Mould‐sensitized adults have lower Th2 cytokines and a higher prevalence of asthma than those sensitized to other aeroallergens

Matheson, Melanie C.; Reece, Jeanette C.; Kandane‐Rathnayake, Rangi; Tang, Mimi L.K.; Simpson, Julie A.; Feather, Iain; Southey, Melissa C.; Tsimiklis, Helen; Hopper, John L.; Morrison, Stephen; Giles, Graham G.; Walters, E. Haydn; Dharmage, Shyamali C.

doi:10.1111/all.12964

Cited by 5 publications

(5 citation statements)

References 42 publications

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“…In addition, our annual NO 2 exposure variable would have been strengthened if the measurement we used encompassed a longer period of exposure, and if seasonal NO 2 variation (in addition to season of blood sampling) was taken into account [31]. Secondly, although we made some adjustment for time to processing, and followed methods for optimizing serum storage duration and conditions [32,33], it is probable that absolute cytokine concentrations were affected by a degree of degradation, absorption and/or cellular production [34], especially with regard to TNF-α which has a half-life of only hours [35]. Thirdly, due to the relatively young age of participants, there were low case numbers in the group reporting cardiovascular events which most likely resulted in insufficient power to examine for effect modification of the NO 2 -IL-6 relationship.…”

Section: Discussionmentioning

confidence: 99%

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The Dose–Response Association between Nitrogen Dioxide Exposure and Serum Interleukin-6 Concentrations

Perret

Bowatte

Lodge

et al. 2017

IJMS

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Systemic inflammation is an integral part of chronic obstructive pulmonary disease (COPD), and air pollution is associated with cardiorespiratory mortality, yet the interrelationships are not fully defined. We examined associations between nitrogen dioxide (NO2) exposure (as a marker of traffic-related air pollution) and pro-inflammatory cytokines, and investigated effect modification and mediation by post-bronchodilator airflow obstruction (post-BD-AO) and cardiovascular risk. Data from middle-aged participants in the Tasmanian Longitudinal Health Study (TAHS, n = 1389) were analyzed by multivariable logistic regression, using serum interleukin (IL)-6, IL-8 and tumor necrosis factor-α (TNF-α) as the outcome. Mean annual NO2 exposure was estimated at residential addresses using a validated satellite-based land-use regression model. Post-BD-AO was defined by post-BD forced expiratory ratio (FEV1/FVC) < lower limit of normal, and cardiovascular risk by a history of either cerebrovascular or ischaemic heart disease. We found a positive association with increasing serum IL-6 concentration (geometric mean 1.20 (95% CI: 1.1 to 1.3, p = 0.001) per quartile increase in NO2). This was predominantly a direct relationship, with little evidence for either effect modification or mediation via post-BD-AO, or for the small subgroup who reported cardiovascular events. However, there was some evidence consistent with serum IL-6 being on the causal pathway between NO2 and cardiovascular risk. These findings raise the possibility that the interplay between air pollution and systemic inflammation may differ between post-BD airflow obstruction and cardiovascular diseases.

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Section: Discussionmentioning

confidence: 99%

“…The methods for the baseline and subsequent follow-up studies have been published [20,32,36,37,38,39,40]. Briefly, the participants (otherwise known as “probands”) who were born in 1961 and schooled in Tasmania in 1968 ( n = 8583 (99%)) were studied by questionnaires and spirometry when seven-years old.…”

Section: Methodsmentioning

confidence: 99%

The Dose–Response Association between Nitrogen Dioxide Exposure and Serum Interleukin-6 Concentrations

Perret

Bowatte

Lodge

et al. 2017

IJMS

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“…The Th2 lymphocytes cytokines, such as interleukin (IL)-4 and -5, play an important role in the pathogenesis of allergic asthma. 1,2 Recently, there has been increasing evidence of vital roles for IL-17 in allergic asthma. 3,4 IL-17 has been recognized as a proinflammatory cytokine in the pathogenesis of various diseases by regulating many inflammatory molecules, including chemokines, cytokines and adhesion molecules.…”

Section: Introductionmentioning

confidence: 99%

Developmental endothelial locus‐1 (Del‐1) antagonizes Interleukin‐17‐mediated allergic asthma

et al. 2018

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Interleukin (IL)-17 is a major contributor to the pathogenesis of allergic asthma. Developmental endothelial locus-1 (Del-1) is an endothelial cell-secreted protein known to inhibit IL-17 expression. However, little is known about the association between Del-1 and IL-17 in the pathogenesis of allergic asthma. Using bronchoalveolar lavage fluid (BALF) and peripheral blood samples collected from allergic asthmatic patients and controls, we explored the role of Del-1 in relation to IL-17 in allergic asthma. We found that the negative correlation between Del-1 and IL-17 was significant in BALF of allergic asthmatics. Del-1 treatment inhibited the expression of IL-17, the differentiation of IL-17-secreting leukocytes and associated cytokines. Contrarily, IL-17 levels were increased after treatment with anti-Del-1 mAb. Consistent with this, Del-1 treatment led to downregulation of IL-5, CCL5 and IL-4, thus reducing secretion of eosinophil cationic protein. Furthermore, Del-1 significantly downregulated the expression of ICAM-1 and may have the potential to reduce leukocyte transendothelial migration. Our data demonstrate that Del-1 can negatively regulate IL-17 and its proinflammatory function, thereby limiting airway inflammation in allergic asthmatics, and suggest Del-1 as a potential candidate for prevention and treatment of allergic asthma.

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“…The Th1 (IFN-γ) and Th2 (IL-4, IL-5 and IL-13) cytokines are reported to be closely associated with the pathogenesis of asthma [15]. The alteration of Th1 and Th2 cytokines induces secretion of allergen-specific IgE, overproduction of airway eosinophilia and mucus secretion [16]. In the present study, CYT treatment reduced the leukocytes number (especially eosinophils) in the BALF, suppressed the IgE production in the serum, decreased the Th1 cytokines (IL-4, IL-5 and IL-13) expression and increased the Th2 cytokine (IFN-γ) expression.…”

Section: Discussionmentioning

confidence: 99%

Effects of caffeoylxanthiazonoside on airway inflammation in an allergic asthma mice model

Wu¹,

Wang²,

Che³

et al. 2021

Trop. J. Pharm Res

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Purpose: To investigate the inhibitory effects of caffeoylxanthiazonoside (CYT) on airway inflammation in mice and its mechanism of action. Methods: An allergic asthma mice model was established by intraperitoneal injection and aerosol nebulization with ovalbumin (OVA). After treatment with CYT, the blood and bronchoalveolar lavage fluid (BALF) were collected from the mice. The leukocytes were classified and counted with Giemsa solution. Enzyme-linked immunosorbent assay (ELISA) was used to determine the serum levels of IgE, and IL-4, IL-5, IL-13 and IFN-γ in the BALF of mice. Lung tissues were obtained from the mice and MUC5AC protein expression was measured by western blot. Results: CYT significantly decreased the serum level of IgE in asthmatic mice. Inflammatory cells in BALF of mice were markedly reduced (p < 0.05) by CYT treatment at varying doses (10, 20, and 40 mg/kg). Treatment with CYT also significantly suppressed the cytokines of IL-4, IL-5 and IL-13 and increased the IFN-γ in the BLAF of OVA-induced allergic asthma mice (p < 0.05). Western blot results indicate that CYT treatment significantly decreased the expression of MUC5AC protein in the lung tissues of asthmatic mice. In addition, no significant effects on the body weight of the mice were found after CYT treatment. Conclusion: Caffeoylxanthiazonoside inhibits airway inflammation in allergic asthma mice by altering Th1/Th2 via re-balancing of related cytokines and downregulation of lung MUC5AC protein expression. Therefore, this compound can potentially be developed for the therapeutic management of inflammation in allergic asthma.

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Mould‐sensitized adults have lower Th2 cytokines and a higher prevalence of asthma than those sensitized to other aeroallergens

Cited by 5 publications

References 42 publications

The Dose–Response Association between Nitrogen Dioxide Exposure and Serum Interleukin-6 Concentrations

The Dose–Response Association between Nitrogen Dioxide Exposure and Serum Interleukin-6 Concentrations

Developmental endothelial locus‐1 (Del‐1) antagonizes Interleukin‐17‐mediated allergic asthma

Effects of caffeoylxanthiazonoside on airway inflammation in an allergic asthma mice model

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