ArticleClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2009
A low dose of Mycoplasma pneumoniae infection enhances an established allergic inflammation in mice: the role of the prostaglandin E2 pathway.
Article in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Glycyrrhizin alleviatesJournal of thoracic disease · 2026Article
- Intermittent hypoxia drives lung microbiome-metabolome remodeling to create a pro-inflammatory landscape in murine OSAHS.Frontiers in microbiology · 2026Article
- Immune dysregulation inFrontiers in immunology · 2026Review
- High-fat diet and palmitic acid amplify airway type 2 inflammation.Frontiers in allergy · 2023Article
- Impact of Therapeutics on Unified Immunity During Allergic Asthma and Respiratory Infections.Frontiers in allergy · 2022Review
- Helicobacter pylori infection increases the risk of adult-onset asthma: a nationwide cohort study.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2017Article
- Changes of serum TNF-α, IL-5 and IgE levels in the patients of mycoplasma pneumonia infection with or without bronchial asthma.International journal of clinical and experimental medicine · 2015Article
- Allergic airway inflammation decreases lung bacterial burden following acute Klebsiella pneumoniae infection in a neutrophil- and CCL8-dependent manner.Infection and immunity · 2014Article
- Mycoplasma pneumoniae CARDS toxin exacerbates ovalbumin-induced asthma-like inflammation in BALB/c mice.PloS one · 2014Article
- Mycoplasma pneumoniae in children with acute and refractory asthma.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2013Article
- Lysophosphatidic acid (LPA) and its receptors: role in airway inflammation and remodeling.Biochimica et biophysica acta · 2013Review
- SPLUNC1 deficiency enhances airway eosinophilic inflammation in mice.American journal of respiratory cell and molecular biology · 2012Article
- Treatment of allergic asthma: modulation of Th2 cells and their responses.Respiratory research · 2011Review
- In vivo function of airway epithelial TLR2 in host defense against bacterial infection.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Developments in the field of allergy in 2009 through the eyes of Clinical and Experimental Allergy.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2010Review
- Effects of atypical infections with Mycoplasma and Chlamydia on asthma.Immunology and allergy clinics of North America · 2010Review
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Authors and funding
4 authors.
Funding
Abstract
backgroundOver 40% of chronic stable asthma patients have evidence of respiratory Mycoplasma pneumoniae (Mp) infection as detected by PCR, but not by serology and culture, suggesting that a low-level Mp is involved in chronic asthma. However, the role of such a low-level Mp infection in the regulation of allergic inflammation remains unknown.
objectiveTo determine the impact of a low-level Mp infection in mice with established airway allergic inflammation on allergic responses such as eosinophilia and chemokine eotaxin-2, and the underlying mechanisms [i.e. the prostaglandin E(2) (PGE(2)) pathway] since PGE(2) inhalation before an allergen challenge suppressed the eosinophil infiltration in human airways.
methodsBALB/c mouse models of ovalbumin (OVA)-induced allergic asthma with an ensuing low- or high-dose Mp were used to assess IL-4 expression, bronchoalveolar lavage (BAL) eosinophil, eotaxin-2 and PGE(2) levels, and lung mRNA levels of microsomal prostaglandin E synthase-1 (mPGES-1). Primary alveolar macrophages (pAMs) from naïve BALB/c mice were cultured to determine whether Mp-induced PGE(2) or exogenous PGE(2) down-regulates IL-4/IL-13-induced eotaxin-2.
resultsLow-dose Mp in allergic mice significantly enhanced IL-4 and eotaxin-2, and moderately promoted lung eosinophilia, whereas high-dose Mp significantly reduced lung eosinophilia and tended to decrease IL-4 and eotaxin-2. Moreover, in both OVA-naïve and allergic mice, lung mPGES-1 mRNA and BAL PGE(2) levels were elevated in mice infected with high-dose, but not low-dose Mp. In pAMs, IL-4/IL-13 significantly increased eotaxin-2, which was reduced by Mp infection accompanied by dose-dependent PGE(2) induction. Exogenous PGE(2) inhibited IL-4/IL-13-induced eotaxin-2 in a dose-dependent manner.
conclusionsThis study highlights a novel concept on how different bacterial loads in the lung modify the established allergic airway inflammation and thus interact with an allergen to further induce Th2 responses. That is, unlike high-level Mp, low-level Mp fails to effectively induce PGE(2) to down-regulate allergic responses (e.g. eotaxin-2), thus maintaining or even worsening allergic inflammation in asthmatic airways.
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