| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
From the Academic Units of Respiratory Medicine* and Cell Biology, Section of Functional Genomics, Division of Genomic Medicine, and the Cardiovascular Research Group, Division of Clinical Sciences (North), University of Sheffield, Sheffield, United Kingdom
The regulation of systemic and local neutrophil activation is crucial to the clearance of infections and the successful resolution of inflammation without progress to tissue damage or disseminated inflammatory reactions. Using purified lipopolysaccharide (pLPS) and highly purified neutrophils, we have previously shown that Toll-like receptor 4 signaling is a potent neutrophil activator, but a poor stimulator of survival. In the presence of peripheral blood mononuclear cells (PBMCs), however, pLPS becomes a potent neutrophil survival factor. Interleukin (IL)-1ß has been identified as an important neutrophil activator and prosurvival cytokine, and is produced in abundance by LPS-stimulated PBMCs. We now show that IL-1ß fails to activate highly purified neutrophils or enhance their survival, but in the presence of PBMCs, IL-1ß induces neutrophil survival. We hypothesized that LPS-primed neutrophils might become responsive to IL-1ß, but were unable to demonstrate this. Moreover, IL-1ra failed to prevent pLPS + PBMC-dependent neutrophil survival. In studies of IL-1R1–/– mice, we found that LPS was still able to mediate neutrophil survival, and neutrophil survival was enhanced by the addition of monocytic cells. Thus an important paradigm of neutrophil regulation needs to be viewed in the context of a cellular network in which actions of IL-1ß on neutrophils are indirect and mediated by other cells.
This article has been cited by other articles:
 |
|
 |
|
  C. A. Loynes, J. S. Martin, A. Robertson, D. M. I. Trushell, P. W. Ingham, M. K. B. Whyte, and S. A. Renshaw Pivotal Advance: Pharmacological manipulation of inflammation resolution during spontaneously resolving tissue neutrophilia in the zebrafish J. Leukoc. Biol., February 1, 2010; 87(2): 203 - 212. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Sabroe, L. C. Parker, D. H. Dockrell, D. E. Davies, S. K. Dower, and M. K. B. Whyte Targeting the Networks that Underpin Contiguous Immunity in Asthma and Chronic Obstructive Pulmonary Disease Am. J. Respir. Crit. Care Med., February 15, 2007; 175(4): 306 - 311. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. von Bernuth, C.-L. Ku, C. Rodriguez-Gallego, S. Zhang, B.-Z. Garty, L. Marodi, H. Chapel, M. Chrabieh, R. L. Miller, C. Picard, et al. A Fast Procedure for the Detection of Defects in Toll-like Receptor Signaling Pediatrics, December 1, 2006; 118(6): 2498 - 2503. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. C. Parker, E. C. Jones, L. R. Prince, S. K. Dower, M. K. B. Whyte, and I. Sabroe Endotoxin tolerance induces selective alterations in neutrophil function J. Leukoc. Biol., December 1, 2005; 78(6): 1301 - 1305. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. C. Parker, M. K. B. Whyte, S. K. Dower, and I. Sabroe The expression and roles of Toll-like receptors in the biology of the human neutrophil J. Leukoc. Biol., June 1, 2005; 77(6): 886 - 892. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. E. Morris, M. K. B. Whyte, G. F. Martin, P. J. Jose, S. K. Dower, and I. Sabroe Agonists of Toll-like Receptors 2 and 4 Activate Airway Smooth Muscle via Mononuclear Leukocytes Am. J. Respir. Crit. Care Med., April 15, 2005; 171(8): 814 - 822. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Francois, J. El Benna, P. M. C. Dang, E. Pedruzzi, M.-A. Gougerot-Pocidalo, and C. Elbim Inhibition of Neutrophil Apoptosis by TLR Agonists in Whole Blood: Involvement of the Phosphoinositide 3-Kinase/Akt and NF-{kappa}B Signaling Pathways, Leading to Increased Levels of Mcl-1, A1, and Phosphorylated Bad J. Immunol., March 15, 2005; 174(6): 3633 - 3642. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
