transmission involving ungulate

222 ction could modulate chemokine production in helminth-LTB coinfection.

223 fections also modulate monocyte responses in helminth-LTBI coinfection has not been fully explored.

224 arization, and impaired monocyte function in helminth-LTBI coinfection.

225 ecifically schistosomiasis, soil-transmitted helminths, lymphatic filariasis, trachoma, onchocerciasi

226 Helminths may protect against cardiometabolic risk throu

227 hat have contributed to current knowledge of helminth-microbiota interactions in species of veterinar

228 Helminth models suggested a contribution of neutrophils

229 ese data reveal a novel mechanism by which a helminth-modified metabolome promotes susceptibility to

230 elling Acanthocheilonema viteae to show that helminth-modulation of the gut microbiome does not requi

231 n during infection with the gastrointestinal helminth Nippostrongylus brasiliensis Our results identi

232 caused by a chronic infection with parasitic helminths of the genus Schistosoma.

233 ondii, to investigate the negative impact of helminthes on the CD8 T cell response, we demonstrate he

234 reatment, there was no effect exerted by the helminths on either eosinophil nor neutrophil activation

235 onship between infection with the fish-borne helminth Opishorchis felineus and specific IgE, skin pri

236 n-relevant, fluorescently-labeled bacterial, helminth or fungal pathogens to track and characterize t

237 humans suggest that intentional exposure to helminths or helminth-derived products may hold promise

238 rs, with mass deworming for soil-transmitted helminths or schistosomiasis (alone or in combination wi

239 earch, including strategies of co-culture of helminths or their products with organoids and the chall

240 The ability of helminth parasite infections to manipulate the immune sy

241 There is increasing interest in helminth parasite modulation of the immune system, both

242 ce exposed to two different Th2 stimuli: the helminth parasite Nippostrongylus brasiliensis (Nb) and

243 he lung and increased ability to expulse the helminth parasite, Nippostrongylus brasiliensis These re

244 Helminth parasites defy immune exclusion through sophist

245 Helminth parasites have been reported to have beneficial

246 an important immune marker of resistance to helminth parasites in wild Soay sheep predict overwinter

247 Infection by helminth parasites is associated with amelioration of al

248 Infection with helminth parasites poses a significant challenge to the

249 Helminth parasites secrete a wide variety of immunomodul

250 Gastrointestinal helminth parasites share their habitat with a myriad of

251 ion drives the clearance of gastrointestinal helminth parasites, which infect over two billion people

252 le are regularly exposed to gastrointestinal helminth parasites.

253 transmission routes and found that ungulate helminth parasitism has evolved some 25 times.

254 the natural mouse small intestine-restricted helminth pathogen Heligmosomoides polygyrus to test the

255 Therefore, we used the gastrointestinal helminth pathogen Trichuris muris to test the hypothesis

256 o-infections with small intestine-restricted helminth pathogens may be important factors that influen

257 y inhibits T cell immunity; however, whether helminthes prevent T cell priming or skew clonal recruit

258 ive response against the early stages of the helminths prior to their establishing long-lasting infec

259 hRetn in sepsis, or whether hRetn influences helminth protection against sepsis, is unknown.

260 elial cells can impair larval development in helminths, providing a novel mechanism contributing to i

261 e complexity of biological symbiosis, intact helminths rather than helminth-derived products are like

262 ase allergy-related diseases, while reducing helminth-related morbidity.

263 ffect on atopy, allergy-related diseases, or helminth-related pathology.

264 The determinants of helminth resistance are not well understood.

265 Interestingly, infection with gut-restricted helminths resulted in immunological and structural chang

266 A murine helminth/RSV coinfection model was developed.

267 gnature was evident in DCs responding to the helminth Schistosoma mansoni or the allergen house dust

268 ot find sufficient evidence to conclude that helminth (Sm) exposure explained rural-urban differences

269 Host suppression of helminth somatic growth may be an important immune strat

270 infection intensity of each soil-transmitted helminth species, and treatment coverage and costs.

271 ect from subsequent infections with multiple helminth species, which occur naturally in endemic areas

272 gulation in rabbits infected with one or two helminth species.

273 control programmes tackling soil-transmitted helminth (STH) infections require sensitive, reliable, a

274 he main strategy to control soil-transmitted helminth (STH) infections.

275 ding in an area endemic for soil-transmitted helminths (STH).

276 the key strategy to control soil-transmitted helminths (STHs) globally.

277 onesia, an area endemic for soil-transmitted helminths (STHs).

278 the relationship between a soil-transmitted helminth, Strongyloides stercoralis (Ss), and T2DM, we e

279 However, zoonotic helminths, such as Toxocara species (spp.), have been as

280 Infection by soil transmitted parasitic helminths, such as Trichuris spp, are ubiquitous in huma

281 Nevertheless, reversal of helminth suppression of the innate IL-12 response of CD8

282 A 2003 national soil-transmitted helminth survey done among schoolchildren found an overa

283 We conclude helminths switch from UQ to RQ synthesis principally via

284 Here, we show helminths synthesize two coq-2 splice forms, coq-2a and

285 Here, we used laboratory data from a rabbit-helminth system and developed a within-host model of inf

286 described can be expected in many other host-helminth systems.

287 stronger correlate of infection outcomes for helminths than host species traits.

288 Although the mechanisms underlying 'helminth therapy' are being evaluated, little attention

289 nflammation during murine infection with the helminth Trichuris muris However, the mechanisms require

290 Helminths trigger multiple immunomodulatory pathways tha

291 Parasitic helminths use two benzoquinones as electron carriers in

292 or pharmaceutical applications or novel anti-helminth vaccines.

293 Protozoa and helminths, vector-borne, foodborne, soilborne and waterb

294 Type 2 immunity serves to resist parasitic helminths, venoms, and toxins, but the role and regulati

295 Helminths were detected using microscopy and malaria par

296 Helminths were detected using microscopy and the presenc

297 Schistosoma haematobium is a parasitic helminth which causes urogenital pathology.

298 ETATION: Mass deworming for soil-transmitted helminths with or without deworming for schistosomiasis

299 fects of mass deworming for soil-transmitted helminths (with or without deworming for schistosomiasis

300 translated in vivo into better clearance of helminth worm infection in mice.