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Updated: Jun 12, 2026

A Neonatal Imaging Model of Gram-Negative Bacterial Sepsis
Published on: August 12, 2020
Neonatal neutrophils with prolonged survival secrete mediators associated with chronic inflammation
Caroline N Nguyen1, Patricia M Schnulle, Nasser Chegini
1Department of Pediatrics, University of Florida, Gainesville, Fla, USA.
Background:
The resolution of inflammation involves the efficient removal of apoptotic neutrophils (PMN). However, a subpopulation of PMN that are resistant to apoptosis may contribute to PMN persistence in tissues, an early hallmark of chronic inflammation. We previously made observations that neonatal PMN with prolonged survival had augmented expression of CD18/CD11b, an adhesion molecule critical to inflammation.
Objectives:
The objectives of this study were to test the hypothesis that surviving neonatal PMN retain the capacity to secrete key mediators associated with chronic inflammation.
Methods:
We profiled cytokine and chemokine secretion patterns of lipopolysaccharide (LPS)-stimulated neonatal and adult PMN using multicytokine array and ELISA.
Results:
We observed that surviving 24-hour neonatal PMN stimulated with LPS had enhanced secretion of interleukin (IL)-8, a chemokine involved in PMN activation and recruitment. In addition, 24-hour neonatal PMN secreted levels of monocyte inhibitory protein (MIP)-1β that were higher than those secreted by 0-hour PMN, but amounts of IL-1 receptor antagonist (IL-1Ra) were lower.
Conclusions:
The results of the present study extend previous observations of augmented function in surviving neonatal neutrophils, and further suggest their potential contribution to the pathogenesis of inflammatory disorders in neonates.
Insights
Neonatal neutrophils resistant to apoptosis may drive chronic inflammation. Surviving neonatal neutrophils show enhanced secretion of key inflammatory mediators like IL-8, suggesting a role in neonatal inflammatory disorders.
Area of Science:
- Immunology
- Neonatal Medicine
- Inflammation Research
Background:
- Neutrophil (PMN) apoptosis is crucial for inflammation resolution.
- Persistent PMN due to impaired apoptosis contributes to chronic inflammation.
- Neonatal PMN exhibit prolonged survival and augmented CD18/CD11b expression.
Purpose of the Study:
- To test if surviving neonatal PMN secrete mediators linked to chronic inflammation.
- Investigate the inflammatory potential of long-lived neonatal neutrophils.
Main Methods:
- Lipopolysaccharide (LPS) stimulation of neonatal and adult PMN.
- Cytokine and chemokine profiling using multicytokine arrays and ELISA.
Main Results:
- LPS-stimulated surviving neonatal PMN showed enhanced IL-8 secretion.
- Neonatal PMN exhibited increased MIP-1β and decreased IL-1Ra secretion compared to 0-hour PMN.
Conclusions:
- Surviving neonatal neutrophils display augmented inflammatory mediator secretion.
- These findings suggest a role for neonatal PMN in the pathogenesis of neonatal inflammatory diseases.
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