Association between specific IgE to Staphylococcus aureus enterotoxins A and B and asthma control

Tanaka, Akihiko; Suzuki, Shintaro; Ohta, Shin; Manabe, Ryo; Furukawa, Hitomi; Kuwahara, Naota; Fukuda, Yoshihiro; Kimura, Takeshi; Jinno, Megumi; Hirai, Kuniaki; Miyata, Yoshito; Yamaguchi, Munehiro; Homma, Tetsuya; Watanabe, Yoshio; Yamamoto, Masayuki; Yokoe, Takuya; Sagara, Hironori

doi:10.1016/j.anai.2015.06.017

Cited by 32 publications

(28 citation statements)

References 38 publications

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“…12,17 • Early sensitization to multiple allergens, but also molecular allergens, conveys a higher risk of asthma exacerbations. [33][34][35][36][37] • Patients with the persistent eosinophilic phenotype have a greater risk of asthma exacerbations. [33][34][35][36][37] • Patients with the persistent eosinophilic phenotype have a greater risk of asthma exacerbations.…”

Section: Discussionmentioning

confidence: 99%

“…21,22,26,27 • Serum staphylococcal enterotoxin may drive a phenotype of lateonset severe asthma associated with chronic rhinosinusitis and nasal polyps. [33][34][35][36][37] • Patients with the persistent eosinophilic phenotype have a greater risk of asthma exacerbations. 14,[60][61][62]64 • Neutrophilic airway inflammation is uncommon in children with asthma and not stable over time.…”

Section: Discussionmentioning

confidence: 99%

“…Serum staphylococcal enterotoxin (SE)-specific IgE levels have been positively associated with the severity of asthma, 34,35 particularly in late-onset asthma, 36 linked to staphylococcal serine protease-like proteins. 37,38 SE may be driving this phenotype of late-onset severe asthma associated with chronic rhinosinusitis and nasal polyps, and sputum eosinophilia leading to raised SE-IgE and eosinophilic asthma.…”

Section: Staphylococcal Enterotoxins and Severe Asthma Phenotypesmentioning

confidence: 99%

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Clinical phenotypes in asthma during childhood

Just

Bourgoin‐Heck

Amat

2017

Clin Experimental Allergy

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Asthma is a heterogeneous disease characterized by numerous phenotypes relating to age of onset, triggers, comorbidities, severity (assessed by multiple exacerbations, lung function pattern) and finally the inflammatory cells involved in the pathophysiologic pathway. These phenotypes can vary over time in relation to changes in the principal triggers involved in the aetiology of the disease. Nevertheless, in a patient with multiple allergies and early-onset disease (defined as multiple sensitizations and allergic comorbidities), the prognosis of asthma is poor with a high risk of persistence and severity of the disease during childhood. Future research will focus on classifying phenotypes into groups based on pathophysiologic mechanisms (endotypes) and the biomarkers attached to these endotypes, which could predict prognosis and lead to targeted therapy. Currently, these biomarkers are related to inflammatory cells associated with the asthma endotype, essentially eosinophils and neutrophils (and related cytokines) attached to Th-2 and non Th-1 pathways, respectively. The most severe asthma (refractory asthma) is linked to neutrophil-derived inflammation (frequently associated with female sex, obesity and possibly disorganized airway microbiota) encountered in very young children or teenagers. Severe asthma is also linked to or a marked eosinophil inflammatory process (frequently associated with multiple atopy and, more rarely, with non-atopic hypereosinophilic asthma in children) and frequently encountered in teenagers. Severe phenotypes of asthma could also play a role in the origin of chronic obstructive pulmonary disease in adult life.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Staphylococcal Enterotoxins and Severe Asthma Phenotypesmentioning

confidence: 99%

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Clinical phenotypes in asthma during childhood

Just

Bourgoin‐Heck

Amat

2017

Clin Experimental Allergy

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“…Staphylococcus aureus is one of the most common human commensal bacteria found in skin and in nasal and bronchial mucosa. Furthermore, it is the most important pathogen associated with atopic dermatitis (AD), and it is also found in allergic rhinitis and allergic asthma . Eosinophils, the main effector cells of the late and chronic phase of allergic inflammation, are also important in host protection against parasitic, bacterial, and viral infections.…”

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confidence: 99%

sCD48 is anti-inflammatory inStaphylococcus aureusEnterotoxin B-induced eosinophilic inflammation

Gangwar

Levi‐Schaffer

2016

Allergy

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“…87 In a meta-analysis, nasal S aureus colonization was only modestly associated with asthma prevalence (OR 1.19) in the general population or, after adjusting for study bias, among a subset of patients with CRS (OR 1.21). 88 However, patients with detectable specific IgE to SAE were more likely to have severe asthma [89][90][91] as well as reduced lung function and increased airway reversibility to bronchodilation. 92 Taken together, specific IgE to SAE and/or S aureus may be important in CRS pathogenesis and related to comorbid asthma in a select group of patients, but the exact mechanisms for these associations are still unclear.…”

Section: Pathogens and Chronic Rhinosinusitismentioning

confidence: 99%

Sinus Infections, Inflammation, and Asthma

Staudacher

Stevens

2019

Immunology and Allergy Clinics of North America

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KEYWORDSAcute rhinosinusitis Chronic rhinosinusitis Nasal polyp Infection Inflammation Asthma Microbiome KEY POINTSRhinosinusitis is clinically defined as the presence of nasal drainage (anterior or posterior), nasal congestion, facial pain/pressure, and/or reduced sense of smell. In acute rhinosinusitis, nasal symptoms last for less than 12 weeks and inflammation is often secondary to a viral or bacterial infection. In chronic rhinosinusitis (CRS), nasal symptoms persist for longer than 12 weeks and the inflammation observed is secondary to impairments in the epithelial barrier, dysregulation of the host immune response, and potentially infections (or colonization) by pathogens. CRS and asthma have a strong clinical association and share similar pathophysiologic mechanisms in support of the unified airway hypothesis.Acute rhinosinusitis (ARS) is defined as the presence of nasal drainage (anterior or posterior), nasal congestion, facial pain/pressure, and/or reduced sense of smell. Depending on which guidelines are followed, ARS symptoms last either for less than 4 weeks 1 or 12 weeks. 2,3 ARS is a clinical diagnosis, and objective confirmation by sinus computed tomography (CT) scan or nasal endoscopy is generally not indicated. Patients can have more than one episode of ARS each year but importantly, they are asymptomatic in the intervening periods.Acute rhinosinusitis is extremely common. Studies specifying ARS found a disease prevalence of 6% to 15%, 2,4 with an estimated 0.035% of the population suffering from recurrent episodes. 5 Between 2006 and 2010, there were an estimated 21.4 million ambulatory care visits with a primary diagnosis of ARS. 6 Furthermore, in 2015 alone, acute upper respiratory infection (or presumed ARS) was one of the top 20 leading diagnoses for outpatient office visits. 7

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Association between specific IgE to Staphylococcus aureus enterotoxins A and B and asthma control

Cited by 32 publications

References 38 publications

Clinical phenotypes in asthma during childhood

Clinical phenotypes in asthma during childhood

sCD48 is anti-inflammatory inStaphylococcus aureusEnterotoxin B-induced eosinophilic inflammation

Sinus Infections, Inflammation, and Asthma

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