Efficacy of nasal Staphylococcus aureus eradication by topical nasal mupirocin in patients with perennial allergic rhinitis

Zeldin, Yuri; Weiler, Zeev; Cohen, Alejandro; Калинин, М. Р.; Schlesinger, M; Kidon, Mona; Magen, Eli

doi:10.1016/s1081-1206(10)60053-1

Cited by 7 publications

(11 citation statements)

References 19 publications

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“…Allergies to pollen represent the most important cause of seasonal allergic rhinitis and inflammatory complications of the respiratory system. It has been reported that individuals suffering from allergic rhinitis are more likely to suffer from bacterial and viral complications of the sinuses and upper respiratory tract and that a history of viral infections worsens the symptoms of allergies (63)(64)(65)(66). Thus, respiratory allergies caused by aeroallergens are highly prevalent and viral and bacterial infections more common in people suffering from allergies.…”

Section: Allergensmentioning

confidence: 99%

Airborne inflammatory factors from the nose to the brain

Tonelli¹

2010

Front Biosci

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The intranasal pathway is a direct route of communication between the environment and the brain. This pathway is currently used for the delivery of several experimental therapeutic peptides and vaccines because it bypasses the blood brain barrier. It is also a route of entrance to the brain for several viruses and toxic substances. Airborne infectious, allergic and pollution agents are among the most common inflammatory factors which may affect brain function via the brain-nose interface. The inflammatory processes triggered in the upper respiratory tract by these agents are positioned to influence the immune response of the brain and therefore, influence its function and alter behavior. Several clinical and epidemiological studies find an association between inflammatory factors affecting the intranasal pathway and neurological disorders such as multiple sclerosis, Alzheimer and Parkinson diseases as well as mental disorders including anxiety and mood disorders. However the mechanisms of interaction between the immune response in the nasal epithelium and the brain are poorly understood. This article discusses current evidence about these mechanisms and associations with neurological and mental diseases.

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Section: Allergensmentioning

confidence: 99%

Airborne inflammatory factors from the nose to the brain

Tonelli¹

2010

Front Biosci

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“…However, there have been reports that S. aureus can be relevant to symptomatology in allergic rhinitis. [19][20][21] This bacterium can be found inside nasal epithelial cells, 22 and S. aureus-derived exotoxin B, serine proteases, and hemolysin A can induce interleukin (IL)6 and IL-8 release from airway epithelial cells, [23][24][25] can induce local neutrophilia, which leads to epithelial damage. 26,27 Neutrophil-derived elastase and reactive oxygen species can be involved in epithelial cell damage.…”

Section: Discussionmentioning

confidence: 99%

Involvement of Staphylococcus aureus and Moraxella catarrhalis in Japanese Cedar Pollinosis

Otsuka

Takanashi

Tokunou

et al. 2016

Am J Rhinol�Allergy

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Nasal symptoms in the preseason are associated with neutrophilia and nasal colonization with S. aureus and M. catarrhalis. Patients with symptoms in the preseason had improved symptom scores when given prophylactic treatment early in season but had more-severe symptom scores late in season than asymptomatic patients in the preseason. Neutrophil-associated tissue damage related to bacterial colonization may underlie these associations.

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“…125 Nasal carriage of S. aureus and skin colonization occur more frequently in children with AD and food allergy and patients with allergic rhinitis. [126][127][128] MRSA colonization is associated with higher levels of peanut specific IgE, 129 and increased and persistent levels of specific IgE to egg white and peanut, independent of eczema severity. 125 In mice models, S. aureus enterotoxins, like SEB, in combination with ovalbumin enhance epicutaneous sensitization with specific IgE against SEB and ovalbumin, 124 and augment ovalbumin induced airway hyperresponsiveness and lung inflammation, via an IL-17A-dependent pathway.…”

Section: The Biological Barrier and Staphylococcus Aureus In Admentioning

confidence: 96%

Epidermal Barrier Dysfunction in Atopic Dermatitis

Gomes¹,

Calado

Gonçalo

2021

SPDV

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Impaired skin barrier is one of the hallmarks of atopic dermatitis (AD), with abnormalities in the cornified envelope, lipid lamellae, tight junctions and cutaneous microbiome. These findings are also present in nonlesional skin of AD individuals, suggesting that epidermal barrier defects may be the initial step towards the development of AD and eventually other atopic diseases (atopic march). It is currently known that pathophysiology of AD involves an interplay between this dysfunctional skin barrier and a predominantly type 2 skewed innate and adaptive immune responses, which further disrupt the skin barrier through type 2 cytokines. In this setting, there is enhanced penetration of environmental and food allergens through a deficient barrier, leading to an increased susceptibility to sensitization. During the sensitization process, thymic stromal lymphopoietin (TSLP) polarizes skin dendritic cells to a T-helper 2 response, and TSLP seems to be a key cytokine in the sensitization of food allergy, allergic asthma and rhinitis. In this review, the authors describe the current knowledge of the pathophysiology of the epidermal barrier, its disruption in AD and how it may be involved in the development of atopic comorbidities and the role of barrier repair therapy on the prevention of the atopic march progression.

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Efficacy of nasal Staphylococcus aureus eradication by topical nasal mupirocin in patients with perennial allergic rhinitis

Cited by 7 publications

References 19 publications

Airborne inflammatory factors from the nose to the brain

Airborne inflammatory factors from the nose to the brain

Involvement of Staphylococcus aureus and Moraxella catarrhalis in Japanese Cedar Pollinosis

Epidermal Barrier Dysfunction in Atopic Dermatitis

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