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Apoptosis in human polymorphonuclear leukocytes: Searching for a genetic roadmap

100%

Kobayashi S. D., DeLeo F. R.

Archivum Immunologiae et Therapiae Experimentalis

2003

vol. 51

issue 1

1-8

Polymorphonuclear leukocytes (PMNs or neutrophils) are essential components of the innate immune system in humans and function primarily to eliminate invading microorganisms. Neutrophil influx to sites of infection is desirable because it also initiates an inflammatory response. Paradoxically, PMNs are also intimately associated with inflammatory disease. As part of normal neutrophil turnover in humans and to limit inflammatory potential, PMNs undergo programmed cell death or apoptosis. Several host factors, including cytokines and growth factors, are capable of extending neutrophil survival, and thus capacity to fight infection. On the other hand, phagocytosis of bacterial pathogens generally accelerates PMN apoptosis. Due in part to the extensive complexity of programmed cell death, relatively little is known about signaling pathways that govern these processes in PMNs. Recently, microarray strategies have been employed to gain an understanding of these processes in activated PMNs, and new evidence indicates that gene transcription is important in the regulation of neutrophil apoptosis and thus inflammation. A series of provocative discoveries led to the hypothesis that neutrophil programmed cell death is the result of an apoptosis differentiation program, a final stage of transcriptionally regulated PMN maturation or hematopoietic differentiation. Further characterization of the apoptosis differentiation program and associated biochemical pathways in mature PMNs will likely yield important insights into the resolution of inflammation and infection.

Neutrophils in the innate immune response

81%

Kobayash S. D., Voyich J. M., Burlak C., DeLeo F. R.

Archivum Immunologiae et Therapiae Experimentalis

2005

vol. 53

issue 6

505-517

Polymorphonuclear leukocytes (PMNs or neutrophils) are an essential component of the human innate immune system. Circulating neutrophils are rapidly recruited to sites of infection by host- and/or pathogen-derived components, which also prime these host cells for enhanced microbicidal activity. PMNs bind and ingest microorganisms by a process known as phagocytosis, which typically triggers production of reactive oxygen species and the fusion of cytoplasmic granules with pathogen-containing vacuoles. The combination of neutrophil reactive oxygen species and granule components is highly effective in killing most bacteria and fungi. Inasmuch as PMNs are the most abundant type of leukocyte in humans and contain an arsenal of cytotoxic compounds that are non-specific, neutrophil homeostasis must be highly regulated. To that end, constitutive PMN turnover is regulated by apoptosis, a process whereby these cells shut down and are removed safely by macrophages. Notably, apoptosis is accelerated following phagocytosis of bacteria, a process that appears important for the resolution of infection and inflammation. This review provides a general overview of the role of human neutrophils in the innate host response to infection and summarizes some of the recent advances in neutrophil biology.

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2 Archivum Immunologiae et Therapiae Experimentalis

1 2005

1 2003

2 DeLeo F. R.

1 Burlak C.

1 Kobayash S. D.

1 Kobayashi S. D.

1 Voyich J. M.

Search results

Apoptosis in human polymorphonuclear leukocytes: Searching for a genetic roadmap

Neutrophils in the innate immune response