Abstract：
:Human neutrophils express Toll-like receptor 4 (TLR4) at low levels, and the role of this receptor in neutrophil responses to microbial stimuli has been questioned. Genetic manipulation of these cells to enable the study of the role of proteins such as TLR4 in their function is challenging. Here, we show that primary human neutrophils rapidly express novel proteins such as enhanced green fluorescent protein (eGFP) after transduction with lentivirus. Stimulation of transduced neutrophils with lipopolysaccharide (LPS) resulted in increased cell survival, which was inhibited when neutrophils were transduced with a lentivirus encoding a dominant negative (dn) TLR4 protein. LPS-induced survival was also inhibited by lentiviruses encoding dnMyD88 or a truncated TRIF (Toll/interleukin-1R homologous domain-containing adapter protein inducing interferon-beta) molecule, whilst, in contrast, neutrophil survival was enhanced by overexpression of kinase-mutated interleukin-1 receptor-associated kinase 1 (kmIRAK-1), which activated nuclear factor (NF)-kappaB. These studies provide proof of the role of TLR4 in human neutrophil biology, have begun to elucidate TLR-dependent pathways regulating neutrophil survival, and demonstrate that neutrophils can be genetically manipulated to enhance or inhibit survival.
journal_name
Immunologyjournal_title
Immunologyauthors
Dick EP,Prince LR,Prestwich EC,Renshaw SA,Whyte MK,Sabroe Idoi
10.1111/j.1365-2567.2008.02949.xsubject
Has Abstractpub_date
2009-06-01 00:00:00pages
249-55issue
2eissn
0019-2805issn
1365-2567pii
IMM2949journal_volume
127pub_type
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