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Lectins Offer New Perspectives in the Development of Macrophage-Targeted Therapies for COPD/Emphysema

Artikel i vetenskaplig tidskrift
Författare V. R. Mukaro
Johan Bylund
G. Hodge
M. Holmes
H. Jersmann
P. N. Reynolds
S. Hodge
Publicerad i Plos One
Volym 8
Nummer/häfte 2
Sidor e56147
ISSN 1932-6203
Publiceringsår 2013
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Sidor e56147
Språk en
Länkar ttp://dx.doi.org/10.1371/journal.po...
Ämnesord OBSTRUCTIVE PULMONARY-DISEASE; MANNOSE-BINDING LECTIN; T-CELL APOPTOSIS; ALVEOLAR MACROPHAGES; GALECTIN-3; EXPRESSION; AIRWAY; EFFEROCYTOSIS; PHAGOCYTOSIS; RECOGNITION
Ämneskategorier Medicinska grundvetenskaper

Sammanfattning

We have previously shown that the defective ability of alveolar macrophages (AM) to phagocytose apoptotic cells ('efferocytosis') in chronic obstructive pulmonary disease/emphysema (COPD) could be therapeutically improved using the C-type lectin, mannose binding lectin (MBL), although the exact mechanisms underlying this effect are unknown. An S-type lectin, galectin-3, is also known to regulate macrophage phenotype and function, via interaction with its receptor CD98. We hypothesized that defective expression of galectin/CD98 would be associated with defective efferocytosis in COPD and that mechanisms would include effects on cytoskeletal remodeling and macrophage phenotype and glutathione (GSH) availability. Galectin-3 was measured by ELISA in BAL from controls, smokers and current/ex-smokers with COPD. CD98 was measured on AM using flow cytometry. We assessed the effects of galectin-3 on efferocytosis, CD98, GSH, actin polymerisation, rac activation, and the involvement of PI3K (using beta-actin probing and wortmannin inhibition) in vitro using human AM and/or MH-S macrophage cell line. Significant decreases in BAL galectin-3 and AM CD98 were observed in BAL from both current- and ex-smoker COPD subjects vs controls. Galectin 3 increased efferocytosis via an increase in active GTP bound Rac1. This was confirmed with beta-actin probing and the role of PI3K was confirmed using wortmannin inhibition. The increased efferocytosis was associated with increases in available glutathione and expression of CD98. We provide evidence for a role of airway lectins in the failed efferocytosis in COPD, supporting their further investigation as potential macrophage-targeted therapies.

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