Role of Chemokines in the Pathogenesis of Acute Lung Injury
Open accessAbstract
Acute lung injury (ALI) is due to an uncontrolled systemic inflammatory response resulting from direct injury to the lung or indirect injury in the setting of a systemic process. Such insults lead to the systemic inflammatory response syndrome (SIRS), which includes activation of leukocytes—alveolar macrophages and sequestered neutrophils—in the lung. Although systemic inflammatory response syndrome is a physiologic response to an insult, systemic leukocyte activation, if excessive, can lead to end organ injury, such as ALI. Excessive recruitment of leukocytes is critical to the pathogenesis of ALI, and the magnitude and duration of the inflammatory process may ultimately determine the outcome in patients with ALI. Leukocyte recruitment is a well orchestrated process that depends on the function of chemokines and their receptors. Understanding the mechanisms that contribute to leukocyte recruitment in ALI may ultimately lead to the development of effective therapeutic strategies.
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Severe COVID-19 patients commonly develop Acute Respiratory Distress Syndrome, characterized by inflammatory injury to the alveoli-capillary membrane, leading to lung over-permeability and increased pulmonary edema fluid into the airspaces, resulting in lack of respiratory capacity.
“Severe COVID-19 patients commonly develop the Acute Respiratory Distress Syndrome [38], which is characterized by inflammatory injury to the alveoli–capillary membrane, leading to lung over-permeability and increased pulmonary edema fluid into the airspaces, resulting in the lack of respiratory capacity [39].”
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [39]
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References 114 · Cited by 274
- Authors
- Bhatia, M., Zemans, R. L., & Jeyaseelan, S.
- Affiliations
- University of Otago (NZ)
- National Jewish Health (US)
- Louisiana State University (US)
- Corresponding author
- Bhatia, Madhav
- Venue
- American Journal of Respiratory Cell and Molecular Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2012-05-01
- Volume
- 46
- Issue
- 5
- Pages
- 566-572
- ISSN
- 1044-1549 (ISSN-L)
- 1535-4989
- PMC
- PMC3361356
- OpenAlex
- W2106398910
- Cited by
- 274
- References
- 114
- Citations by year
- 2026: 18 · 2025: 22 · 2024: 18 · 2023: 29 · 2022: 33 · 2021: 34 · 2020: 21 · 2019: 17 · 2018: 16 · 2017: 14 · 2016: 7 · 2015: 18 · 2014: 12 · 2013: 10 · 2012: 4
- FWCI
- 1.45
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- American Journal of Respiratory Cell and Molecular Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Flight Attendant Medical Research Institute
- University of Otago
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL091958, K08HL103772)
- Topics
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory Support and Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Keywords
- acute lung injury, chemokines, chemokine receptors, leukocyte recruitment, systemic inflammatory response syndrome, alveolar macrophages, neutrophils, leukocyte activation, lung inflammation
- MeSH terms
- Humans, Lymphocyte Activation, Macrophage Activation, Chemokines, Receptors, Chemokine, Acute Lung Injury
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