scholarly journals IL-10 AND IL-35 AS INFLAMMATION REGULATORS IN PATIENTS WITH ALLERGIC RHINITIS AND MILD ATOPIC ASTHMA

2022 ◽  
pp. 1-12
Keyword(s):  
Allergic Rhinitis ◽  
Healthy Subjects ◽  
Respiratory Diseases ◽  
Allergic Inflammation ◽  
Serum Levels ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Atopic Asthma ◽  
Healthy State ◽  
Immunosuppressive Cytokines

Background. Significantly less is known about the immunoregulative cytokines, especially in allergic airway disease. This study aims to present the involvement of IL-35 and IL-10 in patients with allergic rhinitis (AR) and allergic bronchial asthma (BA). Methodology. The study comprised 71 patients –AR, patients with concomitant AR and mild atopic BA, and healthy controls (HC). We examined the serum levels of IL-35 and IL-10, along with other instrumental examinations, between March and September 2021. Findings. Levels of the regulatory cytokines IL-35 and IL-10 were significantly lower in patients than in HC (87.19±11.90 vs. 96.12±1.79 pg/ml; and 30.26±17.55 vs. 111.56±65.03 pg/ml, respectively). Furthermore, threefold higher serum IL-10 levels were found in healthy subjects compared to patients (p = 0.006). No difference in the levels of interleukins was found between the studied groups. Conclusions. Our results indicate that elevated IL-35 and IL-10 may play an essential role in reducing the activity of underlying allergic inflammation in allergic respiratory diseases, although no difference in the levels of the studied cytokines was found between the different groups of patients. Therefore, we can speculate that the immunosuppressive cytokines IL-35 and IL-10 were involved in maintaining the healthy state of no inflammation.

The CX3C-Chemokine Fractalkine (CX3CL1) is Detectable in Serum of Patients Affected by the Inflammatory Diseases Allergic Rhinitis and/or Asthma

2005 ◽  
Vol 3 (3) ◽  
pp. 149-152
Author(s):  
P.L. Minciullo ◽  
M. Patafi ◽  
L. Giannetto ◽  
R.A. Merendino ◽  
G. Di Pasquale ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Potential Role ◽  
Inflammatory Diseases ◽  
Allergic Diseases ◽  
Serum Levels ◽  
Airway Disease ◽  
High Serum ◽  
Allergic Airway Disease ◽  
Inflammatory Conditions ◽  
Healthy Donors

Fractalkine (FKN) is a chemokine able to mediate the initial capture, firm adhesion, and activation of circulating leukocytes. Many tissues express FKN mRNA and FKN expression is increased during inflammatory conditions. To assess a possible involvement in allergic airway disease, we detected serum levels of FKN in a group of patients affected by allergic rhinitis and/or asthma and found high serum levels of FKN in all patients and in only 26% of healthy donors at lower concentrations. The present results underscore the potential role that this chemokine may play in the pathogenesis of respiratory allergic diseases.

scholarly journals Disulfide disruption reverses mucus dysfunction in allergic airway disease

2019 ◽  
Author(s):  
Leslie E. Morgan ◽  
Siddharth K. Shenoy ◽  
Dorota Raclawska ◽  
Nkechinyere A. Emezienna ◽  
Vanessa L. Richardson ◽  
...  
Keyword(s):  
Disulfide Bonds ◽  
Allergic Inflammation ◽  
Airway Disease ◽  
Airway Hyperreactivity ◽  
Allergic Airway Disease ◽  
Mucus Hypersecretion ◽  
Asthma Model ◽  
Targeted Treatments ◽  
Fungal Allergen ◽  
Respiratory Conditions

Airway mucus is essential for healthy lung defense1, but excessive mucus in asthma obstructs airflow, leading to severe and potentially fatal outcomes2–5. Current asthma therapies reduce allergic inflammation and relax airway smooth muscle, but treatments are often inadequate due to their minimal effects on mucus obstruction6,7. The lack of efficacious mucus-targeted treatments stems from a poor understanding of healthy mucus function and pathological mucus dysfunction at a molecular level. The chief macromolecules in mucus, polymeric mucins, are massive glycoproteins whose sizes and biophysical properties are dictated in part by covalent disulfide bonds that link mucin molecules into assemblies of 10 or more subunits8. Once secreted, mucin glycopolymers can aggregate to form plugs that block airflow. Here we show that reducing mucin disulfide bonds depolymerizes mucus in human asthma and reverses pathological effects of mucus hypersecretion in a mouse allergic asthma model. In mice challenged with a fungal allergen, inhaled mucolytic treatment acutely loosened mucus mesh, enhanced mucociliary clearance (MCC), and abolished airway hyperreactivity (AHR) to the bronchoprovocative agent methacholine. AHR reversal was directly related to reduced mucus plugging. Furthermore, protection in mucolytic treated mice was identical to prevention observed in mice lacking Muc5ac, the polymeric mucin required for allergic AHR in murine models9. These findings establish grounds for developing novel fast-acting agents to treat mucus hypersecretion in asthma10,11. Efficacious mucolytic therapies could be used to directly improve airflow, help resolve inflammation, and enhance the effects of inhaled treatments for asthma and other respiratory conditions11,12.

scholarly journals Assessing the expression of immunosuppressive cytokines in the newly diagnosed systemic lupus Erythematosus patients: a focus on B cells

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Mitra Abbasifard ◽  
Zahra Kamiab ◽  
Mohammad Hasani ◽  
Amir Rahnama ◽  
Pooya Saeed-Askari ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
B Cells ◽  
Immune Responses ◽  
Lupus Erythematosus ◽  
Healthy Subjects ◽  
Serum Levels ◽  
Newly Diagnosed ◽  
Systemic Lupus ◽  
Moderate Disease ◽  
Immunosuppressive Cytokines

Abstract Background The immunosuppressive effects of regulatory B-cells (Bregs) and their immunosuppressive cytokines on immune responses in autoimmune disorders, mainly systemic lupus erythematosus (SLE), have been recently established. Therefore, the purpose of this article has been the exploration of the expressions of cytokines produced by B cells in newly diagnosed SLE patients. Results The findings demonstrated that the gene expression of IL-10, TGF-β, IL-35, PD-L1, and FasL was significantly up-regulated in SLE patients compared to healthy subjects (P < 0.05). Additionally, the results revealed that serum levels of IL-10, TGF-β, IL-35, PD-L1 were remarkably increased in patients with SLE compared to healthy subjects (P < 0.0001). However, serum levels of IL-10 and TGF-β decreased significantly with increasing SLEDAI score in studied patients (P < 0.05). Conclusion It was concluded that the release of anti-inflammatory cytokines, particularly IL-10 and TGF-β, might inhibit immune responses and autoreactive immune cells in a compensatory manner in SLE patients with mild to moderate disease activity.

scholarly journals Central role of immunoglobulin (Ig) E in the induction of lung eosinophil infiltration and T helper 2 cell cytokine production: inhibition by a non-anaphylactogenic anti-IgE antibody.

1996 ◽  
Vol 183 (4) ◽  
pp. 1303-1310 ◽  
Author(s):  
A J Coyle ◽  
K Wagner ◽  
C Bertrand ◽  
S Tsuyuki ◽  
J Bews ◽  
...  
Keyword(s):  
Cytokine Production ◽  
Serum Levels ◽  
Airway Disease ◽  
Cell Receptor ◽  
Allergic Airway Disease ◽  
Antigen Challenge ◽  
Eosinophil Infiltration ◽  
T Helper ◽  
Ige Antibody ◽  
Th2 Immune Response

Elevated levels of immunoglobulin (Ig) E are associated with bronchial asthma, a disease characterized by eosinophilic inflammation of the airways. Activation of antigen-specific T helper (Th) 2 cells in the lung with the subsequent release of interleukin (IL) 4 and IL-5 is believed to play an important role in the pathogenesis of this disease. In this study, we have used a non-anaphylactogenic anti-mouse-IgE antibody to investigate the relationship between IgE, airway eosinophil infiltration, and the production of Th2 cytokines. Immunization of mice with house dust mite antigen increased serum levels of IgE and IgG. Antigen challenge of immunized but not control mice induced an infiltration of eosinophils in the bronchoalveolar lavage associated with the production of IL-4 and IL-5 from lung purified Thy1.2+ cells activated through the CD3-T cell receptor complex. Administration of the anti-IgE monoclonal antibody (mAb) 6h before antigen challenge neutralized serum IgE but not IgG and inhibited the recruitment of eosinophils into the lungs and the production of IL-4 and IL-5 but not interferon gamma. Studies performed using an anti-CD23 mAb, CD23 deficient and mast cell deficient mice suggest that anti-IgE mAb suppresses eosinophil infiltration and Th2 cytokine production by inhibiting IgE-CD23-facilitated antigen presentation to T cells. Our results demonstrate that IgE-dependent mechanisms are important in the induction of a Th2 immune response and the subsequent infiltration of eosinophils into the airways. Neutralization of IgE, for example, non-anaphylactogenic anti-IgE mAbs may provide a novel therapeutic approach to the treatment of allergic airway disease.

scholarly journals Alterations of the Murine Gut Microbiome with Age and Allergic Airway Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Marius Vital ◽  
Jack R. Harkema ◽  
Mike Rizzo ◽  
James Tiedje ◽  
Christina Brandenberger
Keyword(s):  
Community Structure ◽  
Gut Microbiota ◽  
Serum Levels ◽  
The Elderly ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Intestinal Microbiome ◽  
16S Rrna Analysis ◽  
Cytokine Analysis ◽  
Old Mice

The gut microbiota plays an important role in the development of asthma. With advanced age the microbiome and the immune system are changing and, currently, little is known about how these two factors contribute to the development of allergic asthma in the elderly. In this study we investigated the associations between the intestinal microbiome and allergic airway disease in young and old mice that were sensitized and challenged with house dust mite (HDM). After challenge, the animals were sacrificed, blood serum was collected for cytokine analysis, and the lungs were processed for histopathology. Fecal pellets were excised from the colon and subjected to 16S rRNA analysis. The microbial community structure changed with age and allergy development, where alterations in fecal communities from young to old mice resembled those after HDM challenge. Allergic mice had induced serum levels of IL-17A and old mice developed a greater allergic airway response compared to young mice. This study demonstrates that the intestinal bacterial community structure differs with age, possibly contributing to the exaggerated pulmonary inflammatory response in old mice. Furthermore, our results show that the composition of the gut microbiota changes with pulmonary allergy, indicating bidirectional gut-lung communications.

scholarly journals 2019 ARIA: care pathways for allergic rhinitis in Russia

2020 ◽  
Vol 17 (1) ◽  
pp. 7-22 ◽  
Author(s):  
Musa Rakhimovich Khaitov ◽  
L Seymurovna Namazova-Baranova ◽  
N Ivanovna Ilyina ◽  
O Mikhaylovna Kurbacheva ◽  
Claus Bachert ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Respiratory Diseases ◽  
National Health System ◽  
Allergic Inflammation ◽  
Asthma Diagnosis ◽  
Predisposing Factor ◽  
Key Issues ◽  
The Russian Federation ◽  
Upper Respiratory ◽  
Treatment And Diagnosis

One of the most common chronic upper respiratory diseases worldwide is allergic rhinitis (AR). Despite advances in understanding the mechanisms of allergic inflammation, the symptoms of AR in most cases are not completely controlled by modern treatment methods. Allergic rhinitis is a precursor and predisposing factor for the development of other respiratory diseases, one of which is asthma. Diagnosis of AR is being actively conducted, but there is still a serious problem of uncontrolled and chaotic treatment of patients, so it is necessary to provide comprehensive medical care within the national health system. ARIA aims to develop and apply internationally recommendations for the management of patients with allergic respiratory diseases. In collaboration with other international associations that deal with the treatment and diagnosis of allergies and respiratory diseases, regulations and programs have been developed for the treatment of patients with AR, as well as when it is combined with asthma, which form the basis of ARIA. This document has been adapted for use in the field of healthcare in the Russian Federation and covers key issues related to the management of patients with AR and in combination with AR and asthma.

scholarly journals The Biology of Prostaglandins and Their Role as a Target for Allergic Airway Disease Therapy

2020 ◽  
Vol 21 (5) ◽  
pp. 1851 ◽  
Author(s):  
Kijeong Lee ◽  
Sang Hag Lee ◽  
Tae Hoon Kim
Keyword(s):  
Nasal Polyposis ◽  
Allergic Inflammation ◽  
Cell Types ◽  
Airway Disease ◽  
G Protein Coupled Receptors ◽  
Allergic Airway Disease ◽  
Airway Diseases ◽  
Disease Therapy ◽  
Lipid Compounds ◽  
G Protein Coupled

Prostaglandins (PGs) are a family of lipid compounds that are derived from arachidonic acid via the cyclooxygenase pathway, and consist of PGD2, PGI2, PGE2, PGF2, and thromboxane B2. PGs signal through G-protein coupled receptors, and individual PGs affect allergic inflammation through different mechanisms according to the receptors with which they are associated. In this review article, we have focused on the metabolism of the cyclooxygenase pathway, and the distinct biological effect of each PG type on various cell types involved in allergic airway diseases, including asthma, allergic rhinitis, nasal polyposis, and aspirin-exacerbated respiratory disease.

scholarly journals Neuroinflammatory Gene Expression Pattern Is Similar between Allergic Rhinitis and Atopic Dermatitis but Distinct from Atopic Asthma

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Paulina Sobkowiak ◽  
Wojciech Langwiński ◽  
Joanna Nowakowska ◽  
Irena Wojsyk-Banaszak ◽  
Dawid Szczepankiewicz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Allergic Rhinitis ◽  
Atopic Dermatitis ◽  
Expression Pattern ◽  
Human Study ◽  
Allergic Inflammation ◽  
Allergic Diseases ◽  
Atopic Asthma ◽  
Control Group ◽  
Altered Expression

Background and Aim. Neurogenic inflammation underlies the pathogenesis of allergic diseases. Interactions between neurons with the immune cells and structural cells (airway epithelium, nasal mucosa, skin keratinocytes) undergo altered regulation during chronic inflammation. Therefore, we hypothesized that the expression of neuroinflammatory genes may be altered allergic diseases, including atopic dermatitis and allergic rhinitis, and that, compared to atopic asthma, the expression pattern may be disease-specific in pediatric patients. Methods. In the study, we included 86 children diagnosed with atopic asthma (n=25), allergic rhinitis (n=20), and atopic dermatitis (n=20) and healthy control subjects (n=21) of Caucasian origin from the Polish population. The blood leukocyte expression of 31 genes involved in neuroinflammatory response (neurotrophins, their receptors, neuropeptides, and histamine signaling pathway) was analysed using TaqMan low-density arrays. The relative expression of selected proteins from plasma was done using TaqMan Protein Assays. Statistical analysis was done using Statistica. Results. Blood expression of 31 genes related to neuroimmune interactions showed significant increase in both allergic diseases, allergic rhinitis and atopic dermatitis, in comparison to the control group. We found 12 genes significantly increased in allergic rhinitis and 9 genes in which the expression was elevated in atopic dermatitis. Moreover, 9 genes with changed expression in atopic dermatitis overlapped with those in allergic rhinitis. Atopic asthma showed 5 genes with altered expression. The peripheral expression of neuroinflammatory genes in the human study was verified in target tissues (nasal epithelium and skin) in a rat model of allergic inflammation. Conclusions. A common pattern of neuroinflammatory gene expression between allergic rhinitis and atopic dermatitis may reflect similar changes in sensory nerve function during chronic allergic inflammation.

scholarly journals Does unified allergic airway disease impact on lung function and type 2 biomarkers?

2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Chris RuiWen Kuo ◽  
Rory Chan ◽  
Brian Lipworth
Keyword(s):  
Allergic Rhinitis ◽  
Lung Function ◽  
Allergic Asthma ◽  
Asthma Control ◽  
Persistent Asthma ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Positive Skin Prick Test ◽  
Positive Skin

AbstractThe concept of the unified allergic airway disease (UAD) recognises the association between allergic inflammation in the upper and lower airways. Patients with asthma and concomitant allergic rhinitis experience more asthma-related primary and secondary care visits. We therefore aimed to determine differences in asthma control (asthma control questionnaire ACQ-6), lung function (spirometry) and T2 biomarkers (FeNO and Eos) in relation to the presence of allergic rhinitis in patients with allergic asthma. Retrospectively, we evaluated a cohort of 60 consecutive patients with persistent asthma attending our research unit for screening into clinical trials. All included subjects were receiving inhaled corticosteroids (ICS) and had a positive skin prick test (SPT) to at least one common aeroallergen to fulfil the criterion of allergic asthma. Patients with UAD had a diagnosis of allergic asthma in addition to established concomitant allergic rhinitis. T2 biomarkers were significantly higher in patients with allergic rhinitis in contrast to those without. FEV1 % predicted and FEF25-75 % predicted were also significantly lower in patients with concomitant allergic rhinitis. However, there was no difference in ACQ-6 observed between groups. In summary, patients with allergic asthma, the presence of concomitant allergic rhinitis is associated with worse lung function and higher type 2 biomarkers.

scholarly journals Cleavage of Fibrinogen by Proteinases Elicits Allergic Responses Through Toll-Like Receptor 4

Science ◽  
2013 ◽  
Vol 341 (6147) ◽  
pp. 792-796 ◽  
Author(s):  
Valentine Ongeri Millien ◽  
Wen Lu ◽  
Joanne Shaw ◽  
Xiaoyi Yuan ◽  
Garbo Mak ◽  
...  
Keyword(s):  
Allergic Disease ◽  
Allergic Inflammation ◽  
Allergic Airway Inflammation ◽  
Airway Disease ◽  
Airway Epithelial Cells ◽  
Allergic Airway Disease ◽  
Airway Epithelial ◽  
Toll Like Receptor ◽  
Defensive Strategy ◽  
Toll Like Receptor 4

Proteinases and the innate immune receptor Toll-like receptor 4 (TLR4) are essential for expression of allergic inflammation and diseases such as asthma. A mechanism that links these inflammatory mediators is essential for explaining the fundamental basis of allergic disease but has been elusive. Here, we demonstrate that TLR4 is activated by airway proteinase activity to initiate both allergic airway disease and antifungal immunity. These outcomes were induced by proteinase cleavage of the clotting protein fibrinogen, yielding fibrinogen cleavage products that acted as TLR4 ligands on airway epithelial cells and macrophages. Thus, allergic airway inflammation represents an antifungal defensive strategy that is driven by fibrinogen cleavage and TLR4 activation. These findings clarify the molecular basis of allergic disease and suggest new therapeutic strategies.

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