A chest physician's guide to mechanisms of sinonasal disease

Hox, Valérie; Maes, Tania; Huvenne, Wouter; Drunen, Cornelis M. van; Vanoirbeek, Jeroen; Joos, Guy; Bachert, Claus; Fokkens, W. J.; Ceuppens, Jan L.; Nemery, Benoît; Hellings, Peter W.

doi:10.1136/thoraxjnl-2014-205520

Cited by 18 publications

(17 citation statements)

References 68 publications

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“…Both allergic rhinitis and CRS, especially in the presence of NP, have been clearly shown to be associated with lower airway diseases such as asthma and COPD and to be a significant and independent negative predictor of quality of life in asthmatics . Asthma diagnosis is frequently ratified by pulmonary function tests, broadly utilized in medical practice .…”

Section: The Relation Between Nasal Flow and Patency Measurements Andmentioning

confidence: 99%

Measurements of nasal airflow and patency: a critical review with emphasis on the use of peak nasal inspiratory flow in daily practice

Ottaviano

Fokkens

2016

Allergy

120

111

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Objective measures can be used to assist the clinician to diagnose and treat nasal obstruction and also to quantify nasal obstruction in research. Objective measurements of nasal obstruction are as important as objective measurements of lung function. peak nasal inspiratory flow (PNIF), acoustic rhinometry (AR) and rhinomanometry (RM), with their specific peculiarity, assess different aspects of nasal obstruction. From the studies available in the literature, it seems that these methods roughly correlate with each other and that all of them can be alternatively utilized very well in research as well as in clinical practice. This review describes the various methods that can be used to measure nasal patency, airflow and resistance, mainly peak nasal inspiratory flow, rhinomanometry and acoustic rhinometry. PNIF has been demonstrated to be reproducible and as good an indication of objective nasal patency as formal rhinomanometry and has the advantage to be cheap, simple and suitable for serial measurements and for home use even in the paediatric population. PNIF normative data are available for children, adults and elderly subjects, and the availability of unilateral PNIF normal values allows evaluation of nasal sides separately. Just as in the lower airways, objective and subjective evaluation gives different information that together optimizes the diagnosis and the treatment of our patients. We argue that PNIF should be used regularly in every outpatient clinic that treats patients with nasal obstruction.

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Section: The Relation Between Nasal Flow and Patency Measurements Andmentioning

confidence: 99%

Measurements of nasal airflow and patency: a critical review with emphasis on the use of peak nasal inspiratory flow in daily practice

Ottaviano

Fokkens

2016

Allergy

120

111

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“…Sensitizer-induced (immunological/allergic) and irritant-induced (non-immunological/non-allergic) asthma are the two physiopathology mechanisms classically proposed for OA ( Figure 1). Sensitizerinduced asthma, induced after a latency period (a few weeks to several years), may be classified in two categories: High Molecular Weight agents (HMW) agent-induced asthma and Low Molecular Weight chemicals (LMW) agent-induced asthma (Figures 1 and 2) 1,2,18,19 . HMW agents, most often animal and vegetal sensitizing proteins, are a major cause of allergic asthma in the workplace 20 .…”

Section: Irritant-induced Asthma Among Current Classifications Of Wormentioning

confidence: 99%

“…HMW agents, most often animal and vegetal sensitizing proteins, are a major cause of allergic asthma in the workplace 20 . They may induce allergic airway inflammation through well-described IgE-dependant immunological mechanisms ( 6,20 , similar to non-work-related asthma caused by common allergens 1,2,18 . In contrast, the underlying mechanism for asthma induced by LMW chemicals, in most cases non-IgE-mediated, is more complex and remains unknown for many agents 1,2,6 .…”

Section: Irritant-induced Asthma Among Current Classifications Of Wormentioning

confidence: 99%

“…It is often difficult to classify LMW agents as either sensitizer or irritant 18 , as some irritants have sensitizing properties and vice versa. Some LMW agents, especially those with highly reactive side chains, may induce immune sensitization after a latency period, whereas others may cause IIA particularly after a high-level exposure 18 (Figure 1). It has been suggested, for some chemicals, that sensitizer and irritant properties might depend on the level/intensity of exposure, with potentially interlinked mechanisms.…”

Section: Irritant-induced Asthma Among Current Classifications Of Wormentioning

confidence: 99%

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Do chronic workplace irritant exposures cause asthma?

Dumas

Moual

2016

Current Opinion in Allergy &Amp; Clinical Immunology

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Evidence of a causal effect of chronic workplace irritant exposure in new-onset asthma remains limited, mainly because of a lack of longitudinal studies and the difficulty to evaluate irritant exposures. However, recent epidemiological studies strengthen the evidence of an effect of chronic exposure to irritants in work-related asthma. The underlying mechanism remains unknown but may be related to oxidative stress, neurogenic inflammation and dual irritant and adjuvant effects. However, disentangling chronic irritant effects from either acute irritant-induced asthma or immunological low molecular weight agent-induced asthma is difficult for some agents. Further research is needed to improve assessment of irritant exposures and identify biomarkers.

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“…Because of its position at the entry into the airways, the nasal mucosa is continuously exposed to inhaled agents from the environment [ 1 ]. To prevent stimulation of inflammation by these agents, the nasal mucosa has developed various mechanical mechanisms including tight junction molecules, mucus production, and ciliary movement.…”

Section: Introductionmentioning

confidence: 99%

Diesel Exhaust Particles Upregulate Interleukins IL-6 and IL-8 in Nasal Fibroblasts

et al. 2016

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BackgroundDiesel exhaust particles (DEP) are a major source of air pollution. Nasal fibroblasts are known to produce various cytokines and chemokines. The aim of this study was to evaluate DEP-induced cytokines and chemokines in nasal fibroblasts and to identify the signaling pathway involved.MethodsA cytokine and chemokine array performed after stimulation of nasal fibroblasts with DEP revealed that levels of IL-6 and IL-8 were increased most significantly among various cytokines and chemokines. RT—PCR and ELISA were used to determine the mRNA and protein expression levels of IL-6 and IL-8. Signaling pathways of p-38, Akt, and NF-κB were analyzed by western blotting, luciferase assay, and ELISA. Organ cultures of nasal interior turbinate were also developed to demonstrate the ex vivo effect of DEP on the expression of IL-6 and IL-8 and the associated signaling pathway.ResultsDEP increased the expressions of IL-6 and IL-8 in nasal fibroblasts at mRNA and protein levels. DEP induced phosphorylation of p38, Akt, and NF-κB, whereas inhibitors of p38, Akt, and NF-κB blocked these phophorylations and the expressions of IL-6 and IL-8. These findings were also observed in ex vivo organ culture of nasal inferior turbinate.ConclusionsDEP induces expression of IL-6 and IL-8 via p38, Akt, and NF-κB signaling pathways in nasal fibroblasts. This finding suggests that air pollution might induce or aggravate allergic rhinitis or chronic rhinosinusitis.

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A chest physician's guide to mechanisms of sinonasal disease

Cited by 18 publications

References 68 publications

Measurements of nasal airflow and patency: a critical review with emphasis on the use of peak nasal inspiratory flow in daily practice

Measurements of nasal airflow and patency: a critical review with emphasis on the use of peak nasal inspiratory flow in daily practice

Do chronic workplace irritant exposures cause asthma?

Diesel Exhaust Particles Upregulate Interleukins IL-6 and IL-8 in Nasal Fibroblasts

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