Association of Mycoplasma pneumoniae antigen with initial onset of bronchial asthma.

Wilsher, Margaret; Kolbe, J.

doi:10.1164/ajrccm.151.2.7842224

Cited by 6 publications

(3 citation statements)

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“…Mycoplasma pneumoniae has long been appreciated as a trigger for acute asthmatic attacks (Seggev et al, 1986;Leibowitz et al, 1988;Lieberman et al, 2003;Biscardi et al, 2004) and some studies have shown that the organism can be isolated in higher prevalence from asthmatics (Esposito et al, 2000;Teig et al, 2005). In addition, some studies and case reports document the initial onset of asthma following M. pneumoniae infection (Petrovsky, 1990;Yano et al, 1994;Wilsher & Kolbe, 1995;Biscardi et al, 2004). Follow-up studies in children have demonstrated prolonged airway dysfunction that can persist for years, perhaps consistent with a persistent infection.…”

Section: Role Of M Pneumoniae In Chronic Asthmamentioning

confidence: 99%

Epidemiology, clinical manifestations, pathogenesis and laboratory detection ofMycoplasma pneumoniaeinfections: Figure 1

2008

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Since its initial description in the 1940s and eventual elucidation as a highly evolved pathogenic bacterium, Mycoplasma pneumoniae has come to be recognized as a worldwide cause of primary atypical pneumonia. Beyond its ability to cause severe lower respiratory illness and milder upper respiratory symptoms it has become apparent that a wide array of extrapulmonary infectious and postinfectious events may accompany the infections in humans caused by this organism. Autoimmune disorders and chronic diseases such as asthma and arthritis are increasingly being associated with this mycoplasma, which frequently persists in individuals for prolonged periods. The reductive evolutionary process that has led to the minimal genome of M. pneumoniae suggests that it exists as a highly specialized parasitic bacterium capable of residing in an intracellular state within the respiratory tissues, occasionally emerging to produce symptoms. This review includes discussion of some of the newer aspects of our knowledge on this pathogen, characteristics of clinical infections, how it causes disease, the recent emergence of macrolide resistance, and the status of laboratory diagnostic methods.

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Section: Role Of M Pneumoniae In Chronic Asthmamentioning

confidence: 99%

Epidemiology, clinical manifestations, pathogenesis and laboratory detection ofMycoplasma pneumoniaeinfections: Figure 1

2008

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“…However, bronchial asthma patients often exhibit AHR following infection with bacteria or viruses (38). It is wellknown evidence that infection with Mycoplasma pneumoniae or influenza A often induces asthma-like AHR even in the nonallergic patients (39)(40)(41). Therefore, it is very important to reveal the mechanism of how these infections exacerbates bronchial asthma independently of Ag.…”

Section: Discussionmentioning

confidence: 99%

Contribution of IL-18-induced innate T cell activation to airway inflammation with mucus hypersecretion and airway hyperresponsiveness

Ishikawa¹,

Yoshimoto²,

Nakanishi³

2006

International Immunology

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Human bronchial asthma is characterized by airway hyperresponsiveness (AHR), eosinophilic airway inflammation, mucus hypersecretion and high serum level of IgE. IL-18 was originally regarded to induce T(h)1-related cytokines from Th1 cells in the presence of IL-12. However, our previous reports clearly demonstrated that IL-18 with IL-2 promotes Th2 cytokines production from T cells and NK cells. Furthermore, IL-18 with IL-3 stimulates basophils and mast cells to produce Th2 cytokines. Thus, we examined the capacity of IL-2 and IL-18 to induce AHR, airway eosinophilic inflammation and goblet cell metaplasia. Intranasal administration of IL-2 and IL-18 induces AHR, mucus hypersecretion and eosinophilic inflammation in the lungs of naive mice. CD4+ T cells are prerequisite for this IL-2 plus IL-18-induced bronchial asthma, because CD4+ T cells-depleted or Rag-2-deficient (Rag-2-/-) mice did not develop bronchial asthma after IL-2 plus IL-18 treatment. Both STAT6-/- mice and IL-13-neutralized wild-type mice failed to develop AHR, goblet cell metaplasia and airway eosinophilic inflammation, while IL-4-/- mice almost normally developed, suggesting that IL-13 is a major causative factor and IL-4 mainly enhances the degree of AHR and eosinophilic inflammation. Both IL-4 and IL-13 equally induce eotaxin in mouse embryonic fibroblasts. However, only IL-13 blockade inhibited asthma symptoms, suggesting that IL-13 but not IL-4 is produced abundantly and plays a critical role in the pathogenesis of bronchial asthma in this model. As airway epithelial cells store robust IL-18, IL-18 might be critically involved in pathogen-induced bronchial asthma, in which pathogens stimulate epithelial cells to produce IL-18 without IL-12 induction.

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“…In addition to its role as a cause of community-acquired pneumonia, M. pneumoniae is also known to trigger acute asthmatic exacerbations 5,6,78.…”

Section: Introductionmentioning

confidence: 99%

Serial Changes in Serum Eosinophil-associated Mediators between Atopic and Non-atopic Children afterMycoplasma pneumoniaepneumonia

Kim

Cho

Moon

et al. 2014

Allergy Asthma Immunol Res

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PurposeMycoplasma pneumoniae pneumonia (MP) is associated with the exacerbation, timing, and onset of asthma. The goal of this study was to elucidate the impact of MP on eosinophil-related hyper-reactive amplification in atopic children.MethodsWe studied 48 patients with MP (26 atopic, 22 non-atopic), between 3 and 12 years of age. Serial changes in blood eosinophil counts, serum interleukin-5 (IL-5), and serum eosinophil cationic protein (ECP) levels were measured in atopic and non-atopic children with MP upon admission, recovery, and at 2 months post-recovery. Serum IL-5 and ECP levels were measured by enzyme-linked immunosorbent assays; eosinophil counts were measured using an autoanalyzer.ResultsSerial changes in serum IL-5, ECP, and total eosinophil counts were significantly higher in atopic patients, relative to non-atopic controls (P≤0.001). Serum IL-5 and ECP levels were significantly higher in atopic patients at all three time points tested, while eosinophil counts were higher in the clinical recovery and follow-up phases, but not in the acute phase. Furthermore, among atopic patients, serum ECP levels were significantly higher in the recovery and follow-up phases than in the acute phase.ConclusionsThe present study demonstrated significant differences in eosinophil counts, serum IL-5, and serum ECP levels between atopic and non-atopic children with MP at admission, recovery, and 2 months after clinical recovery. These outcomes are suggestive of eosinophil-related hyperreactivity in atopic children, with this status maintained for at least 2 months after MP.

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Association of Mycoplasma pneumoniae antigen with initial onset of bronchial asthma.

Cited by 6 publications

References 0 publications

Epidemiology, clinical manifestations, pathogenesis and laboratory detection ofMycoplasma pneumoniaeinfections: Figure 1

Epidemiology, clinical manifestations, pathogenesis and laboratory detection ofMycoplasma pneumoniaeinfections: Figure 1

Contribution of IL-18-induced innate T cell activation to airway inflammation with mucus hypersecretion and airway hyperresponsiveness

Serial Changes in Serum Eosinophil-associated Mediators between Atopic and Non-atopic Children afterMycoplasma pneumoniaepneumonia

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