Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 321, Issue 4, Pages L726-L733Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00080.2021
Keywords
LCN2; lipocalin-2; lung inflammation; neutrophil gelatinase-associated lipocalin; NGAL
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Funding
- National Institute of Environmental Health Sciences [R00ES025819]
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Lipocalin-2 (LCN2) functions as an inflammatory mediator with roles in immune response, iron sequestration, cell migration, and apoptosis regulation. Research aims to differentiate between the protective and detrimental roles of LCN2 in immune response to various inflammatory stimuli.
Lipocalin-2 (LCN2) is an inflammatory mediator best known for its role as an innate acute-phase protein. LCN2 mediates the innate immune response to pathogens by sequestering iron, thereby inhibiting pathogen growth. Although LCN2 and its bacteriostatic properties are well studied, other LCN2 functions in the immune response to inflammatory stimuli are less well understood, such as its role as a chemoattractant and involvement in the regulation of cell migration and apoptosis. In the lungs, most studies thus far investigating the role of LCN2 in the immune response have looked at pathogenic inflammatory stimuli. Here, we compile data that explore the role of LCN2 in the immune response to various inflammatory stimuli in an effort to differentiate between protective versus detrimental roles of LCN2.
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