The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Pathophysiological roles of interleukin-8/CXCL8 in pulmonary diseases
Abstract
Fifteen years have passed since the first description of interleukin (IL)-8/CXCL8 as a potent neutrophil chemotactic factor. Accumulating evidence has demonstrated that various types of cells can produce a large amount of IL-8/CXCL8 in response to a wide variety of stimuli, including proinflammatory cytokines, microbes and their products, and environmental changes such as hypoxia, reperfusion, and hyperoxia. Numerous observations have established IL-8/CXCL8 as a key mediator in neutrophil-mediated acute inflammation due to its potent actions on neutrophils. However, several lines of evidence indicate that IL-8/CXCL8 has a wide range of actions on various types of cells, including lymphocytes, monocytes, endothelial cells, and fibroblasts, besides neutrophils. The discovery of these biological functions suggests that IL-8/CXCL8 has crucial roles in various pathological conditions such as chronic inflammation and cancer. Here, an overview of its protein structure, mechanisms of production, and receptor system will be discussed as well as the pathophysiological roles of IL-8/CXCL8 in various types of lung pathologies.
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Cited by
Bansal, T., Alaniz, R. C., Wood, T. K., & Jayaraman, A. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0906112107 · Cited by 868
Molecular mechanisms of fluoride toxicity
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Mediators of Chronic Obstructive Pulmonary Disease
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A spatially resolved atlas of the human lung characterizes a gland-associated immune niche
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Metadata
- Authors
- Mukaida, N.
- Venue
- American Journal of Physiology-Lung Cellular and Molecular Physiology
- Publisher
- American Physiological Society
- Published
- 2003-04-01
- Volume
- 284
- Issue
- 4
- Pages
- L566-L577
- ISSN
- 1040-0605 (ISSN-L)
- 1522-1504
- OpenAlex
- W2136822492
- Cited by
- 472
- References
- 8
- FWCI
- 8.58
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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