Mycoplasma pneumoniae and Asthma in Children

Biscardi, Sandra; Lorrot, Mathie; Marc, E.; Moulin, F.; Boutonnat-Faucher, Bénédicte; Heilbronner, Claire; Iniguez, Jean-Luc; Chaussain, M; Nicand, Elizabeth; Raymond, Josette; Gendrel, D.

doi:10.1086/392498

Cited by 200 publications

(174 citation statements)

References 31 publications

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“…In the majority of exacerbation studies looking for a wide array of pathogens, the relative proportion of atypical bacteria is rather low. However, M. pneumoniae was identified in 20% of exacerbations in asthmatic children requiring hospitalisation, and in 50% of children experiencing their first asthmatic attack [55]. More recently, atypical infection has been associated with more severe asthma exacerbations, as shown by spirometry and symptom severity scores [56].…”

Section: Infection Among Factors Precipitating Asthma Exacerbationsmentioning

confidence: 99%

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Xepapadaki¹,

Papadopoulos²

2010

Eur Respir J

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Respiratory infections have been implicated in the origin and exacerbation of asthma in a variety of ways; however, systemisation of this knowledge in a way helpful for disease management remains suboptimal.Several conceptual issues need to be taken into account: the fact that the effects of an infection may vary according to genetic background, the current immune status of the host, and parallel environmental stimuli, in addition to the particular infectious agent itself. Moreover, childhood is a very special period because of the continuous processes taking place, such as neural, immune and respiratory maturation.Epidemiological studies have convincingly demonstrated that the majority of asthma exacerbations, in both adults and children, follow viral upper respiratory tract infections. Asthma exacerbations are still often unresponsive to current asthma treatment, and new therapeutic approaches are required.This review presents current knowledge on the associations between infection and exacerbation of established asthma with respect to definitions, epidemiology, mechanisms and treatment.

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Section: Infection Among Factors Precipitating Asthma Exacerbationsmentioning

confidence: 99%

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Xepapadaki¹,

Papadopoulos²

2010

Eur Respir J

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“…Mycoplasma pneumoniae is a human pathogen primarily colonizing the respiratory tract. While the most common clinical manifestations of infection are tracheobronchitis and atypical or "walking" pneumonia (7,12,14,30), recent studies indicate a strong correlation with asthma (5,24,38), and extrapulmonary complications are not uncommon (53). Adherence of M. pneumoniae cells to host respiratory epithelium (cytadherence) is required for colonization and pathogenesis (20) and is mediated largely by a differentiated terminal organelle (9,39).…”

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confidence: 99%

Mutant Analysis Reveals a Specific Requirement for Protein P30 inMycoplasma pneumoniaeGliding Motility

2005

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The cell-wall-less prokaryote Mycoplasma pneumoniae, long considered among the smallest and simplest cells capable of self-replication, has a distinct cellular polarity characterized by the presence of a differentiated terminal organelle which functions in adherence to human respiratory epithelium, gliding motility, and cell division. Characterization of hemadsorption (HA)-negative mutants has resulted in identification of several terminal organelle proteins, including P30, the loss of which results in developmental defects and decreased adherence to host cells, but their impact on M. pneumoniae gliding has not been investigated. Here we examined the contribution of P30 to gliding motility on the basis of satellite growth and cell gliding velocity and frequency. M. pneumoniae HA mutant II-3 lacking P30 was nonmotile, but HA mutant II-7 producing a truncated P30 was motile, albeit at a velocity 50-fold less than that of the wild type. HA-positive revertant II-3R producing an altered P30 was unexpectedly not fully wild type with respect to gliding. Complementation of mutant II-3 with recombinant wild-type and mutant alleles confirmed the correlation between gliding defect and loss or alteration in P30. Surprisingly, fusion of yellow fluorescent protein to the C terminus of P30 had little impact on cell gliding velocity and significantly enhanced HA. Finally, while quantitative examination of HA revealed clear distinctions among these mutant strains, gliding defects did not correlate strictly with the HA phenotype, and all strains attached to glass at wild-type levels. Taken together, these findings suggest a role for P30 in gliding motility that is distinct from its requirement in adherence.Mycoplasmas are cell-wall-less prokaryotes with minimal genomes and limited biosynthetic capabilities, dictating a strict dependence on host species for survival in nature (43). Mycoplasma pneumoniae is a human pathogen primarily colonizing the respiratory tract. While the most common clinical manifestations of infection are tracheobronchitis and atypical or "walking" pneumonia (7,12,14,30), recent studies indicate a strong correlation with asthma (5, 24, 38), and extrapulmonary complications are not uncommon (53). Adherence of M. pneumoniae cells to host respiratory epithelium (cytadherence) is required for colonization and pathogenesis (20) and is mediated largely by a differentiated terminal organelle (9, 39). This well-defined apical structure is a membrane-bound extension of the mycoplasma cell distinguished ultrastructurally by an electron-dense core (4), which is a major constituent of the M. pneumoniae cytoskeleton (17, 35).M. pneumoniae cells exhibit gliding motility, with the terminal organelle always the leading end (6), but details regarding the biological significance and the mechanism of gliding are largely unknown. Although the M. pneumoniae genome has been sequenced and twice annotated (11, 19), close inspection reveals no homology to proteins known to be involved in bacterial motility of any type in walled bact...

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“…It is generally believed that MP closely correlates with the occurrence, development, and deterioration of pediatric asthma (Biscardi et al, 2004;Ou et al, 2008;Varshney et al, 2009;Guilbert and Denlinger, 2010). However, the relationship between MP infection and the pathogenesis of pediatric asthma remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Effects of Mycoplasma pneumoniae infection on airway neurokinin-1 receptor expression in BALB/c mice

Zhang¹,

Wei²,

Shang³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to establish a BALB/c mouse model of Mycoplasma pneumoniae (MP) infection and to explore the expression of neurokinin-1 receptor (NK1-R) in the trachea and lung tissue and changes in its relative content at different time points (on the 3rd, 7th, 14th, 21st, and 30th days after infection) in MP-infected BALB/c mice. Immunohistochemistry and Western blot analysis were performed to determine NK1-R expression in the trachea and lung tissue and changes in relative content in MP-infected BALB/c mice. After MP infection, the expression of NK1-R on the surfaces of upper tracheal and bronchial epithelial cells, submucosa, and alveolar epithelial cells, as well as around the smooth muscle, was upregulated more significantly in the infection group than in the control group (P < 0.05); NK1-R protein expression was enhanced on the 3rd, 7th, 14th, 21st, and 30th days after infection compared with that of the control 8321 ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 13 (4): 8320-8328 (2014) MP infection on airway NK1-R expression in BALB/c mice group (P < 0.05). NK1-R expression in the trachea, bronchus, and lung tissue increased in MP-infected BALB/c mice, which may explain why wheezing occurs after MP infection.

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Mycoplasma pneumoniae and Asthma in Children

Cited by 200 publications

References 31 publications

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Mutant Analysis Reveals a Specific Requirement for Protein P30 inMycoplasma pneumoniaeGliding Motility

Effects of Mycoplasma pneumoniae infection on airway neurokinin-1 receptor expression in BALB/c mice

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