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1 n species (ROS), and prostaglandins (PGs) by pulmonary macrophages.
2 llectin-mediated killing by rapid entry into pulmonary macrophages.
3 saline-treated controls but did not prevent pulmonary macrophage accumulation or the development of
4 in of SP-D is required for the regulation of pulmonary macrophage activation, airspace remodeling, an
6 DMCs also expressed argI(high)iNOS(low), but pulmonary macrophages adopted argI(high)iNOS(low) polari
7 evasion of this restriction by sG, involves pulmonary macrophages and complement, but not neutrophil
9 mined the role of IL-13 in the activation of pulmonary macrophages and DCs and in the priming of an i
10 istered to the lungs of mice causes death of pulmonary macrophages and the release of proinflammatory
11 1Delta was more efficiently contained within pulmonary macrophages and was further delayed in causing
12 n IPS-1-deficient alveolar epithelial cells, pulmonary macrophages, and CD11b(+) dendritic cells (DC)
13 We have previously implicated activation of pulmonary macrophage by TNF-alpha and/or MCP-1 in the me
14 lted in increased intracellular infection of pulmonary macrophages by C. neoformans, increasing the p
17 rgets, cathepsins S and B, were increased in pulmonary macrophages from smokers and patients with chr
20 tructive pulmonary disease, WT mice had more pulmonary macrophages, higher histopathology scores, and
21 tide inhibited the alternative activation of pulmonary macrophages in the lungs of HDM-challenged mic
22 animal models suggest an important role for pulmonary macrophages in the pathogenesis of pulmonary h
23 hronic obstructive pulmonary disease (COPD), pulmonary macrophages increase in number, release increa
26 Principal components analysis correlated pulmonary macrophage inflammatory peptide-2 and interleu
29 odest decrease in the phagocytic capacity of pulmonary macrophage populations following HDM exposure.
30 d TNF-alpha-secreting T cells, and increased pulmonary macrophage production of TNF-alpha to lipopoly
31 nt infection, we investigated the ability of pulmonary macrophages (PuM) to phagocytize C. neoformans
32 parasite of aquatic amoebae and pathogen of pulmonary macrophages, replicates intracellularly, utili
33 that TSLP changes the quiescent phenotype of pulmonary macrophages toward an aaM phenotype during TSL
34 ith CSF2RA or CSF2RB mutations, we show that pulmonary macrophage transplantation (PMT) of either wil
35 ant in the lung was found to be dependent on pulmonary macrophages, underscoring the importance of co
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