Related Experiment Video
Updated: Mar 29, 2026
Culturing of Human Nasal Epithelial Cells at the Air Liquid Interface
Published on: October 8, 2013
Bactericidal antibiotics promote reactive oxygen species formation and inflammation in human sinonasal epithelial
Michael A Kohanski1, Anuj Tharakan1, Andrew P Lane1
1Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD.
Background:
Bactericidal antibiotics have been shown to stimulate reactive oxygen species (ROS) formation in mammalian cells through mitochondrial dysfunction. This results in oxidative tissue damage that may have negative consequences for long-term antibiotic use. Antibiotics are widely and heavily used in the treatment of acute and chronic sinusitis; however, the relationship between antibiotics and ROS formation in sinonasal epithelial cells (SNECs) has not yet been demonstrated.
Methods:
Human SNECs were collected from patients during endoscopic sinus surgery and grown in culture at the air-liquid interface. Differentiated SNECs were stimulated with the bactericidal antibiotics amoxicillin and levofloxacin and the bacteriostatic antibiotic clarithromycin for 24 hours. ROS were quantified via fluorescence. Cell death was quantified by lactate dehydrogenase (LDH) secretion. Expression of inflammatory markers such as tumor necrosis factor α (TNF-α) and nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidant genes were measured by real-time polymerase chain reaction (RT-PCR).
Results:
Cultured SNECs treated with the bactericidal antibiotics amoxicillin and levofloxacin resulted in a significant increase in production of ROS (p < 0.05) and secretion of LDH (p < 0.05). The increase in ROS formation correlated with an increase in expression of Nrf2-mediated antioxidant genes as well as the expression and production of proinflammatory cytokine TNF-α, and interleukin 1 β (IL-1β) (p < 0.05). SNECs treated with clarithromycin did not demonstrate statistically significant increases in ROS or proinflammatory cytokine production.
Conclusion:
In this study, we show that treatment of cultured human SNECs with bactericidal antibiotics leads to formation of ROS with an associated increase in inflammatory and antioxidant gene expression and cell death. This suggests that long-term or inappropriate antibiotic use in the treatment of sinusitis may result in oxidative tissue damage to the sinonasal epithelium. Future studies will explore the clinical implications of such damage to the sinonasal epithelium.
Insights
Bactericidal antibiotics like amoxicillin increase reactive oxygen species (ROS) and inflammation in sinonasal cells, potentially causing oxidative damage. This highlights risks of long-term antibiotic use for sinusitis.
Area of Science:
- Otolaryngology
- Cell Biology
- Pharmacology
Background:
- Bactericidal antibiotics can induce reactive oxygen species (ROS) via mitochondrial dysfunction, leading to oxidative damage.
- This oxidative stress has potential negative implications for prolonged antibiotic therapy.
- The effect of antibiotics on ROS in sinonasal epithelial cells (SNECs) remains underexplored.
Purpose of the Study:
- To investigate the impact of bactericidal and bacteriostatic antibiotics on ROS production in cultured human SNECs.
- To assess the correlation between antibiotic-induced ROS and inflammatory/antioxidant gene expression and cell death in SNECs.
Main Methods:
- Human SNECs were cultured at the air-liquid interface.
- Cells were exposed to amoxicillin, levofloxacin (bactericidal), or clarithromycin (bacteriostatic) for 24 hours.
- ROS production, cell death (LDH), and expression of TNF-α and Nrf2-mediated genes were quantified.
Main Results:
- Bactericidal antibiotics (amoxicillin, levofloxacin) significantly increased ROS production and LDH secretion in SNECs (p < 0.05).
- Increased ROS correlated with elevated expression of antioxidant genes and pro-inflammatory cytokines (TNF-α, IL-1β) (p < 0.05).
- Clarithromycin (bacteriostatic) did not cause significant increases in ROS or inflammation.
Conclusions:
- Bactericidal antibiotics induce ROS formation, inflammation, and cell death in cultured human SNECs.
- This suggests potential oxidative tissue damage in the sinonasal epithelium from long-term or inappropriate antibiotic use for sinusitis.
- Further research is needed to clarify the clinical significance of these findings for sinonasal health.
More Related Videos
07:36Contact-Free Co-Culture Model for the Study of Innate Immune Cell Activation During Respiratory Virus Infection
Published on: February 28, 2021
09:02Infection of Primary Nasal Epithelial Cells Grown at an Air-Liquid Interface to Characterize Human Coronavirus-Host Interactions
Published on: September 22, 2023
Related Concept Videos
01:29Microbiota of the Respiratory Tract
01:31Defense Against Bacterial Pathogens
Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...
01:30Epistaxis
Etiology
Possible causes of this condition include high blood pressure, trauma, low humidity, upper respiratory tract infections, allergies, foreign bodies, nasal inhalation of corticosteroids or illicit drugs, excessive use of decongestant nasal sprays, facial or nasal surgery, anatomic malformation, tumors, or systemic...
01:25Clinical Significance of Antibiotic Resistance
01:16Drugs Used in Upper Respiratory Disorders: Overview
Antihistamines (e.g., Benadryl) block histamines from binding. Histamines are chemicals released during an allergic reaction in the body. As a...
01:25Mechanism of Antibiotic Resistance in MRSA