Asthmatic Children Have Increased Specific Anti–Mycoplasma pneumoniae IgM but not IgG or IgE—Values Independent of History of Respiratory Tract Infection

Smith‐Norowitz, Tamar A.; Silverberg, Jonathan I.; Kusonruksa, Melanie; Weaver, Diana; Ginsburg, David; Norowitz, Kevin B.; Durkin, Helen G.; Hammerschlag, Margaret R.; Bluth, Martin H.; Kohlhoff, Stephan

doi:10.1097/inf.0b013e3182862ea8

Cited by 23 publications

(16 citation statements)

References 20 publications

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“…Following M. pneumoniae infection, the IgM level has been shown to markedly increase in normal children, which usually occurred 7–14 days following infection, peaked in weeks 3–4 and persisted for months (51). M. pneumoniae infection can cause an increase in the level of total IgE in the serum, whereas delayed-type and anaphylactic-type allergic reactions induce asthma as an immediate reaction and delayed-phase reaction or a dual-phase reaction, which induce the IgE-mediated airway inflammation and airway hyper-reactivity (52). However, there is no direct evidence that M. pneumoniae is the direct cause of asthma.…”

Section: Humoral Immune Damagementioning

confidence: 99%

Insights into the pathogenesis of Mycoplasma pneumoniae

Liu

et al. 2016

Molecular Medicine Reports

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Mycoplasma are the smallest prokaryotic microbes present in nature. These wall-less, malleable organisms can pass through cell filters, and grow and propagate under cell-free conditions in vitro. Of the pathogenic Mycoplasma Mycoplasma pneumoniae has been examined the most. In addition to primary atypical pneumonia and community-acquired pneumonia with predominantly respiratory symptoms, M. pneumoniae can also induce autoimmune hemolytic anemia and other diseases in the blood, cardiovascular system, gastrointestinal tract and skin, and can induce pericarditis, myocarditis, nephritis and meningitis. The pathogenesis of M. pneumoniae infection is complex and remains to be fully elucidated. The present review aimed to summarize several direct damage mechanisms, including adhesion damage, destruction of membrane fusion, nutrition depletion, invasive damage, toxic damage, inflammatory damage and immune damage. Further investigations are required for determining the detailed pathogenesis of M. pneumoniae.

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Section: Humoral Immune Damagementioning

confidence: 99%

Insights into the pathogenesis of Mycoplasma pneumoniae

Liu

et al. 2016

Molecular Medicine Reports

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“…71 In another cross-sectional study, asymptomatic asthmatic patients had higher acquisition rates, as measured by reverse transcriptase-PCR, of M pneumoniae (45%) and Chlamydia pneumoniae (13%), than nonasthmatic persons (9% and 0%, respectively). 72 The potential negative impact of Th2-biased response on immunity has been further demonstrated for leishmaniasis, 73 toxoplasmosis, 74 schistosomiasis, 75 and candidiasis.…”

Section: Effect Of Atopic Conditions On the Risk Of Microbial Infectionsmentioning

confidence: 94%

“…72 The potential negative impact of Th2-biased response on immunity has been further demonstrated for leishmaniasis, 73 toxoplasmosis, 74 schistosomiasis, 75 and candidiasis. 76 If patients with asthma and other atopic conditions have normal IgM responses to exposure to microbial organisms (eg, as evidence for mycoplasma infection 71 ) but suboptimal IgG response as discussed in the mechanism section, these data may suggest some impairment in the immune pathways post-IgM production by B-cells (e.g., impairment in isoclass switching, postswitch defect, or a more rapid waning of humoral immunity).…”

Section: Effect Of Atopic Conditions On the Risk Of Microbial Infectionsmentioning

confidence: 99%

Risks for infection in patients with asthma (or other atopic conditions): Is asthma more than a chronic airway disease?

Juhn¹

2014

Journal of Allergy and Clinical Immunology

128

124

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Most of the research effort regarding asthma has been devoted to its causes, therapy, and prognosis. There is also evidence that the presence of asthma can influence patients’ susceptibility to infections, yet research in this aspect of asthma has been limited. There is additional debate in this field, with current literature tending to view the increased risk of infection among atopic patients as due to opportunistic infections secondary to airway inflammation, especially in severe atopic diseases. Other evidence, however, suggests that such risk and its underlying immune dysfunction may be a phenotypic or clinical feature of atopic conditions. This review argues that 1) improved understanding of the effects of asthma or other atopic conditions on the risk of microbial infections will bring important and new perspectives to clinical practice, research, and public health concerning atopic conditions and that 2) research efforts into the causes and effects of asthma must be juxtaposed because they are likely to guide each other.

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“…2 Previous studies have shown that individuals with asthma have an increased risk of serious and common infections of the respiratory tract, such as invasive pneumococcal diseases, 3,4 Streptococcus pyogenes , 5 Bordetella pertussis , 6 Staphylococcus aureus , 7 otitis media, 7 otitis media, 8 and Mycoplasma pneumoniae. 9 and adaptive immunity, 10 which may partly explain this increased propensity for infection. A recent review has posited that asthma may be more than a just a chronic airway disease as asthma also appears to possess features characteristic of systemic immune dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Asthma and Risk of Appendicitis in Children: A Population-Based Case-Control Study

Hasassri

Jackson

Ghawi

et al. 2017

Academic Pediatrics

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Objective To assess whether asthma is associated with risk of appendicitis in children. Methods We used a population-based case-control study design utilizing a comprehensive medical record review and predetermined criteria for appendicitis and asthma. All children (age<18 years) who resided in Olmsted County, Minnesota, and developed appendicitis between 2006 and 2012 were matched to controls (1:1) with regard to birthday, gender, registration date, and index date. Asthma status was ascertained using predetermined criteria. Active (current) asthma was defined as the presence of asthma symptoms or asthma-related events (eg, medication use, clinic visits, emergency department, or hospitalization) within one year prior to the index date. Inactive asthma was defined as subjects without these events. A conditional logistic regression model was used. Results Among the 309 appendicitis cases identified, when stratified by asthma status, active asthma was associated with significantly increased risk of appendicitis when compared to inactive asthma (OR=2.48; 95% CI, 1.22–5.03) and to no asthma (OR=1.88; 95% CI, 1.07–3.27) (overall p-value=0.035). When controlling for potential confounders such as gender, age, and smoking status, active asthma was associated with a higher odds of developing appendicitis compared to non-asthmatics (adjusted OR=1.75, 95% CI 0.99–3.11) whereas inactive asthma was not (overall p-value=0.049). Tobacco smoke exposure within three months was associated with an increased risk of appendicitis (adjusted OR=1.66; 95% CI, 1.02, 2.69). Among asthma medications, leukotriene receptor antagonists reduced the risk of appendicitis (OR=0.18; 95% CI, 0.04–0.74). Conclusions Active asthma may be an unrecognized risk factor for appendicitis in children while a history of inactive asthma does not pose such risk. Further investigation exploring the underlying mechanisms is warranted.

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Asthmatic Children Have Increased Specific Anti–Mycoplasma pneumoniae IgM but not IgG or IgE—Values Independent of History of Respiratory Tract Infection

Abstract: Increased specific IgM anti-M. pneumoniae responses may indicate an important role for M. pneumoniae infection in asthma.

Cited by 23 publications

References 20 publications

Insights into the pathogenesis of Mycoplasma pneumoniae

Insights into the pathogenesis of Mycoplasma pneumoniae

Risks for infection in patients with asthma (or other atopic conditions): Is asthma more than a chronic airway disease?

Asthma and Risk of Appendicitis in Children: A Population-Based Case-Control Study

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