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A blast from the past: clearance of apoptotic cells regulates immune responses
Apoptosis, which is a programmed and physiological form of cell death, is known to shape the immune system by regulating populations of effector lymphocytes. However, the binding and ingestion ofExpand
Macrophage phagocytosis of aging neutrophils in inflammation. Programmed cell death in the neutrophil leads to its recognition by macrophages.
TLDR
Changes in the senescent neutrophil that are associated with their recognition by macrophages are the subject of this investigation, and these processes may represent a mechanism for the removal of neutrophils during inflammation that also serves to limit the degree of tissue injury. Expand
Resolution of in flammation: state of the art, definitions and terms
TLDR
A consensus report was needed that addresses the rapid progress in this emerging field and details how the specific study of resolution of acute inflammation provides leads for novel anti‐inflammatory therapeutics, as well as defines the terms and key components of interest in the resolution process within tissues as appreciated today. Expand
Thrombospondin cooperates with CD36 and the vitronectin receptor in macrophage recognition of neutrophils undergoing apoptosis.
TLDR
Newly defined roles for TSP and CD36 in phagocytic clearance of senescent neutrophils, which may limit inflammatory tissue injury and promote resolution are indicated. Expand
Cyclin-dependent kinase inhibitors enhance the resolution of inflammation by promoting inflammatory cell apoptosis
TLDR
It is shown that the CDK inhibitor R-roscovitine markedly enhances resolution of established neutrophil-dependent inflammation in carrageenan-elicited acute pleurisy, bleomycin-induced lung injury, and passively induced arthritis in mice. Expand
Inhibition of apoptosis and prolongation of neutrophil functional longevity by inflammatory mediators
TLDR
Inhibition of apoptosis of aging neutrophil populations was associated with prolongation of the functional life span of the population as assessed by the ability of neutrophils to spread on glass surfaces, to polarize in response to deliberate stimulation with N‐formyl‐Met‐Leu‐Phe, and to release the granule enzyme marker myeloperoxidase on fMLP stimulation. Expand
Extracellular matrix proteins protect small cell lung cancer cells against apoptosis: A mechanism for small cell lung cancer growth and drug resistance in vivo
TLDR
It is shown here that SCLC is surrounded by an extensive stroma of extracellular matrix (ECM) at both primary and metastatic sites, which enhances tumorigenicity and confers resistance to chemotherapeutic agents as a result of β1 integrin-stimulated tyrosine kinase activation suppressing chemotherapy-induced apoptosis. Expand
NF-κB Activation Is a Critical Regulator of Human Granulocyte Apoptosis in Vitro*
  • C. Ward, E. Chilvers, +5 authors Adriano G. Rossi
  • Biology, Medicine
  • The Journal of Biological Chemistry
  • 12 February 1999
TLDR
Light is shed on the biochemical and molecular mechanisms regulating human granulocyte apoptosis and, in particular, on the transcription factor NF-κB, which plays a crucial role in regulating the physiological cell death pathway in granulocytes. Expand
Granulocyte apoptosis and its role in the resolution and control of lung inflammation.
  • C. Haslett
  • Medicine
  • American journal of respiratory and critical care…
  • 1 November 1999
TLDR
Although it had been assumed that extravasated neutrophils disintegrated (undergo necrosis) in situ, this work has demonstrated an alternative fate, whereby the cell undergoes apoptosis, a process that has different implications for the control of inflammation. Expand
Interleukin-8 and development of adult respiratory distress syndrome in at-risk patient groups
TLDR
Evidence is provided of a relation between the presence of interleukin-8 in early BAL samples and the development of ARDS, which reinforces the likely importance of neutrophils and the effects of their accumulation and activation in the pathogenesis of many cases of AR DS. Expand
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