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Updated: Feb 10, 2026
Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
Chlamydia pneumoniae-induced tumour necrosis factor alpha responses are lower in children with asthma compared with
Tamar Anne Smith-Norowitz1, Kobkul Chotikanatis1, Diana Weaver1
1Department of Pediatrics, Division of Infectious Diseases, State University of New York Downstate Medical Center, Brooklyn, New York, USA.
Insights
Patients with asthma show lower tumor necrosis factor alpha (TNF-α) responses to Chlamydia pneumoniae infection. Antibiotics like ciprofloxacin, azithromycin, and doxycycline partially restored TNF-α levels in asthma patients.
Area of Science:
- Immunology
- Infectious Diseases
- Respiratory Medicine
Background:
- Chlamydia pneumoniae infection is linked to asthma pathogenesis.
- Impaired innate immune responses, specifically cytokine production, may contribute to asthma.
- Tumor necrosis factor alpha (TNF-α) is a key monocyte cytokine that may inhibit C. pneumoniae.
Purpose of the Study:
- To investigate TNF-α responses in C. pneumoniae-infected peripheral blood mononuclear cells (PBMCs) from asthma patients and non-asthma controls.
- To determine if antibiotics (ciprofloxacin, azithromycin, doxycycline) affect TNF-α responses in this context.
Main Methods:
- PBMCs from pediatric asthma patients (n=19) and non-asthma controls (n=6) were infected with C. pneumoniae.
- Cells were cultured with or without antibiotics (ciprofloxacin, azithromycin, doxycycline) for 48 hours.
- TNF-α levels in supernatants were quantified using ELISA.
Main Results:
- Asthma patients exhibited significantly lower TNF-α levels upon C. pneumoniae infection compared to non-asthma controls.
- Baseline TNF-α levels (without infection) were similar between groups.
- Antibiotic treatment (ciprofloxacin, azithromycin, doxycycline) increased TNF-α levels in infected PBMCs from asthma patients, an effect not seen in non-asthma controls.
Conclusions:
- Distinct differences exist in TNF-α production by C. pneumoniae-infected PBMCs between asthma and non-asthma individuals.
- Antibiotics may modulate the inflammatory response in C. pneumoniae-infected asthma patients.
Introduction:
Chlamydia pneumoniae respiratory tract infection has been implicated in the pathogenesis of reactive airway disease and asthma. Innate cytokine responses that are protective of infection with intracellular pathogens may be impaired in patients with asthma. Tumour necrosis factor alpha (TNF-α) is a cytokine related to functions of monocytes and may inhibit C. pneumoniae infection. We investigated TNF-α responses in C. pneumoniae-infected peripheral blood mononuclear cells (PBMCs) in patients with asthma and non-asthma, and whether ciprofloxacin, azithromycin or doxycycline affects TNF-α responses.
Methods:
PBMC (1.5×106) from paediatric patients with asthma (n=19) and non-asthmatic controls (n=6) were infected or mock infected for 1 hour with or without C. pneumoniae AR-39 at a multiplicity of infection=0.1, and cultured+ciprofloxacin, azithromycin or doxycycline (0.1 ug/mL) for 48 hours. TNF-α levels were measured in supernatants by ELISA.
Results:
When PBMC from patients with asthma were infected with C. pneumoniae, levels of TNF-α were significantly lower than in subjects without asthma (48 hours) (5.5±5.6, 38.4±53.7; p=0.0113). However, baseline responses (no infection with C. pneumoniae) were similar in asthma and non-asthma (1.0±1.7, 1.1±1.2; p=0.89). When PBMC frompatiens with asthma were infected with C. pneumoniae+ciprofloxacin, azithromycin or doxycycline, TNF-α levels increased (25%-45%); this affect was not observed in PBMC from patients without asthma.
Conclusions:
We identified differences in the quantity of TNF-α produced by C. pneumoniae-infected PBMC in asthma compared with non-asthma.
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