ライフサイエンスコーパス: pulmonary inflammation

1 ive functions of HDL and could contribute to pulmonary inflammation.

2 as a major cofactor of ILC2 function during pulmonary inflammation.

3 a might serve as a unique strategy to lessen pulmonary inflammation.

4 T cells to these same LDLNs without inducing pulmonary inflammation.

5 e role of alveolar macrophages in regulating pulmonary inflammation.

6 utic strategies to limit the damage of acute pulmonary inflammation.

7 2a(+/-) mice was exacerbated in both EAE and pulmonary inflammation.

8 cies was efficient in preventing spontaneous pulmonary inflammation.

9 ic inflammation, cutaneous vasculopathy, and pulmonary inflammation.

10 d vascular responses in LPS- or acid-induced pulmonary inflammation.

11 av1 in modulating Gc action in two models of pulmonary inflammation.

12 nd to ameliorate airway hyper-resistance and pulmonary inflammation.

13 nonatopic and viral-induced exacerbations of pulmonary inflammation.

14 t of impaired PMN recruitment, which reduced pulmonary inflammation.

15 cacy of targeting the IL-17/IL-22 pathway in pulmonary inflammation.

16 in house dust mite (HDM)-triggered allergic pulmonary inflammation.

17 ors (TLRs) play in A. baumannii OMV-mediated pulmonary inflammation.

18 cer development is associated with extensive pulmonary inflammation.

19 tion in vitro and in a murine model of acute pulmonary inflammation.

20 uit T cells to amplify the effector phase of pulmonary inflammation.

21 cal responses associated with acute allergic pulmonary inflammation.

22 RD-like phenotype in a model of eosinophilic pulmonary inflammation.

23 PD is multifactorial, but all triggers cause pulmonary inflammation.

24 hus implicating HXA3 in pneumococcus-induced pulmonary inflammation.

25 egrin engagement during K pneumoniae-induced pulmonary inflammation.

26 t sufficient to induce the effector phase of pulmonary inflammation.

27 ated with IKKalpha downregulation and marked pulmonary inflammation.

28 r IL-6 downstream of OSM in the induction of pulmonary inflammation.

29 ctions that facilitate the effector phase of pulmonary inflammation.

30 ckroach allergen model of murine asthma-like pulmonary inflammation.

31 ght serve as a unique strategy for lessening pulmonary inflammation.

32 ed drops in lung function and an increase in pulmonary inflammation.

33 as a mechanism of development of asthma-like pulmonary inflammation.

34 lomas mitigates widespread cytokine-mediated pulmonary inflammation.

35 ays of mice would dampen acute smoke-induced pulmonary inflammation.

36 ous inhibitor of T cell function in allergic pulmonary inflammation.

37 genomes in BALF and the degree of histologic pulmonary inflammation.

38 e had increased gut epithelial apoptosis and pulmonary inflammation.

39 ry airway epithelial cells, neutrophilia and pulmonary inflammation.

40 mediate these parameters of Df-elicited Th2 pulmonary inflammation.

41 ich results in a dramatic reduction in fatal pulmonary inflammation.

42 responses in vitro and in a murine model of pulmonary inflammation.

43 cells to promote neutrophil recruitment and pulmonary inflammation.

44 onary Sendai virus infection, with increased pulmonary inflammation.

45 netic programs influencing Th2 cell-mediated pulmonary inflammation.

46 esentation and downstream phases of allergic pulmonary inflammation.

47 to the lungs of C57BL/6 mice with Ag-induced pulmonary inflammation.

48 the CCL2/CCR2 axis in recruiting MCps during pulmonary inflammation.

49 for the circadian clock in a mouse model of pulmonary inflammation.

50 ittle is known about DC recruitment in acute pulmonary inflammation.

51 maging of the lungs is feasible and reflects pulmonary inflammation.

52 uate the influence of SD on allergen-induced pulmonary inflammation.

53 ssues under steady-state conditions and upon pulmonary inflammation.

54 ation of WGA-Fc also dramatically diminished pulmonary inflammation.

55 nt pathways also contribute to PLY-triggered pulmonary inflammation.

56 t target to modulate NK cell response during pulmonary inflammation.

57 hyperplasia, airway eosinophilia, and type 2 pulmonary inflammation.

58 icial action on both bronchoconstriction and pulmonary inflammation.

59 st cardinal asthma manifestations, including pulmonary inflammation.

60 osure can cause oxidative stress, leading to pulmonary inflammation.

61 ting that MGL1 is required for resolution of pulmonary inflammation.

62 tment to the lung in a murine model of acute pulmonary inflammation.

63 d chlamydial clearance and the resolution of pulmonary inflammation.

64 er that is responsible for the regulation of pulmonary inflammation.

65 s formulation of IgG 43RCA-G1 did not induce pulmonary inflammation.

66 In a murine model of LPS-induced pulmonary inflammation, activation of each PGD2 receptor

67 However, NKG2D was not required for pulmonary inflammation after a single inoculation of all

68 . aureus EV and OVA resulted in neutrophilic pulmonary inflammation after OVA challenge alone.

69 d mice showed significantly less disease and pulmonary inflammation after RSV infection associated wi

70 old SP-C/TNF-alpha mice displayed pronounced pulmonary inflammation, airspace enlargement, increased

71 kines typically associated with eosinophilic pulmonary inflammation, airway eosinophilia was signific

72 In lipopolysaccharide-induced acute pulmonary inflammation, alveolar recruitment of neutroph

73 injury is characterized by both systemic and pulmonary inflammation and activation of neutrophils, as

74 CD8(+) T cell response was increased, as was pulmonary inflammation and airway cytokine/chemokine exp

75 Airway epithelial KIF3A suppresses Th2 pulmonary inflammation and airway hyperresponsiveness fo

76 athogenesis of asthma including neutrophilic pulmonary inflammation and airway hyperresponsiveness.

77 in infants and the older population, causes pulmonary inflammation and airway occlusion that leads t

78 Effector CD8 T cells attenuate pulmonary inflammation and alter the ability of DCs with

79 trate that acute exposure to OSPM results in pulmonary inflammation and alteration of innate/adaptive

80 e, we demonstrate that BET inhibition limits pulmonary inflammation and alters the Th17-related infla

81 agonizing BAFF in CS-exposed mice attenuates pulmonary inflammation and alveolar destruction.

82 so suggest that Cif contributes to sustained pulmonary inflammation and associated loss of lung funct

83 of Pseudomonas infection, significantly less pulmonary inflammation and bacterial load was observed i

84 ted CS-induced impairment of MCC, CS-induced pulmonary inflammation and CS-associated lung injury in

85 sodes, can progress to a critical stage with pulmonary inflammation and death in young infants.

86 rtial neutrophil depletion led to diminished pulmonary inflammation and decreased host morbidity.

87 reatment of mice with 12,13-diHOME increased pulmonary inflammation and decreased the number of regul

88 Increases in pulmonary inflammation and decreases in lung function ar

89 R-Fc administration significantly attenuated pulmonary inflammation and destruction of alveolar walls

90 oxidative stress, nor do they reduce chronic pulmonary inflammation and disease progression in all pa

91 amma expression in AM is crucial to suppress pulmonary inflammation and diseases and to promote fast

92 ard CD36 are more potent at inhibiting acute pulmonary inflammation and dysfunction.

93 former more profoundly inhibited LPS-induced pulmonary inflammation and elevation of plasma level of

94 e surfactant protein (SP)-C promoter develop pulmonary inflammation and emphysema but are resistant t

95 Overwhelming pulmonary inflammation and endothelium disruption are co

96 le Haemophilus influenzae (NTHi)] that cause pulmonary inflammation and exacerbations.

97 th models and correlated with development of pulmonary inflammation and expression of hypoxia specifi

98 e of type-I IFN signaling results in chronic pulmonary inflammation and fibrosis despite clearance.

99 Considering that GRP blockade abrogates pulmonary inflammation and fibrosis in hyperoxic baboons

100 rsensitivity pneumonitis is characterized by pulmonary inflammation and fibrosis in response to repea

101 st that HSM may be used for the treatment of pulmonary inflammation and fibrosis.

102 Pulmonary inflammation and goblet cell differentiation w

103 , and asthma, are associated with persistent pulmonary inflammation and goblet cell metaplasia and co

104 ermatophagoides farinae had markedly reduced pulmonary inflammation and goblet cell metaplasia compar

105 role of IL-17 in mediating neutrophil-driven pulmonary inflammation and highlight a new mouse model t

106 ung disease, Itk-deficient mice show reduced pulmonary inflammation and IL-9 production by T cells an

107 ing and maturation of DCs and contributes to pulmonary inflammation and immune response against D. fa

108 receptor for interleukin 33 (IL-33) mediates pulmonary inflammation and immune system-related disorde

109 piratory disease and is a known regulator of pulmonary inflammation and immunity.

110 rtant implications for the control of excess pulmonary inflammation and immunopathology while preserv

111 reduced COX, were protected from CS-induced pulmonary inflammation and impairment of MCC.

112 ePPARgamma) knockout exacerbated LPS-induced pulmonary inflammation and injury as shown by several me

113 ed cells as well as fine tune the control of pulmonary inflammation and injury.

114 f virus infected cells and the resolution of pulmonary inflammation and injury.

115 response to RSV by limiting T-cell-mediated pulmonary inflammation and injury.

116 brosis progression, possibly by exacerbating pulmonary inflammation and intensifying the fibrotic res

117 in the experimental murine model of allergic pulmonary inflammation and is likely to contribute to th

118 mmatory cytokines in the airways, leading to pulmonary inflammation and lung injury.

119 These immunodeficient mice develop chronic pulmonary inflammation and lung tumors at a high frequen

120 infection has the potential to induce excess pulmonary inflammation and massive tissue damage in the

121 le of CB2 activation during allergen-induced pulmonary inflammation and natural killer (NK) cell effe

122 ry immune response, and we hypothesized that pulmonary inflammation and NETosis are defective after B

123 actor, soluble CD40 ligand, and P-selectin), pulmonary inflammation and oxidative stress (exhaled nit

124 responsible for the observed transient local pulmonary inflammation and oxidative stress.

125 Pulmonary inflammation and quasi-static lung compliance

126 experienced greater mortality with increased pulmonary inflammation and reduced numbers and activity

127 ozone exposure led to early and exaggerated pulmonary inflammation and remodeling.

128 h time-of-day variation and the magnitude of pulmonary inflammation and responses to bacterial infect

129 n complex interrelated pathways that lead to pulmonary inflammation and subsequently promote resoluti

130 ) from arachidonic acid (AA), promotes acute pulmonary inflammation and systemic infection after lung

131 s were required for Df-elicited eosinophilic pulmonary inflammation and Th2 cytokine generation in th

132 of Df-elicited eosinophilic and neutrophilic pulmonary inflammation and Th2 cytokine generation in th

133 se A2 (gV-sPLA2) showed reduced eosinophilic pulmonary inflammation and Th2 cytokine generation when

134 h) background, mev mice had markedly reduced pulmonary inflammation and Th2 cytokine production.

135 not solely a consequence of malnutrition or pulmonary inflammation and that loss of cystic fibrosis

136 ed by CD4 T cells in the context of allergic pulmonary inflammation and the asthma surrogate, airway

137 conidia leads to the development of chronic pulmonary inflammation and the coevolution of Th1, Th2,

138 direct cytolysis but may also contribute to pulmonary inflammation and tissue damage via the release

139 er 12 weeks, we measured airway pathologies, pulmonary inflammation, and airspace enlargement.

140 k-out (UG-KO) mice, which are susceptible to pulmonary inflammation, and B16F10 melanoma cells, which

141 severe infection (increased viral titer and pulmonary inflammation, and compromised lung function).

142 eposition, propagation of acute eosinophilic pulmonary inflammation, and development of airway hyperr

143 oss of capillary barrier function, exuberant pulmonary inflammation, and extensive microthrombus form

144 alpha activity limited murine Th9-associated pulmonary inflammation, and human allergic inflammation

145 ma symptoms, health care use, lung function, pulmonary inflammation, and indoor pollutants were asses

146 Asthma symptoms, morbidity, pulmonary inflammation, and lung function were monitored

147 ages, is critical for inhibiting spontaneous pulmonary inflammation, and pulmonary inflammation cause

148 cancer, cigarette smoke and asbestos, induce pulmonary inflammation, and pulmonary inflammation has r

149 ral clearance, enhances disease severity and pulmonary inflammation, and regulates the production of

150 Airway hyper-responsiveness (AHR), pulmonary inflammation, and T-cell subsets were assessed

151 esponsiveness, bronchoalveolar eosinophilia, pulmonary inflammation, and Th2 cytokine production that

152 ay pivotal roles in modulating host defense, pulmonary inflammation, and tissue injury following resp

153 iology and lung cell biology studies such as pulmonary inflammation, angiogenesis, vessel permeabilit

154 bronchoalveolar lavage fluid; and decreased pulmonary inflammation, as well as activation of NF-kapp

155 monoclonal antibody (MAb) would decrease the pulmonary inflammation associated with primary RSV infec

156 tantially reduced CD4(+) cells and decreased pulmonary inflammation at 18 h postinfection compared to

157 irway mucociliary clearance (MCC) and higher pulmonary inflammation at baseline, whereas mice deficie

158 ma deletion in lung macrophages induced mild pulmonary inflammation at the steady state and surprisin

159 tically engineered mice reported that during pulmonary inflammation, basophil-derived interleukin-4 c

160 ith S. pneumoniae is associated with altered pulmonary inflammation but not enhanced bacterial cleara

161 on with a PT-deficient strain induced severe pulmonary inflammation but not mortality in neonatal mic

162 Intrapulmonary H1N1 infection induced lethal pulmonary inflammation, but anti-Axl mAb treatment of in

163 is early IL-33 release resulted in a greater pulmonary inflammation by 24 hours after challenge relat

164 stitial cells such as SMC in promoting acute pulmonary inflammation by ADAM17-dependent transactivati

165 ermined airway hyperresponsiveness (AHR) and pulmonary inflammation by histologic and flow cytometric

166 ates the development of cys-LT-dependent Th2 pulmonary inflammation by inhibiting both CysLT(1)R sign

167 the lung against exuberant allergen-induced pulmonary inflammation by inhibiting the activation of e

168 In this paper, we show that RGS16 constrains pulmonary inflammation by regulating chemokine-induced T

169 sfunction of these Na(+) transporters during pulmonary inflammation can contribute to pulmonary edema

170 ting spontaneous pulmonary inflammation, and pulmonary inflammation caused by dysfunctional autophagy

171 Pulmonary inflammation causes multiple alterations withi

172 in increased bacillary burden and excessive pulmonary inflammation characterized by neutrophil infil

173 endonasal instillation of OVA+SEB induced a pulmonary inflammation, characterized by an increase in

174 f8 deficiency is associated with exacerbated pulmonary inflammation, characterized by enhanced neutro

175 stic bone marrow, neutrophilic cutaneous and pulmonary inflammation, chondritis, and vasculitis.

176 31-2G significantly decreased RSV-associated pulmonary inflammation compared to either antibody alone

177 flammasome pathway genes modify systemic and pulmonary inflammation, contributing to respiratory impa

178 suggest that NK cells significantly augment pulmonary inflammation, contributing to the pathogenesis

179 In acute pulmonary inflammation, danger is first recognized by ep

180 osure and health care use, lung function, or pulmonary inflammation did not differ by weight.

181 or (S1PR) agonists have been shown to reduce pulmonary inflammation during Bordetella pertussis infec

182 at treatment with S1PR agonist AAL-R reduces pulmonary inflammation during infection.

183 reatment with the S1PR agonist AAL-R reduces pulmonary inflammation during infection.

184 rotective properties, reducing the extent of pulmonary inflammation during lung injury.

185 cPLA2alpha plays a crucial role in eliciting pulmonary inflammation during pneumococcal infection and

186 me Network strategy did not attenuate global pulmonary inflammation during the first 27 hours after s

187 LT formed in mouse lungs as a consequence of pulmonary inflammation during the neonatal period.

188 etween lymphoid follicles and development of pulmonary inflammation, emphysema, and airway wall remod

189 lated with Pneumocystis, a vigorous Th2-like pulmonary inflammation ensued and peaked at 14 days post

190 4c(-/-) CD19(+)CD138(+) cells induced marked pulmonary inflammation, eosinophilia, and increased bron

191 on in M is sufficient for the development of pulmonary inflammation, even when inflammation is induce

192 Uncontrolled neutrophil-driven pulmonary inflammation exacerbates this disease.

193 es to influenza during pregnancy could drive pulmonary inflammation, explaining increased morbidity a

194 ted in enhanced host morbidity and increased pulmonary inflammation following both IAV and RSV infect

195 esponse during pregnancy could contribute to pulmonary inflammation following influenza A virus infec

196 rotected from airway hyperresponsiveness and pulmonary inflammation following ozone exposure.

197 asbestos, induce pulmonary inflammation, and pulmonary inflammation has recently been implicated in s

198 ed with vaccinia virus developed more severe pulmonary inflammation, higher lung virus titers and gre

199 ing phase of events leading to Th2-polarized pulmonary inflammation, (ii) the suppression Th1/Th17 pa

200 fect of CD4-mediated Treg-cell activation on pulmonary inflammation in a humanized mouse model of all

201 receptor P2Y12 is required for LTE4 mediated pulmonary inflammation in a mouse model of asthma and si

202 st particulates (DEPs) aggravate asthma-like pulmonary inflammation in a mouse model of asthma induce

203 signaling in the lung may be responsible for pulmonary inflammation in acute lung injury.

204 al alcohol exposure will trigger asthma-like pulmonary inflammation in allergen-sensitized mice, prov

205 thysmography (WBP), assesses the severity of pulmonary inflammation in animal models of inflammatory

206 CT and Patlak analysis for quantification of pulmonary inflammation in experimental ARDS.

207 K(i)) is the gold standard for assessment of pulmonary inflammation in experimental studies of acute

208 g clearly delineated tuberculosis-associated pulmonary inflammation in live animals.

209 sk, suggesting an etiologic role for chronic pulmonary inflammation in lung carcinogenesis.

210 phaCD11b PET/CT successfully tracked ear and pulmonary inflammation in mice and differentiated acute

211 caused significant morbidity, mortality, and pulmonary inflammation in mice, manifesting as increased

212 tosis and the outcome of neutrophil-mediated pulmonary inflammation in mice.

213 hat IL-17A is crucial for the development of pulmonary inflammation in murine models of experimental

214 In vivo studies showed greater LPS-induced pulmonary inflammation in Nrf2(-/-) mice that was signif

215 suggest that A-SAA is functionally linked to pulmonary inflammation in our O3 exposure model and that

216 muscle, but elicits airflow obstruction and pulmonary inflammation in patients with asthma.

217 thma, we studied the development of allergic pulmonary inflammation in periostin-deficient mice.

218 associated with reduction of viral load and pulmonary inflammation in RSV-infected mice.

219 Finally, LPS-induced pulmonary inflammation in SM22-Adam17(-/-) mice was rest

220 PIEZO1 in innate immune cells showed ablated pulmonary inflammation in the context of bacterial infec

221 Finally, dissection of the role of pulmonary inflammation in the initiation and promotion o

222 nockout mouse model to determine the role of pulmonary inflammation in the pathophysiology due to exp

223 lts suggest that the fungus elicits aberrant pulmonary inflammation in the setting of CFTR mutation,

224 Following acute LPS-induced pulmonary inflammation in vivo, chemokine-like receptor

225 nt roles of TLRs in A. baumannii OMV-induced pulmonary inflammation in vivo.

226 Targeting Axl significantly inhibited pulmonary inflammation, including the expression of IL-1

227 exposed to inhaled OVA showed no evidence of pulmonary inflammation, indices of remodeling, or airway

228 To determine the role of adiponectin in the pulmonary inflammation induced by extended (48-72 h) low

229 The ability of glucocorticoids to suppress pulmonary inflammation induced by non-typeable Haemophil

230 The effect of the COX pathway on innate pulmonary inflammation induced by protease-containing fu

231 Pulmonary inflammation, infection, and structural lung d

232 We examined which clinical outcomes (pulmonary inflammation, infection, structural lung disea

233 for survival and subsequently for markers of pulmonary inflammation, influx of lymphocytes and neutro

234 al factor in sickle cell disease by lowering pulmonary inflammation, iron overload, and mortality.

235 Pulmonary inflammation is associated with altered lipid

236 Pulmonary inflammation is believed to be central to the

237 Our data suggest that pneumococcal pulmonary inflammation is required for high-level bacter

238 Acute pulmonary inflammation is still a frightening complicati

239 efense against Klebsiella pneumoniae-induced pulmonary inflammation is unknown.

240 ell type is essential for the development of pulmonary inflammation, likely a cell in which group V s

241 damage (nephropathy, pulmonary hypertension, pulmonary inflammation, liver function, inflammatory inf

242 7(-/-)) were investigated in models of acute pulmonary inflammation (LPS, cytokine, and acid instilla

243 n up without inducing ATII cell dysfunction, pulmonary inflammation, lung damage, or excessive system

244 reus EV can induce Th1 and Th17 neutrophilic pulmonary inflammation, mainly in a TLR2-dependent manne

245 Th1 and Th17 cell responses and neutrophilic pulmonary inflammation, mainly via a Toll-like receptor

246 Here we show, using readily resolving pulmonary inflammation models, that loss of this seconda

247 ) mice resulted in a significant increase in pulmonary inflammation, mucous cell metaplasia, airway h

248 omplex disease characterized by eosinophilic pulmonary inflammation, mucus production and reversible

249 l the respective role of chronic hypoxia and pulmonary inflammation on soleus muscle hypertrophic cap

250 ure at a level of dietary intake potentiates pulmonary inflammation on subsequent infection with RSV.

251 ng ENDS vapor for 4 months failed to develop pulmonary inflammation or emphysema.

252 xemia, lung dysfunction, pulmonary edema, or pulmonary inflammation over a 6-day period.

253 identified and tested in an in vivo model of pulmonary inflammation, proving its efficacy.

254 We evaluated associations between pulmonary inflammation, recovery of pathogen-specific CD

255 sion of Foxm1 in macrophages is required for pulmonary inflammation, recruitment of macrophages into

256 humans, cadmium is poorly excreted, triggers pulmonary inflammation, reduces pulmonary function, and

257 m signals that regulate ILC2 function during pulmonary inflammation remain poorly understood.

258 or the promotion of Th2-mediating pathogenic pulmonary inflammation remains to be defined.

259 molecular mechanism of Mina's involvement in pulmonary inflammation remains unknown, our recent work

260 differentiation of TH17 cells, which promote pulmonary inflammation, requires the cooperation of a ne

261 2G) showed therapeutic efficacy for reducing pulmonary inflammation RSV infection in BALB/c mice.

262 ion from eosinophilic, neutrophilic, and Th2 pulmonary inflammation seen in Clec4n(-/-) recipients.

263 The protection from pulmonary inflammation seen with the Dectin-2 mAb or in

264 showed a marked augmentation of eosinophilic pulmonary inflammation, serum IgE, and Th2 cytokines.

265 Our murine model of allergic pulmonary inflammation suggested that HC-HA may contribu

266 a histone deacetylases expression, following pulmonary inflammation, suggested a putative role for hi

267 eness, mucus production, and IL-17A-dominant pulmonary inflammation, suggesting a regulatory role of

268 ells (DCs) also had less D. farinae-elicited pulmonary inflammation, supporting an effector function

269 in the EC-SOD KO group demonstrated greater pulmonary inflammation than did wild-type mice, there wa

270 caused significantly greater weight loss and pulmonary inflammation than the peptide without it (due

271 onses in vivo but showed attenuated allergic pulmonary inflammation that corresponded to lower expres

272 fluenza viral infection results in excessive pulmonary inflammation that has been linked to the damag

273 ibrosis (CF) is characterized by progressive pulmonary inflammation that is infection-triggered.

274 pulmonary disease (COPD) is characterized by pulmonary inflammation that persists after the cessation

275 MCps) to the lung is a feature of Ag-induced pulmonary inflammation that requires sensitization and c

276 rophages have a key role in tumor-associated pulmonary inflammation that supports the proliferation o

277 ion in lung macrophages in the modulation of pulmonary inflammation, the development of acute host di

278 Roflumilast reduces pulmonary inflammation through decreasing prolyl endopep

279 s to macFoxm1(-/-) mice restored BHT-induced pulmonary inflammation to the levels observed in control

280 Pulmonary inflammation totally inhibited this hypertroph

281 CD8 T cells presented with severe cachexia, pulmonary inflammation, viral dissemination, and 100% mo

282 e that is limited by alternative activation, pulmonary inflammation was ameliorated in mice lacking H

283 Pulmonary inflammation was assessed by histological feat

284 In vivo pulmonary inflammation was assessed in male BALB/c mice.

285 r receptor 2) and FoxF1, known regulators of pulmonary inflammation, was decreased in enFoxm1(-/-) mi

286 , nonatopic and virally exacerbated forms of pulmonary inflammation, we compared inflammatory respons

287 AP12 plays a role in cigarette smoke-induced pulmonary inflammation, we exposed wild-type and DAP12-d

288 In addition, survival and pulmonary inflammation were measured in mice undergoing

289 ells, and multiple parameters of asthma-like pulmonary inflammation were triggered.

290 y ablated O(3)-induced AHR without affecting pulmonary inflammation; whereas in obese mice, TNFR2 def

291 eased lung tumor multiplicity and attenuated pulmonary inflammation, which including reduced influx o

292 l introduction of A. baumannii OMVs mediated pulmonary inflammation, which is associated with neutrop

293 ificantly reduced lipopolysaccharide-induced pulmonary inflammation, which was evidenced by a decreas

294 ynamic biomarker for leukemia patients (with pulmonary inflammation) who might be suitable for a nove

295 a model of house dust mite-induced allergic pulmonary inflammation, wild type mice develop a mixed c

296 ed the pivotal role of the receptor CXCR7 in pulmonary inflammation with a predominant effect on the

297 a novel regulatory pathway in ILC2-mediated pulmonary inflammation with important clinical implicati

298 mice during lipopolysaccharide (LPS)-induced pulmonary inflammation, with altered intercellular adhes

299 anced loss of barrier function and increased pulmonary inflammation, with few differences in indexes

300 d had increased bacterial burdens and severe pulmonary inflammation, with increased myeloid and lymph