Abstract
This chapter focuses on the repair of environmental injury in normal, full term postnatal lung after exposure to environmental toxicants and compares it to adult lung. 'Repair' is defined as all the processes that are involved in resolving an injury, and includes both cellular and acellular components. Several factors may influence both susceptibility and the capability of the lung to properly repair injury. The alterations seen in repair of the developing lung following exposure to environmental toxicants may be due to a temporary or permanent disruption of the epithelial mesenchymal trophic unit resulting in either an inability to heal the initial wound or disruption of critical morphogenic events. Many factors regulate the repair process following injury by P450-mediated toxicants, including various soluble cytokines and growth factors, interactions with integrins and matrix elements as well as cell-cell interactions. Various studies have demonstrated that when the developing lung does not repair, abnormalities may persist into adulthood. Acute ozone toxicity generates a reversible lesion without a defined long-term pathology but involving a substantial inflammatory cell response. Repair following acute injury is characterized by both proliferation and ciliary regeneration detectable in the surviving cells 24 h after exposure. In case of ozone exposure in adults, the overall response is characterized by a large influx of inflammatory cells into the lung. This influx is predominately neutrophils in the early phase while elevated macrophages persist throughout exposure.
| Original language | English (US) |
|---|---|
| Title of host publication | The Lung: Development, Aging and The Environment |
| Publisher | Elsevier Inc. |
| Pages | 353-362 |
| Number of pages | 10 |
| ISBN (Print) | 9780080481357, 9780123247513 |
| DOIs | |
| State | Published - Dec 3 2003 |
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ASJC Scopus subject areas
- Medicine(all)
Cite this
Repair of Environmental Lung Injury During Development. / Smiley-Jewell, Suzette; Van Winkle, Laura S.
The Lung: Development, Aging and The Environment. Elsevier Inc., 2003. p. 353-362.Research output: Chapter in Book/Report/Conference proceeding › Chapter
}
TY - CHAP
T1 - Repair of Environmental Lung Injury During Development
AU - Smiley-Jewell, Suzette
AU - Van Winkle, Laura S.
PY - 2003/12/3
Y1 - 2003/12/3
N2 - This chapter focuses on the repair of environmental injury in normal, full term postnatal lung after exposure to environmental toxicants and compares it to adult lung. 'Repair' is defined as all the processes that are involved in resolving an injury, and includes both cellular and acellular components. Several factors may influence both susceptibility and the capability of the lung to properly repair injury. The alterations seen in repair of the developing lung following exposure to environmental toxicants may be due to a temporary or permanent disruption of the epithelial mesenchymal trophic unit resulting in either an inability to heal the initial wound or disruption of critical morphogenic events. Many factors regulate the repair process following injury by P450-mediated toxicants, including various soluble cytokines and growth factors, interactions with integrins and matrix elements as well as cell-cell interactions. Various studies have demonstrated that when the developing lung does not repair, abnormalities may persist into adulthood. Acute ozone toxicity generates a reversible lesion without a defined long-term pathology but involving a substantial inflammatory cell response. Repair following acute injury is characterized by both proliferation and ciliary regeneration detectable in the surviving cells 24 h after exposure. In case of ozone exposure in adults, the overall response is characterized by a large influx of inflammatory cells into the lung. This influx is predominately neutrophils in the early phase while elevated macrophages persist throughout exposure.
AB - This chapter focuses on the repair of environmental injury in normal, full term postnatal lung after exposure to environmental toxicants and compares it to adult lung. 'Repair' is defined as all the processes that are involved in resolving an injury, and includes both cellular and acellular components. Several factors may influence both susceptibility and the capability of the lung to properly repair injury. The alterations seen in repair of the developing lung following exposure to environmental toxicants may be due to a temporary or permanent disruption of the epithelial mesenchymal trophic unit resulting in either an inability to heal the initial wound or disruption of critical morphogenic events. Many factors regulate the repair process following injury by P450-mediated toxicants, including various soluble cytokines and growth factors, interactions with integrins and matrix elements as well as cell-cell interactions. Various studies have demonstrated that when the developing lung does not repair, abnormalities may persist into adulthood. Acute ozone toxicity generates a reversible lesion without a defined long-term pathology but involving a substantial inflammatory cell response. Repair following acute injury is characterized by both proliferation and ciliary regeneration detectable in the surviving cells 24 h after exposure. In case of ozone exposure in adults, the overall response is characterized by a large influx of inflammatory cells into the lung. This influx is predominately neutrophils in the early phase while elevated macrophages persist throughout exposure.
UR - http://www.scopus.com/inward/record.url?scp=84942248993&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84942248993&partnerID=8YFLogxK
U2 - 10.1016/B978-012324751-3/50060-7
DO - 10.1016/B978-012324751-3/50060-7
M3 - Chapter
SN - 9780080481357
SN - 9780123247513
SP - 353
EP - 362
BT - The Lung: Development, Aging and The Environment
PB - Elsevier Inc.
ER -