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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
5 era, and 4) increased hallmarks of classical pulmonary macrophage activation.
6 led interrogation of molecular mechanisms of pulmonary macrophage adaptation.
7 DMCs also expressed argI(high)iNOS(low), but pulmonary macrophages adopted argI(high)iNOS(low) polari
8  evasion of this restriction by sG, involves pulmonary macrophages and complement, but not neutrophil
9 ed in C. neoformans phagocytosis by resident pulmonary macrophages and DC.
10 mined the role of IL-13 in the activation of pulmonary macrophages and DCs and in the priming of an i
11 tracellular replication of R. equi in equine pulmonary macrophages and in an in vivo mouse infection
12 cling by AT2 cells, with some degradation by pulmonary macrophages and loss up the bronchial tree.
13 SC, as well as abnormal interactions between pulmonary macrophages and respiratory resident T cells,
14 istered to the lungs of mice causes death of pulmonary macrophages and the release of proinflammatory
15 1Delta was more efficiently contained within pulmonary macrophages and was further delayed in causing
16 n IPS-1-deficient alveolar epithelial cells, pulmonary macrophages, and CD11b(+) dendritic cells (DC)
17  We have previously implicated activation of pulmonary macrophage by TNF-alpha and/or MCP-1 in the me
18 lted in increased intracellular infection of pulmonary macrophages by C. neoformans, increasing the p
19                                              Pulmonary macrophages comprise the first line of host de
20       We hypothesized that NTHi infection of pulmonary macrophages drives neutrophilic inflammation i
21 t mechanisms that regulate the activation of pulmonary macrophages during inflammation are poorly und
22  (DMRP(NOCas)) for the dynamic monitoring of pulmonary macrophages during influenza A virus (IAV) inf
23                                 Furthermore, pulmonary macrophages expressed argI(high)iNOS(low) on t
24                                              Pulmonary macrophages expressed arginase I (subtype M2)
25 rgets, cathepsins S and B, were increased in pulmonary macrophages from smokers and patients with chr
26                                              Pulmonary macrophages from STAT1 KO mice exhibited defec
27                                 In contrast, pulmonary macrophage function was defective in TNFRI-/-
28 tructive pulmonary disease, WT mice had more pulmonary macrophages, higher histopathology scores, and
29 or normal physiological GM-CSF secretion and pulmonary macrophage homeostasis.
30 recise number and anatomic location of human pulmonary macrophages in nondiseased lungs and to quanti
31 ELMalpha also suppressed the Sirt1 signal in pulmonary macrophages in the early posthypoxic period.
32 tide inhibited the alternative activation of pulmonary macrophages in the lungs of HDM-challenged mic
33  animal models suggest an important role for pulmonary macrophages in the pathogenesis of pulmonary h
34 hronic obstructive pulmonary disease (COPD), pulmonary macrophages increase in number, release increa
35           Furthermore, ActRIIA-Fc normalized pulmonary macrophage infiltration and corrected cardiopu
36 lation and significantly reduced viremia and pulmonary macrophage infiltration.
37  TJ and PPAR-gamma expression, and increased pulmonary macrophage infiltration.
38     Principal components analysis correlated pulmonary macrophage inflammatory peptide-2 and interleu
39                        NTHi persistence with pulmonary macrophages may contribute to chronic airway i
40 short-lived free radical that is secreted by pulmonary macrophages (Mo).
41                                              Pulmonary macrophages (Mphi), airway epithelium, and den
42 ell as cell death were examined in lungs and pulmonary macrophages of mice with cigarette smoke (CS)-
43  macrophages (IMs) constitute a second major pulmonary macrophage population.
44 knowledge) data comparing effects on the two pulmonary macrophage populations demonstrate that the ac
45 odest decrease in the phagocytic capacity of pulmonary macrophage populations following HDM exposure.
46 d TNF-alpha-secreting T cells, and increased pulmonary macrophage production of TNF-alpha to lipopoly
47 nt infection, we investigated the ability of pulmonary macrophages (PuM) to phagocytize C. neoformans
48  parasite of aquatic amoebae and pathogen of pulmonary macrophages, replicates intracellularly, utili
49 eria to instruct an immune-tolerant state of pulmonary macrophages through Fc gamma receptor IIb sign
50 that TSLP changes the quiescent phenotype of pulmonary macrophages toward an aaM phenotype during TSL
51 ith CSF2RA or CSF2RB mutations, we show that pulmonary macrophage transplantation (PMT) of either wil
52 NOCas) enables in vivo dynamic monitoring of pulmonary macrophages, uncovering extensive recruitment
53                                              Pulmonary macrophages undergo dynamic changes in populat
54 ant in the lung was found to be dependent on pulmonary macrophages, underscoring the importance of co
55 nvasive assessment of cardiac, arterial, and pulmonary macrophages using the nanotracer (64)Cu-Macrin
56                                              Pulmonary macrophages were analyzed for uptake of PKH-26
57 nclusions: The precise locations occupied by pulmonary macrophages were defined in nondiseased human
58                               Stimulation of pulmonary macrophages with TNF-alpha and/or MCP-1 induce