ライフサイエンスコーパス: pulmonary inflammation

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

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

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

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

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

6 cer development is associated with extensive pulmonary inflammation.

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

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

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

10 cal responses associated with acute allergic pulmonary inflammation.

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

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

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

14 hus implicating HXA3 in pneumococcus-induced pulmonary inflammation.

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

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

17 ated with IKKalpha downregulation and marked pulmonary inflammation.

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

19 ctions that facilitate the effector phase of pulmonary inflammation.

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

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

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

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

24 lomas mitigates widespread cytokine-mediated pulmonary inflammation.

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

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

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

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

29 e had increased gut epithelial apoptosis and pulmonary inflammation.

30 ry airway epithelial cells, neutrophilia and pulmonary inflammation.

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

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

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

34 cells to promote neutrophil recruitment and pulmonary inflammation.

35 onary Sendai virus infection, with increased pulmonary inflammation.

36 netic programs influencing Th2 cell-mediated pulmonary inflammation.

37 esentation and downstream phases of allergic pulmonary inflammation.

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

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

40 tor of innate immunity, normally suppressing pulmonary inflammation.

41 eduction has been blamed on malnutrition and pulmonary inflammation.

42 rus titers, and prevent body weight loss and pulmonary inflammation.

43 icial action on both bronchoconstriction and pulmonary inflammation.

44 2Y12) receptor is required for LTE4-mediated pulmonary inflammation.

45 st cardinal asthma manifestations, including pulmonary inflammation.

46 the viral titer but had a minimal effect on pulmonary inflammation.

47 oting the development of innate and adaptive pulmonary inflammation.

48 y epithelial cells in orchestrating allergic pulmonary inflammation.

49 the ability of DCs to elicit pathologic Th2 pulmonary inflammation.

50 showed significantly reduced antigen-induced pulmonary inflammation.

51 ory zone 1), particularly during the peak of pulmonary inflammation.

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

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

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

55 d chlamydial clearance and the resolution of pulmonary inflammation.

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

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

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

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

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

61 e role of alveolar macrophages in regulating pulmonary inflammation.

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

63 2a(+/-) mice was exacerbated in both EAE and pulmonary inflammation.

64 cies was efficient in preventing spontaneous pulmonary inflammation.

65 ic inflammation, cutaneous vasculopathy, and pulmonary inflammation.

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

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

68 nonatopic and viral-induced exacerbations of pulmonary inflammation.

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

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

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

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

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

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

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

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

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

78 2B)R double-knockout mice exhibited enhanced pulmonary inflammation and airway destruction.

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

80 or IL-17RA completely blocked IL-25-induced pulmonary inflammation and airway hyperresponsiveness in

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

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

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

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

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

86 Infected mice demonstrated increased pulmonary inflammation and alveolar epithelial cell apop

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

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

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

90 ADA-deficient mice would lead to diminished pulmonary inflammation and damage.

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

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

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

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

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

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

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

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

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

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

101 a the Fas/FasL pathway in the development of pulmonary inflammation and fibrosis in reovirus 1/L-indu

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

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

104 ransduce an apoptotic signal, do not develop pulmonary inflammation and fibrotic lesions associated w

105 Pulmonary inflammation and goblet cell differentiation w

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

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

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

109 ), are devastating disorders of overwhelming pulmonary inflammation and hypoxemia, resulting in high

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

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

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

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

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

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

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

117 ion of crocidolite asbestos in mice leads to pulmonary inflammation and injury that is enhanced in EC

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

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

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

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

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

123 (eff) cell-derived IL-10 results in enhanced pulmonary inflammation and lethal injury.

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

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

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

127 s of Pneumocystis in the lungs may stimulate pulmonary inflammation and may play a role in the develo

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

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

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

131 Pulmonary inflammation and quasi-static lung compliance

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

133 ted molecular pattern-induced (PAMP-induced) pulmonary inflammation and remodeling in mice.

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

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

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

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

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

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

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

141 le than D. farinae-loaded WT BMDCs to induce pulmonary inflammation and Th2 polarization in WT mice.

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

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

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

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

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

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

148 red, with increased fungal burden, increased pulmonary inflammation, and decreased survival.

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

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

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

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

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

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

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

156 ture from remodeling during allergen-induced pulmonary inflammation, and these effects may be mediate

157 sinophil homing into the airways in allergic pulmonary inflammation, and thus is a potential therapeu

158 e had significantly exacerbated eosinophilic pulmonary inflammation, as assessed in bronchoalveolar l

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

160 astases and suggest that amelioration of the pulmonary inflammation associated with asthma will have

161 activity of RSV G protein might decrease the pulmonary inflammation associated with infection in BALB

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

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

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

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

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

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

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

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

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

171 ophages in the development of ricin-mediated pulmonary inflammation by employing transgenic (MAFIA) m

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

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

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

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

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

177 Pulmonary inflammation causes multiple alterations withi

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

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

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

181 31-2G significantly decreased RSV-associated pulmonary inflammation compared to either antibody alone

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

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

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

185 lial cells reduced the phenotype of allergic pulmonary inflammation due to loss of IL-17-induced neut

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

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

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

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

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

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

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

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

194 4c(-/-) CD19(+)CD138(+) cells induced marked pulmonary inflammation, eosinophilia, and increased bron

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

196 Uncontrolled neutrophil-driven pulmonary inflammation exacerbates this disease.

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

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

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

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

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

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

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

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

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

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

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

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

209 Pulmonary inflammation in asthma is orchestrated by the

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

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

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

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

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

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

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

217 We hypothesize that EC-SOD may inhibit pulmonary inflammation in part by preventing superoxide-

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

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

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

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

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

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

224 ng the pathogenesis of Th2 cytokine-mediated pulmonary inflammation, in part through the regulation o

225 This worsening of pulmonary inflammation, in response to persistent Pneumo

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 mined virus replication and the character of pulmonary inflammation induced by MHV-1 infection in sus

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

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 ensuing inflammation in a model of allergic pulmonary inflammation, initiated by inhalation sensitiz

235 Pulmonary inflammation is associated with altered lipid

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

237 Acute pulmonary inflammation is still a frightening complicati

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

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

240 7(-/-)) were investigated in models of acute pulmonary inflammation (LPS, cytokine, and acid instilla

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

242 nsgenic lungs was associated with persistent pulmonary inflammation, macrophage infiltration and incr

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

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

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

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

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

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

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

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

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

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

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

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

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

256 These studies showed that allergen-induced pulmonary inflammation resulted in a >3-fold increase in

257 2G) showed therapeutic efficacy for reducing pulmonary inflammation RSV infection in BALB/c mice.

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

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

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

261 inistration of IL-25 into naive mice induces pulmonary inflammation similar to that seen in patients

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

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

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

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

266 sthma model selectively reduced eosinophilic pulmonary inflammation, TGF-beta1 and collagen expressio

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

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

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

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

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

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

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

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

275 Roflumilast reduces pulmonary inflammation through decreasing prolyl endopep

276 role of epithelial-derived Act1 in allergic pulmonary inflammation through the distinct impact of th

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

278 Pulmonary inflammation totally inhibited this hypertroph

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

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

281 Pulmonary inflammation was assessed by histological feat

282 stasis to the lung as a function of allergic pulmonary inflammation was assessed following the i.v. i

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

284 ngs and the eventual death of infected mice, pulmonary inflammation was generally absent, and there w

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 Using a mouse model of allergic pulmonary inflammation, we observed diminished Th2 respo

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

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

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

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

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

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

295 (SARS) is characterized by substantial acute pulmonary inflammation with a high mortality rate.

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