Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.2.1.7 (BAL)
 1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Activated polymorphonuclear leukocytes (PMNs) are implicated in the pathogenesis of acute lung injury (ALI) associated with sepsis. Adhesion of activated PMNs to endothelial monolayers is mediated by the CD18 adhesion-receptor complex on the PMN cell surface. Monoclonal antibody 60.3 (MoAb 60.3) blocks CD18-dependent PMN-endothelial adhesion in vitro and in vivo. This study was designed to determine the role of CD18-dependent PMN adhesion in ALI associated with gram-negative sepsis. Anesthetized, ventilated (FiO2 0.5, positive end-expiratory pressure 5 cm H2O) pigs received sterile saline (control, n = 8) or live Pseudomonas aeruginosa, 5 x 10(8) colony-forming units/ml at 0.3 ml/20 kg/min (septic, n = 9) for 1 hour. A third group (n = 7) received MoAb 60.3, 2 mg/kg intravenously, 15 minutes before Pseudomonas infusion. Animals were studied for 300 minutes. MoAb 60.3 significantly (p less than 0.05) attenuated the neutropenia seen in sepsis (15 +/- 1 vs 6 +/- 1 x 10(3) PMNs/mm3 at 300 min). Alveolar-capillary membrane injury was assessed by bronchoalveolar-lavage protein content and extravascular lung water determination. MoAb 60.3 significantly (p less than 0.05) reduced BAL protein at 300 minutes (388 +/- 75 vs 1059 +/- 216 micrograms/ml in septic animals) and attenuated the increase in extravascular lung water to 240 minutes (7.1 +/- 2 vs 14.2 +/- 1.2 ml/kg in septic animals). Systemic hypotension, decreased cardiac index, pulmonary hypertension, and relative hypoxemia, all characteristic of this model, were not altered by MoAb 60.3. These data suggest that, in this model of septic ALI, neutropenia is, in part, CD18 dependent and that blocking CD18-dependent PMN adhesion protects the alveolar-capillary membrane independently of altered hemodynamic status.
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PMID:Anti-CD18 antibody attenuates neutropenia and alveolar capillary-membrane injury during gram-negative sepsis. 167 91

Macrophages and monocytes play important proinflammatory roles in allergic inflammation. We hypothesized that these cells would express an activated phenotype in allergic disease of the airways. We therefore compared the expression of 17 activation markers on the surface of alveolar macrophages (AM) and peripheral blood monocytes (PBM) in 13 subjects with asymptomatic allergic asthma (AA), nine subjects with asymptomatic allergic rhinitis (AR), and 11 nonallergic (N). AM were obtained by BAL, and PBM were simultaneously obtained by phlebotomy; both were analyzed for expression of surface markers using a new two-color flow cytometry method that essentially eliminates background autofluorescence. The proportions of AM in BAL fluid from AA, AR, and N subjects were 84 +/- 2, 85 +/- 4, and 91 +/- 1%, respectively; viability always exceeded 92%. Expression of eight markers (CD16, CD18, CD32, CD44, CD71, HLA Class I, HLA DR, and HLA DQ) was significantly (p < 0.05) higher on AM of AA than on N; expression of six markers (CD11a, CD16, CD18, CD71, HLA Class I, and HLA DR) was higher on AM of AR than on N, with differences in CD44 levels approaching statistical significance (p = 0.07). Expression of one marker, CD44, was significantly higher on AM of AA than on those of AR, with differences in HLA Class I levels approaching statistical significance (p = 0.07). In contrast, no significant differences were found among the three groups in the expression in eight other markers (CD11b, CD14, CD23, CD29, CD33, CD35, CD63, and CD64). Finally, similar analysis of PBM from these same subjects failed to find any difference between the three groups in any of the 17 activation markers studied. These data suggest that AM are activated in allergic respiratory diseases, and that levels of HLA Class I and CD44 on AM are altered during allergic inflammation in the upper and lower airways.
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PMID:Phenotypic analysis of alveolar macrophages and monocytes in allergic airway inflammation. I. Evidence for activation of alveolar macrophages, but not peripheral blood monocytes, in subjects with allergic rhinitis and asthma. 911 17