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1 terstitial mononuclear cell infiltration and alveolitis.
2 st levels were detected in SSc patients with alveolitis.
3 cytokines is associated with the presence of alveolitis.
4  inflammation in IgG immune complex-mediated alveolitis.
5 lity in models of chemotactic factor-induced alveolitis.
6 , and TNF-alpha and would have a concomitant alveolitis.
7 ty and neutrophil infiltration in a model of alveolitis.
8 ly suppressed endotoxin-induced neutrophilic alveolitis.
9 ividuals and strongly correlated with T-cell alveolitis.
10  histologically simulated extrinsic allergic alveolitis.
11  not a consequence of excessive neutrophilic alveolitis.
12 thelium and mild to moderate peribronchiolar alveolitis.
13 y correlated with the severity of the T cell alveolitis.
14 lymorphonuclear neutrophil (PMN)-predominant alveolitis.
15 e in some, but not all, patients with active alveolitis.
16 resence of lung granulomas and a CD4+ T cell alveolitis.
17 reathlessness, the primary symptom of active alveolitis.
18 ents of lung be performed for diagnosing SSc alveolitis.
19  challenge, with no ERD signs in the form of alveolitis.
20  having active alveolitis and 1 as having no alveolitis.
21 ula may underestimate the presence of active alveolitis.
22 o produce lesions resembling human fibrosing alveolitis.
23 which is the time point of peak neutrophilic alveolitis.
24 lammatory response using a mouse model of IC alveolitis.
25 HIV disease progression than was lymphocytic alveolitis.
26 ave restrictive lung disease and evidence of alveolitis.
27 erminal airspace cell population to diagnose alveolitis, a condition that predicts changes in lung fu
28 rstitial pneumonia characterized by a marked alveolitis, accompanied by loss of appetite, weight loss
29 ell numbers, and resolution of CD8(+) T-cell alveolitis after ART in 9 of 12 individuals.
30 dients predict the intensity of neutrophilic alveolitis after treatment with endotoxin.
31                         In SSc patients with alveolitis, all 8 domains of the SF-36 were significantl
32                                T lymphocytic alveolitis also was found in the affected but not the un
33                                  Lymphocytic alveolitis, although present at all stages of HIV infect
34  patients were reclassified as having active alveolitis and 1 as having no alveolitis.
35 ving 890 subjects with cryptogenic fibrosing alveolitis and 5, 884 control subjects drawn from the Un
36 acute exacerbations" (AE), marked by diffuse alveolitis and altered gas exchange, resulting in a sign
37  In the lung, CO suppressed LPS-induced lung alveolitis and associated edema formation, while in the
38 ease (CBD) is characterized by a CD4+ T cell alveolitis and granulomatous inflammation in the lung.
39 hereas these mice had increased neutrophilic alveolitis and greater lung injury compared with WT cont
40 mma-producing CD8 T cells mediated pulmonary alveolitis and inflammation, which were dependent upon C
41 d enhanced pulmonary pathology consisting of alveolitis and interstitial pneumonitis after a live-vir
42 ere were marked differences in severities in alveolitis and interstitial pneumonitis when each of the
43 als primed with FG vaccine showed quite mild alveolitis and interstitial pneumonitis, which were elim
44  with Go6976 showed significantly suppressed alveolitis and neutrophil influx in bronchial alveolar l
45 eased mortality, consistent with more severe alveolitis and pneumonitis.
46 lung disorder characterized by CD4(+) T cell alveolitis and progressive lung fibrosis.
47                           Extrinsic allergic alveolitis and pulmonary sarcoidosis are granulomatous d
48 ogically similar to human extrinsic allergic alveolitis and sarcoidosis, respectively.
49 symptoms in patients with evidence of active alveolitis and scleroderma-related interstitial lung dis
50 is higher than those in SSc patients without alveolitis and than those in normal controls), and RANTE
51                   MBV decreased long-lasting alveolitis and the proportion of lung undergoing inflamm
52 formed on patients with SSc (with or without alveolitis) and on normal control subjects.
53 alveolar damage, hyaline membrane formation, alveolitis, and death were noted in 12-month-old mice in
54 ivation in the lungs, increased neutrophilic alveolitis, and greater lung inflammation/injury compare
55 hed AEC2-driven recruitment of granulocytes, alveolitis, and lung injury.
56  to the recruitment of alveolar macrophages, alveolitis, and subsequent granuloma development.
57 eased in patients with cryptogenic fibrosing alveolitis, and that this effect is independent of the e
58 onary edema and develops into a neutrophilic alveolitis, and, later, pulmonary fibrosis.
59 reduced histological evidence of PcP-related alveolitis as compared with infected wild-type mice.
60 y be a risk factor for cryptogenic fibrosing alveolitis as well as for lung cancer, and so may confou
61                                  C5a-induced alveolitis, as measured by cell counts and total protein
62                  These findings suggest that alveolitis associated with HIV-1 infection is caused by
63 o the lungs with acute, focal bronchitis and alveolitis associated with massive pulmonary oedema, hae
64  fibrosing alveolitis (CFA) and in fibrosing alveolitis associated with systemic sclerosis (FASSc).
65                          At low RSV F doses, alveolitis-associated histopathology was unexpectedly ob
66 th the development of a macrophage-dominated alveolitis at sites of infection, with increased synthes
67        This evidence suggests that fibrosing alveolitis begins much earlier in the course of clinical
68 itical pathway to end-stage fibrosis is not "alveolitis" but rather the ongoing epithelial damage and
69 sion structures, from necrotic granulomas to alveolitis, but the mechanisms regulating their developm
70 t CRP has a significant protective effect in alveolitis by reducing neutrophil influx and protein lea
71  (HP) is a T(H)1 lymphocyte-biased fibrosing alveolitis caused by antigens ranging from avian excreta
72 stitial vascularity in cryptogenic fibrosing alveolitis (CFA) and in fibrosing alveolitis associated
73                   Lone cryptogenic fibrosing alveolitis (CFA) is a progressive interstitial lung dise
74 viously suggested that cryptogenic fibrosing alveolitis (CFA) may be caused by occupational exposures
75 use model of intratracheal endotoxin-induced alveolitis, coexposure to FRT (core temperature approxim
76 dence in patients with cryptogenic fibrosing alveolitis compared with the general population in a pop
77          Interventions to limit neutrophilic alveolitis could either be targeted to block local lung
78 imited (n = 57) cutaneous disease and active alveolitis (determined by bronchoalveolar lavage and/or
79                              Thus, fibrosing alveolitis develops after intratracheal bleomycin irresp
80 s, neither crescentic glomerulonephritis nor alveolitis ensued, likely because of the predominance of
81                                    Fibrosing alveolitis (FA) is characterized by persistent inflammat
82 long-term followup, patients with persistent alveolitis had a decline in lung function (mean +/- SD c
83                         Although lymphocytic alveolitis has been associated with viremia and an incre
84                        Cryptogenic fibrosing alveolitis has been reported to be associated with an in
85 ected mouse lung tissues demonstrated severe alveolitis, hemorrhaging, and spread of the virus throug
86 P = 0.0005, with levels in SSc patients with alveolitis higher than those in normal controls), IL-8 (
87  = 0.03, with levels in SSc patients without alveolitis higher than those in normal controls).
88 (P = 0.009, with levels in SSc patients with alveolitis higher than those in SSc patients without alv
89 Open lung biopsy revealed extrinsic allergic alveolitis (hypersensitivity pneumonitis).
90 D8(+) T cells, often resolving CD8(+) T-cell alveolitis in active smokers.
91       Influenza is known to cause persistent alveolitis in animal models; however, little is known ab
92                                  Lymphocytic alveolitis in HIV-1-infected individuals is associated w
93          These data suggest that lymphocytic alveolitis in HIV-infected subjects occurs in response t
94              The usefulness of BAL to define alveolitis in SSc is questionable.
95 ea, along with mucosal damage and multifocal alveolitis in the lungs.
96 s opacification on HRCT accurately predicted alveolitis in the middle lung fields, HRCT did not detec
97 hoalveolar lavage (BAL), in the diagnosis of alveolitis in these patients.
98  necessary for the full development of acute alveolitis in this model of lung injury.
99 causes a slowly unfolding, spatially limited alveolitis in which alveolar macrophages containing SARS
100 protein C and proCPB, attenuated C5a-induced alveolitis in WT but not in proCPB-/- mice, indicating t
101 C5a instillation was ineffective in reducing alveolitis in WT mice, suggesting that the beneficial ef
102                To study the effect of CRP on alveolitis induced by different chemoattractants, transg
103                           Extrinsic allergic alveolitis is caused by inhaled antigens, whereas the na
104 othesized that the intensity of neutrophilic alveolitis is related to establishing a gradient of neut
105 ells in the lung, and this failure of a CD4+ alveolitis limits an effective immune response.
106 t histologic features, including lymphocytic alveolitis, lymphocytic interstitial pneumonitis, bronch
107 though early identification and treatment of alveolitis may prevent deterioration of lung function, t
108                           Lung inflammation (alveolitis) may cause lung fibrosis in scleroderma.
109  the results derived from our immune complex alveolitis model.
110 sma protein affects leukocyte recruitment in alveolitis models of lung inflammation.
111 ype DBP(+/+) counterparts in three different alveolitis models, two acute and one chronic.
112 round-glass opacification and the finding of alveolitis on BAL from segments in the same lung regions
113 between fibrosis on HRCT and the presence of alveolitis on BAL was significant for the lower lobes bu
114   Despite viral clearance, bronchiolitis and alveolitis persisted at day 14 postinfection; histopatho
115                                  Lymphocytic alveolitis portends a poor prognosis in human immunodefi
116 d cell count obtained after CYC treatment of alveolitis predicts long-term lung function outcomes and
117 ed among patients with cryptogenic fibrosing alveolitis (rate ratio [RR] 7.31, 95% confidence interva
118           Nine of the 18 patients had active alveolitis recorded in both lavaged segments, while in 4
119 e poor prognosis associated with lymphocytic alveolitis reflects a high pulmonary viral burden.
120 ion, the best approach for diagnosing active alveolitis remains controversial.
121 ected a lower doses and volumes, significant alveolitis required exposure to 5 mg of silica in 50 mul
122 une complex glomerulonephritis and pulmonary alveolitis, similar to that caused by cells treated with
123 ell depletion and dysfunction, CD8(+) T-cell alveolitis, smoking, and poor control of human immunodef
124 almost completely abolished the neutrophilic alveolitis that occurs in rats following i.p. injection
125 cause of infection (six deaths), hemorrhagic alveolitis (three deaths), or bleeding (one death).
126 ical changes consisting of bronchiolitis and alveolitis typical of virus-induced changes.
127                                       Active alveolitis was defined as the presence of > or =3.0% pol
128                       An immature macrophage alveolitis was found in the affected lung and the unaffe
129         To test this hypothesis, C5a-induced alveolitis was studied in wild-type (WT) and proCPB-defi
130  gelatinase B in bleomycin-induced fibrosing alveolitis, we instilled bleomycin intratracheally into
131  bronchiolocentric granulomatous lymphocytic alveolitis, which evolves to fibrosis in chronic advance
132 nchoalveolar lavage or biopsy, patients with alveolitis who did not receive cyclophosphamide therapy
133 s and survival are improved in patients with alveolitis who receive cyclophosphamide.
134 median follow-up of 16 months, patients with alveolitis who received cyclophosphamide were more likel
135 a lung-centric 'second wave' cytokine-driven alveolitis with associated immunothrombosis; this phenom

 
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