ライフサイエンスコーパス: inflammatory response

1 , IKKalpha and IKKbeta, during the canonical inflammatory response.

2 d causes the systemic hyperactivation of the inflammatory response.

3 is clearly compatible with an effective anti-inflammatory response.

4 x, inducing local pancreatic fibrosis and an inflammatory response.

5 4 and IL-13, key cytokines that drive type 2 inflammatory response.

6 the role of TLR4 in the ML exosome-mediated inflammatory response.

7 d decrease PGN, S. aureus and MRSA-triggered inflammatory response.

8 n NOD-SCID/gamma mice, resulting in a robust inflammatory response.

9 esult in a potent and sometimes pathological inflammatory response.

10 rhinovirus challenge exacerbated the type 2 inflammatory response.

11 lar glucose metabolism as well as the innate inflammatory response.

12 rized by epithelial-autonomous activation of inflammatory response.

13 in the glaucoma samples suggesting an innate inflammatory response.

14 rfaces, i.e., corrosion, that aggravate this inflammatory response.

15 rthritis by cooperating with IL-17 to induce inflammatory response.

16 The instigating agent typically triggers an inflammatory response.

17 lymphocytes, we will be able to regulate the inflammatory response.

18 gainst infections by initiating an inducible inflammatory response.

19 pleen, and liver and an exaggerated systemic inflammatory response.

20 nfiltration is critical to program the acute inflammatory response.

21 y but success is likely to be limited by the inflammatory response.

22 ves periodontitis largely by modulating host inflammatory response.

23 attempts to improve outcome by modifying the inflammatory response.

24 nce in key peripheral organs, and an altered inflammatory response.

25 produces a known toxin nor induces a robust inflammatory response.

26 sis is difficult due to the ongoing systemic inflammatory response.

27 into the airways of WT hosts suppressed the inflammatory response.

28 to immune cells, unshielded RN7SL1 drives an inflammatory response.

29 we found almost 25% to express markers of an inflammatory response.

30 rcoralis infection and is associated with an inflammatory response.

31 nd a subsequent type I interferon-associated inflammatory response.

32 cytes and leukocytes, and attenuated overall inflammatory response.

33 by robust virus replication and strong host inflammatory response.

34 rrelated with, and dependent upon, the acute inflammatory response.

35 gering a switch from proinflammatory to anti-inflammatory responses.

36 rast, Delta5G infection elicited only modest inflammatory responses.

37 nd central nervous system cytokine/chemokine inflammatory responses.

38 tervention initiated in the midst of rampant inflammatory responses.

39 d cells (ILC2s) are key regulators of type 2 inflammatory responses.

40 , but it also inflicts secondary injury from inflammatory responses.

41 proliferation, differentiation, immunity and inflammatory responses.

42 B cells (Bregs) that suppress autoimmune and inflammatory responses.

43 ly regulates both virus replication and host inflammatory responses.

44 mune system balance by negatively regulating inflammatory responses.

45 of ML had no effect on in vitro and in vivo inflammatory responses.

46 ry T (Treg) cells are well known to modulate inflammatory responses.

47 lular ATP is a central signaling molecule in inflammatory responses.

48 onstrated in vitro as negative regulators of inflammatory responses.

49 y impact both virus replication and cellular inflammatory responses.

50 roglia may be an important mechanism to tune inflammatory responses.

51 res to the resolution of neutrophil-mediated inflammatory responses.

52 terferon-gamma, which prolongs and heightens inflammatory responses.

53 es results in unique virulence potential and inflammatory responses.

54 nd tissues from collateral damage induced by inflammatory responses.

55 rdiovascular system, including reductions in inflammatory responses.

56 transcription in macrophages for modulating inflammatory responses.

57 f danger signals to propagate and perpetuate inflammatory responses.

58 ly plays an important role in the immune and inflammatory responses.

59 est that this interaction may play a role in inflammatory responses.

60 icrobial clearance while minimizing damaging inflammatory responses.

61 stration of the initiation and resolution of inflammatory responses.

62 e considered as immunosuppressors to various inflammatory responses.

63 etermine the role of H2 R in modulating lung inflammatory responses.

64 ent example of how ubiquitin signals control inflammatory responses.

65 or and a central regulator of cell death and inflammatory responses.

66 cells in the prevention of diverse types of inflammatory responses.

67 failed to suppress pyroptotic cell death and inflammatory responses.

68 f dendritic cell maturation and promotion of inflammatory responses.

69 ole of lncRNAs in transcriptional control of inflammatory responses.

70 ance of the actin cytoskeleton in modulating inflammatory responses.

71 and an important mediator of autoimmune and inflammatory responses.

72 prevent infection without inducing damaging inflammatory responses.

73 ated in clinical HAT and associated with CNS inflammatory responses.

74 y potential differences in the upper airways inflammatory response after exposure to LMW and HMW agen

75 the relevance of pericardial clusters during inflammatory responses after MI, we surgically removed t

76 recognized as signaling mediators of sterile inflammatory responses after trauma and injury.

77 The patients were unable to orchestrate an inflammatory response against LPS and expressed three fa

78 Large but not small cholangiocytes show inflammatory responses against large but not small chola

79 ive in later stages of disease when the host inflammatory response and blood-brain barrier integrity

80 Thus, Spata2 can regulate inflammatory response and cell death in both RIPK1-depen

81 anscription, T cell differentiation, and the inflammatory response and correlated with subject age, s

82 umans, which is characterized by exacerbated inflammatory response and extensive lung pathology.

83 gulatory mechanisms that maintain a balanced inflammatory response and highlight important difference

84 t, GSTO1-1 deficient mice show a more severe inflammatory response and increased escape of bacteria f

85 enriched in pathways and diseases related to inflammatory response and inhibition of matrix metallopr

86 the diversity and spatiotemporal role of the inflammatory response and its interactions with resident

87 s 0 and 4 of inoculation for analysis of the inflammatory response and microbiota.

88 Here, He et al. show that the inflammatory response and phagocytosis mediated by the i

89 ntous Pf phage alters the progression of the inflammatory response and promotes phenotypes typically

90 er, the role of 15-epi LXA4 in post-MI acute inflammatory response and resolving phase is unclear.

91 ate-like lymphocyte populations in the early inflammatory response and subsequent parasite control fo

92 ead cells after MI, resulting in exacerbated inflammatory responses and a substantial decrease in sur

93 nfection induced metabolic dysregulation and inflammatory responses and affected the immune cell cont

94 study, we investigated the role of TRIM28 in inflammatory responses and angiogenic activity of ECs fo

95 hear flow, is a critical process involved in inflammatory responses and cancer metastasis.

96 ay a role in post-myocardial infarction (MI) inflammatory responses and cardiac outcome.

97 ipids, endogenous to brain tissue, influence inflammatory responses and cell survival in vitro.

98 atory reflex are physiological regulators of inflammatory responses and cytokine production.

99 stimulating IA production could promote anti-inflammatory responses and have therapeutic benefits.

100 re euthanized 18 months after infection, and inflammatory responses and histologic alterations were a

101 Cortistatin reduced Th1/Th17-driven inflammatory responses and increased regulatory T cells

102 rong induction of multiple genes involved in inflammatory responses and mobilization of innate immune

103 Hypoxia augments inflammatory responses and osteoclastogenesis by incompl

104 Honokiol repressed cardiac inflammatory responses and oxidative stress in mice subj

105 volved in the pathogenesis of AD by inducing inflammatory responses and regulating tolerogenic proces

106 hydrocarbon receptor ligand that attenuated inflammatory responses and shows therapeutic potential f

107 dentified role for peroxisomes in macrophage inflammatory responses and suggest that peroxisomes are

108 Such recognition, in turn, triggers inflammatory responses and the engagement of previously

109 NF-kappaB is a key mediator of the inflammatory response, and its dysregulation has been as

110 d by impairment of organ perfusion, systemic inflammatory response, and multiple organ failure.

111 consistent with a type 2 helper T-cell-type inflammatory response, and subacute fibrosis were recogn

112 rated at the level of chromatin to reprogram inflammatory responses, and identify previously unknown

113 iological processes, including angiogenesis, inflammatory responses, and vascular stabilization.

114 , the key transcription factor that mediates inflammatory responses, and were unable to induce the ex

115 ion; DLG4 is a hub protein in the microglial inflammatory response; and genetic variation in DLG4 is

116 d whether inflammation and components of the inflammatory response are altered in females compared wi

117 Antiviral inflammatory responses are a crucial component of WNV pa

118 Inflammatory responses are elicited through lipid produc

119 ant suppression of the magnitude of the skin inflammatory response as assessed by changes in ear thic

120 e that TNF-alpha is a major component of the inflammatory response associated with altered neurodevel

121 Despite similar initial viral titers and inflammatory responses between wild-type and SCD animals

122 ng PLK2 attenuated HDG-induced apoptosis and inflammatory responses both in vitro and in vivo.

123 ogenic diet, and hyperglycemia influence the inflammatory response, but how this occurs is unclear.

124 Activin is a critical modulator of inflammatory responses, but has not been assessed in pan

125 -2 suppresses the lipopolysaccharide-induced inflammatory response by abrogating IL-1beta expression.

126 The reduced inflammatory response by HOCl treatment was demonstrated

127 Therefore, dampening the inflammatory response by targeting microbiota-derived me

128 site of skin injury, which in turn modulates inflammatory responses by directing the M2 polarization

129 ulating saturated fatty acids, which trigger inflammatory responses by engaging pattern recognition r

130 lectrophilic fatty acids (EFAs) mediate anti-inflammatory responses by modulating metabolic and infla

131 at suppressed adipogenic differentiation and inflammatory responses by negatively regulating PPARgamm

132 ack between tumor and stroma subverts normal inflammatory responses by triggering the release of exos

133 cellular processes, including DNA repair and inflammatory response, by suppressing downstream targets

134 ered previously unidentified roles of PXR in inflammatory response, cell proliferation, and cell migr

135 rtant genes; including genes involved in the inflammatory response, cell proliferation, leukocyte ext

136 A chronic, neutrophil-rich inflammatory response characterizes this infection.

137 The inflammatory response coincides with raised levels of im

138 gnancy in the opossum is characterized by an inflammatory response consistent with implantation in hu

139 ction, greater than or equal to two systemic inflammatory response criteria, greater than or equal to

140 eement, NOD2(-/-) decreased the CVB3-induced inflammatory response, CVB3 copy number, and apoptosis i

141 The comparison of the inflammatory response, cytokine profiles and Th-1, Th-2

142 ich, in turn, through regulation of the host inflammatory response, determines disease severity.

143 s, regulatory regions near genes involved in inflammatory response displayed decreased chromatin acce

144 onjunctiva is a common site for the allergic inflammatory response due to it being highly vascularize

145 uld play an important role in regulating the inflammatory response during chronic liver disease.

146 vide targets for therapies that modulate the inflammatory response during Ebola virus disease.

147 local and remote organ injury attributed to inflammatory response during the reperfusion phase.

148 ay an essential role in mediating epithelial inflammatory responses during injury.

149 l role for NLRP10 in the resolution of local inflammatory responses during L. major infection.

150 sized that IL-15(-/-) mice will have reduced inflammatory responses during the development of allergi

151 red response is coordinated, we examined the inflammatory response elicited in mouse macrophages by i

152 s that glycosylation of Env modulates innate/inflammatory responses elicited by cells of monocyte/mac

153 ry network enables a robust yet time-limited inflammatory response essential for functional immunity.

154 y to enhance viral resistance and induce pro-inflammatory responses essential for confronting infecti

155 lly improves liver pathology as reflected by inflammatory response, fibrosis, and apoptotic death of

156 efore involution revealed down-regulation of inflammatory response genes, pointing to the suppression

157 elf-limiting response to prevent unnecessary inflammatory responses harmful to the organism.

158 BACKGROUND & AIMS: Despite inducing an inflammatory response, Helicobacter pylori can persist i

159 chemokines, but not of cytokines typical of inflammatory responses (IL-1beta, IL-6, IL-10, TNF).

160 ict is associated with greater viral-induced inflammatory response in adulthood and in turn with incr

161 seased tissue elicits an EDA-dependent fibro-inflammatory response in dermal fibroblasts.

162 uimod induces a monomorphic and self-limited inflammatory response in healthy subjects, as well as pa

163 owed measurement of RSV load and the mucosal inflammatory response in infants.

164 prepsoriatic skin produces a "feed forward" inflammatory response in keratinocytes that is self-ampl

165 oduces a polysaccharide that induces an anti-inflammatory response in macrophages, providing a potent

166 rrent study extends our investigation to the inflammatory response in mouse embryonic stem cells and

167 ve state of NF-kappaB, the deficiency in the inflammatory response in mouse embryonic stem cells is a

168 ll, we demonstrate an important role for the inflammatory response in regulating MERS-CoV pathogenesi

169 llergen of S aureus and induces a TH2-biased inflammatory response in the airways in an IL-33-depende

170 e receptor 4 (TLR4)- and NF-kappaB-dependent inflammatory response in the CPE that is associated with

171 ermore, the expansion of ILC2s modulated the inflammatory response in the diseased kidney in favor of

172 naling, H. hepaticus induces an IL-23-driven inflammatory response in the intestine.

173 -cell activation in the peripheral blood and inflammatory response in the nasal compartment, coupled

174 LPS administration induced an inflammatory response in the OM, including the infiltrat

175 g DHI's role in stroke and CAD treatment was inflammatory response in the process of atherosclerosis.

176 that GSTO1-1 is critical for a TLR4-like pro-inflammatory response in vivo.

177 Muscle injury precipitates a complex inflammatory response in which a multiplicity of cell ty

178 ion significantly attenuated obesity-induced inflammatory responses in adipose tissue.

179 athway, an effect that may be exacerbated by inflammatory responses in immunocompetent hosts.

180 B10 cells can regulate inflammatory responses in innate immunity.

181 actions of IRF-1 resulted in decreased local inflammatory responses in joint-associated tissues, whic

182 and that glucocorticoid deficiency promotes inflammatory responses in keratinocytes.

183 dy viral infection, has been shown to elicit inflammatory responses in lungs and to exacerbate pulmon

184 es demonstrated that oxLDL ICs elicit potent inflammatory responses in macrophages.

185 etinopathy and that Muller cells orchestrate inflammatory responses in myeloid cells through a CD40-A

186 viral infection, all of which induce robust inflammatory responses in naturally differentiated cells

187 These LPS-derived EVs induce inflammatory responses in other cholangiocytes including

188 EBOV replication coinciding with systematic inflammatory responses in otherwise asymptomatic rhesus

189 Here we characterized these inflammatory responses in patients with erythema migrans

190 ne the in vivo role of versican in mediating inflammatory responses in poly(I:C)-induced lung inflamm

191 ular mechanism is responsible for triggering inflammatory responses in primary mouse macrophages.

192 previous data, IDR-1002 suppressed in vitro inflammatory responses in RAW 264.7 murine monocyte/macr

193 e results highlight critical roles of innate/inflammatory responses in SIVmac239 infection.

194 n, which may be important for the control of inflammatory responses in the CNS and neurotoxicity.

195 s and HAI titers with reduced viral load and inflammatory responses in the cVLP group.

196 a demonstrate MyD88 signaling mediates early inflammatory responses in the joint but also contributes

197 alance, glucose metabolism, and postprandial inflammatory responses.In a randomized controlled crosso

198 ched cells with salmeterol could inhibit the inflammatory response induced by Escherichia coli lipopo

199 The mucosal inflammatory response induced by Salmonella serovar Typh

200 Moreover, a prominent inflammatory response involving both activation of resid

201 Inhibiting the excessive inflammatory response is essential for improving the neu

202 For gliomas, the tumor-associated inflammatory response is pivotal to support growth and i

203 A controlled inflammatory response is required for protection against

204 tion to their well-characterized role in pro-inflammatory responses, keratinocytes also directly supp

205 ifferences exist in the microbial insult and inflammatory responses leading to gingivitis and peri-im

206 f many immune responses as well as prolonged inflammatory responses, leading to an overall weakened r

207 re of cytotoxic T cells to limit or contract inflammatory responses may propagate injury and lead to

208 We conclude that the inflammatory response mechanism is not active in mouse e

209 entiation can trigger the development of the inflammatory response mechanism, as indicated by the tra

210 nstrated that VISTA critically regulates the inflammatory responses mediated by DCs and IL-17-produci

211 herapeutic target for modulating the chronic inflammatory response observed in healthy tissues or for

212 noyl glycerol (2-AG) on the permeability and inflammatory response of intestinal epithelium under nor

213 h in vitro and in vivo, resulted in a higher inflammatory response of the encountering macrophages, m

214 terol had a similar inhibitory effect on the inflammatory response of the murine macrophage cell line

215 , the functional role of these organelles in inflammatory responses of myeloid immune cells is largel

216 ly responsible for histone deacetylation and inflammatory responses of primary microglia to classic i

217 T cells and are important for the control of inflammatory responses of T cells.

218 These inflammatory responses often become chronic and non-reso

219 Age-associated differences in the inflammatory response only became evident at twenty hour

220 F) and human AD cortices correlated with the inflammatory response or immunological disease.

221 ributors to the triggering of human ILC2s in inflammatory responses, particularly when combined with

222 Inflammatory response plays an important role in Parkins

223 An enhanced inflammatory response predicts worse outcomes in heart f

224 ond, we demonstrate that targeting the acute inflammatory response reduces cognitive impairments, the

225 ns occurs in the presence or absence of host inflammatory responses remain unknown.

226 wever, its contribution to sepsis-associated inflammatory response remains to be explored.

227 ar glucose metabolism can influence cellular inflammatory responses.Several metabolic factors affect

228 of death worldwide and an elevated systemic inflammatory response (SIR) is associated with reduced s

229 GSTO1-1 deficiency ameliorates the inflammatory response stimulated by LPS and attenuates t

230 B lymphocytes in the presence of detectable inflammatory responses, suggesting the involvement of co

231 s from greater than or equal to two systemic inflammatory response syndrome "and" lactate ordered, or

232 score discrimination was lowest for systemic inflammatory response syndrome (median area under the re

233 ive identification of patients with systemic inflammatory response syndrome (SIRS) and sepsis at low

234 quick SOFA (qSOFA), and removed the systemic inflammatory response syndrome (SIRS) criteria from the

235 for sepsis, excluding the need for systemic inflammatory response syndrome (SIRS) criteria.

236 primary outcome was a composite of systemic inflammatory response syndrome and dysfunction of at lea

237 Systemic Inflammatory Response Syndrome and quick Sequential Orga

238 psis (suspected infection plus >/=2 systemic inflammatory response syndrome criteria) and hypotension

239 ted Organ Failure Assessment score, systemic inflammatory response syndrome criteria, the National an

240 s for a serious infection with >/=2 systemic inflammatory response syndrome criteria.

241 al Organ Failure Assessment and the Systemic Inflammatory Response Syndrome criteria.

242 eceiver operating characteristic of Systemic Inflammatory Response Syndrome for critical care interve

243 bility to distinguish noninfectious systemic inflammatory response syndrome from sepsis, though the p

244 patients (defined: infection, >/= 2 systemic inflammatory response syndrome, and hypoperfusive organ

245 from mortality in a mouse model of systemic inflammatory response syndrome.

246 s ascertained by examining changes in airway inflammatory responses, Th2 responses, and lung histopat

247 bacteremia, is a key mediator of IL-10 anti-inflammatory response that portends poor clinical outcom

248 sts that surgical trauma launches a systemic inflammatory response that reaches the brain and associa

249 reactive protein (CRP) is a biomarker of the inflammatory response that shows significant prognostic

250 ull mutants were found to induce an elevated inflammatory response that was dependent on the cag PAI

251 Surgical trauma induces local and systemic inflammatory responses that can also contribute to the a

252 turb mitochondria, and initiate degenerative inflammatory responses that resemble sporadic inclusion

253 itis rat model, CHMFL-BTK-11 ameliorated the inflammatory response through blockage of proliferation

254 DHEA regulates microglial inflammatory responses through phosphorylation of TrkA a

255 the first time that di-C18 LPAs trigger pro-inflammatory responses through Toll-like receptor 2 (TLR

256 Meanwhile, decreased local/systemic inflammatory response (TNF-alpha downward arrow, IL-1bet

257 of the alveolar bone due to an aberrant host inflammatory response to a dysbiotic oral microbiome.

258 permitted rapid progression from a skin pro-inflammatory response to a lethal systemic condition.

259 and cellular immunity, and regulation of the inflammatory response to Ags.

260 significant decrease in the nociceptive and inflammatory response to allyl isothiocyanate (the agoni

261 el downstream mediator of the joint-specific inflammatory response to B. burgdorferi.

262 expression is precisely regulated during the inflammatory response to control infection and limit the

263 threatening condition caused by dysregulated inflammatory response to infection with no effective the

264 implant dentistry that have investigated the inflammatory response to known microbial biofilms observ

265 for NLRP10 as a suppressor of the cutaneous inflammatory response to Leishmania major infection.

266 ite of GSTO1-1 can be used to ameliorate the inflammatory response to LPS.

267 an uncontrolled and amplified host systemic inflammatory response to microbial infection-is a life-t

268 re involved in stimulating and resolving the inflammatory response to pathogens.

269 of enteric glia in mediating this secondary inflammatory response to prolonged treatment with morphi

270 been shown to be important for generating an inflammatory response to the pathogen.

271 nase subunit beta (IKKbeta) to fine-tune the inflammatory response to the strength of the offending s

272 ion and phagocytosis, and this may limit the inflammatory response to this nonapoptotic form of cell

273 al, a high dose of vitamin D attenuated the inflammatory response to UV radiation in a small group o

274 s cholesterol metabolism and tempers chronic inflammatory responses to atherogenic diet by restrainin

275 n the production of IFN-beta during the host inflammatory responses to bacterial infection and sugges

276 Sepsis, resulting from uncontrolled inflammatory responses to bacterial infections, continue

277 r circadian influence; time-of-day may alter inflammatory responses to chemotherapeutics.

278 These data suggest that inflammatory responses to chemotherapy depend on time-of

279 istory of major depressive disorder (MDD) on inflammatory responses to high-fat meals.

280 It also decreases the immune and inflammatory responses to His6-OPH in vivo as determined

281 Inflammatory responses to IL-1beta and LPS-induced morta

282 Systemic inflammatory responses to malaria during pregnancy predi

283 of glycolytic machinery and is essential for inflammatory responses to myelin.

284 nt are often seen at the early stage of lung inflammatory responses to noxious stimuli.

285 the hypothalamic-pituitary-adrenal axis and inflammatory responses to stress.

286 n cells and induced stronger host immune and inflammatory responses to viral infection.

287 vement of the alpha7 nAChR in regulating the inflammatory response via the cholinergic anti-inflammat

288 ndant in atherosclerotic plaques and promote inflammatory responses via the complement system and inf

289 signaling on immune cells may impact on the inflammatory response, we evaluated the role of ecto-5'-

290 ification of early signs of Lyme disease and inflammatory responses; we used this information to deve

291 d non-pathogenic stimuli, and only induce an inflammatory response when they are exposed to high leve

292 eperfusion injury (PIRI) triggers an intense inflammatory response which is essential for repair but

293 y in the onset of immunity, particularly the inflammatory response, which led to a 2-day delay in the

294 ata demonstrate that BCD inhibits CC-induced inflammatory responses, which may be explained by BCD-me

295 sponsible for allergic sensitization and the inflammatory response, while IgE binding to CD23 is invo

296 especially the DI domain, drive a local Th1 inflammatory response, with subsequent plaque instabilit

297 s and ubiquitination events that orchestrate inflammatory responses, with an emphasis on the NLRP3 in

298 pathways that are important to coordinating inflammatory responses within immune cells (p<0.05, Benj

299 overed an additional mechanism that controls inflammatory responses within the CNS milieu under injur

300 olymorphonuclear leukocytes [PMNs]) generate inflammatory responses within the joints of gout patient