scholarly journals The role of eosinophilic leukocytes in pathogenesis of bronchial asthma

2004 ◽  
Vol 23 (4) ◽  
pp. 333-341 ◽  
Author(s):  
Danijela Vucevic ◽  
Tatjana Radosavljevic ◽  
Gordana Djordjevic-Denic

Pathogenesis of bronchial asthma has not been completely understood. Eosinophilic leukocytes accumulate in high numbers in the lungs, blood and sputum of asthmatic patients. Peripheral blood eosinophilia has been identified as a risk factor for the development of airway obstruction. Prominent eosinophilic inflammatory infiltrate in the bronchial mucosa and correlation between eosinophil numbers and disease severity supports the hypothesis that eosinophils are central inflammatory cells capable of inducing pathophysiological features of asthma. Activated eosinophils secrete a wide range of preformed and newly generated mediators that damage the bronchial epithelium, contract smooth muscle, increase mucous secretion and cause vasodilatation. There is ample evidence that oxidants generation is increased during an asthma exacerbation. Many investigations indicate that airway and blood eosinophils produce more oxidants in asthmatic patients compared with control subjects.

Acta Naturae ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 54-64
Author(s):  
I. P. Shilovskiy ◽  
M. E. Dyneva ◽  
O. M. Kurbacheva ◽  
D. A. Kudlay ◽  
M. R. Khaitov

Cytokines of the interleukin-1 (IL-1) family play an important role in the realization of the protective functions of innate immunity and are the key mediators involved in the pathogenesis of a wide range of diseases, including various manifestations of allergy. The IL-1 family includes more than 11 members. However, the functions of many of them remain to be elucidated. Recently, new members of the IL-1 family have been discovered. In 2000, several independent research groups reported the discovery of a new interleukin of this family, which was named IL-37, or IL-1F7 (according to the new nomenclature). IL-37 was assigned to the IL-1 family based on its structural similarity with other members of this family. The study of its biological properties showed that its activity changes in inflammatory diseases, such as rheumatoid arthritis, psoriasis, as well as allergic diseases (allergic rhinitis, bronchial asthma, and atopic dermatitis). However, unlike most members of the IL-1 family, IL-37 acts as a negative regulator of inflammation. Activation of IL-37 suppresses inflammation, resulting in the suppression of inflammatory cytokines and chemokines, which in turn prevents infiltration of pro-inflammatory cells, mainly eosinophils and neutrophils. The exact molecular and cellular mechanisms of the anti-inflammatory effect of IL-37 in the development of allergic diseases (AD) have not been fully studied. This review summarizes and analyzes the accumulated experimental data on the role of IL-37 in the pathogenesis of AD, such as allergic rhinitis, bronchial asthma, and atopic dermatitis.


Inflammation ◽  
2021 ◽  
Author(s):  
Fei Chen ◽  
Min Yu ◽  
Yonghong Zhong ◽  
Lina Wang ◽  
Huaqiong Huang

Abstract Asthma is a common chronic respiratory disease that affects millions of people worldwide. The incidence of asthma has continued to increase every year. Bronchial asthma involves a variety of cells, including airway inflammatory cells, structural cells, and neutrophils, which have gained more attention because they secrete substances that play an important role in the occurrence and development of asthma. Neutrophil extracellular traps (NETs) are mesh-like structures composed of DNA, histones, and non-histone molecules that can be secreted from neutrophils. NETs can enrich anti-bacterial substances and limit pathogen migration, thus having a protective effect in case of inflammation. However, despite of their anti-inflammatory properties, NETs have been shown to trigger allergic asthma and worsen asthma progression. Here, we provide a systematic review of the roles of NETs in asthma.


2003 ◽  
Vol 2 (2) ◽  
pp. 38-43
Author(s):  
I. I. Ivanchuk ◽  
A. E. Sazonov ◽  
F. I. Petrovsky ◽  
I. S. Lescheva ◽  
A. P. Kopieva ◽  
...  

Investigations of the mRNA expression of apoptosis intracellular regulators, bcl-2 and bcl-xL antagonists and bax, bcl-xL agonists of cellular destruction as well as mRNA expression of IL-5 were carried out. As a result of investigation of potential role of IL-5 in the regulation of programmable bcl-2-dependent destruction we found the increase of vitality and mRNA expression stimulation of bcl-2 peripheral blood eosinophils in patients with bronchial asthma (BA). It was found that fresh-isolated peripheral blood eosinophils in all investigated groups expressed bax and bcl-xL mRNA, bcl-xS had the less activity. In peripheric blood eosinophils of healthy donors the bcl-2 expression was not found, however, the increase of mRNA expression by IL-5 was shown in group of patients with bronchial asthma and, possibly connected with this, the appearance of bcl-2 activity. Thus, the decrease of apoptotic activity in peripheral blood eosinophils in patients with bronchial asthma may lead to the increase of eosinophil portion that is subjected to necrotic destruction and this may significantly contribute into bronchial asthma pathogenesis.


2020 ◽  
Vol 13 (4) ◽  
pp. 1765-1772
Author(s):  
Assem Metwally Abo-Shanab ◽  
Hala Elnady ◽  
Iman Helwa ◽  
Rania Fawzy Mahmoud Abdelkawy ◽  
Hanan Atta ◽  
...  

Bronchial asthma (BA) is usually persistent through allergic sensitization, which is likely to result in bronchial hyper-responsiveness and acute bronchoconstriction due to reactions to specific and non-specific trigger stimuli. Many research focused on the role of T cells; particularly, T helper 2 (Th2) cells which linked to controlling immunoglobulin E (IgE) production due to their role in producing different cytokines, like Interleukin-13 (IL-13), in addition to influencing the function of eosinophils through the actions of IL-5. From this perspective, we decided to study the role of IgE, IL-13, and IL-5 in asthmatic children. IL-5, IL-13, and total IgE have been measured by ELISA technique in the serum of 57 children with bronchial asthma and compared to that of 20 healthy controls. Our results reported that 38/57 (66.67%) of the patient group had a family history for allergy, and parental consanguinity was found in 4/57 families (0.07%). IgE levels showed high statistical significance in asthmatic patients in comparison to controls (p = 0.00001), while IL-13 and IL-5 levels were not significantly different in patients versus control groups (P= 0.96, P = 0.81). Moreover, IgE was found significantly increased in both groups with/without family history for allergy (p = 0.009), whereas IL-13 was significantly elevated only in the group of patients with family history for allergy (0.01). This study demonstrates that asthma is strongly related to the family history of allergy, where IgE, as well as IL-13 levels, were found high in these asthmatic patients suggesting their association with underlying symptoms. Unexpectedly IL-5 was found insignificantly decreased.


2018 ◽  
Vol 27 (1) ◽  
pp. 10-13
Author(s):  
M Obaidulla Ibne Ali ◽  
Nur E Atia ◽  
Tohorul Islam ◽  
MN Islam ◽  
PM Basak ◽  
...  

In chronic bronchial asthma inflammation may be accompanied by intensive air flow limitation. Endogenous oxidants produced by overactive inflammatory cells destroy airway epithelium which slough into bronchial lumen and thus aggravates asthma. When oxidant overwhelm anti-oxidants, tissue injury and disease results. It is observed that decrease level of anti-oxidants in the lungs is a feature of chronic bronchial asthma and that there is a marked decrease of these levels during acute asthmatic attacks. These observations highlight the positive correlation between anti-oxidant therapy in asthmatic patients. The study was carried out to observe the changes in lung function in patients with chronic bronchial asthma both before and after supplementation of anti-oxidant vitamin A. Pulmonary function variables such as FVE, FEV1, FEV1/FVC%and PEFR were measured by spirometer in patients with chronic bronchial asthma both before and three month after supplementation of vitamin A 10,000 I.U orally daily. The mean FVC, FEV1, FEV1/FVC% and PEFR following vitamin A was unchanged significantly (P<0.001) than the pre supplementation values in patients with chronic bronchial asthma. This study reveals that no improvement of pulmonary functions occur after supplementation of anti-oxidant vitamin A in chronic bronchial asthma patients.TAJ 2014; 27(1): 10-13


2020 ◽  
Vol 2 (4) ◽  
pp. 243-271
Author(s):  
Salina Nicoleau ◽  
Beata Wojciak-Stothard

Pulmonary Hypertension (PH) is a multifactorial and lethal disease, characterised by elevated pulmonary arterial pressure and progressive right heart failure. PH pathobiology rests on four pillars: vascular remodelling, vasoconstriction, inflammation and thrombosis. While vascular and inflammatory cells have been the focus of PH research over the past decades, platelets have received relatively less attention, despite their associations with key pathophysiological processes of the disease. Platelets contain a wide range of vasoactive, inflammatory and pro-thrombotic mediators, likely to promote PH development and progression. There is currently no cure for PH, and platelet-associated pathways may help identify new therapeutic strategies. This review summarises available evidence on the role of platelets in different forms of PH, and comments on the current state of platelet-targeting therapies. It also describes the latest advances in the in vitro technologies that enable exploration of platelet function under dynamic and physiologically relevant conditions. Doi: 10.28991/SciMedJ-2020-0204-7 Full Text: PDF


2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Luiz H. C. Vasconcelos ◽  
Sarah R. D. Ferreira ◽  
Maria da C. C. Silva ◽  
Paula B. Ferreira ◽  
Iara L. L. de Souza ◽  
...  

Asthma is a chronic inflammatory disease of the airways related to epithelial damage, bronchial hyperresponsiveness to contractile agents, tissue remodeling, and luminal narrowing. Currently, there are many data about the pathophysiology of asthma; however, a new aspect has emerged related to the influence of reactive oxygen and nitrogen species (ROS and RNS) on the origin of this disease. Several studies have shown that an imbalance between the production of ROS and RNS and the antioxidant enzymatic and nonenzymatic systems plays an important role in the pathogenesis of this disease. Considering this aspect, this study is aimed at gathering data from the scientific literature on the role of oxidative distress in the development of inflammatory airway and lung diseases, especially bronchial asthma. For that, articles related to these themes were selected from scientific databases, including human and animal studies. The main findings of this work showed that the respiratory system works as a highly propitious place for the formation of ROS and RNS, especially superoxide anion, hydrogen peroxide, and peroxynitrite, and the epithelial damage is reflected in an important loss of antioxidant defenses that, in turn, culminates in an imbalance and formation of inflammatory and contractile mediators, such as isoprostanes, changes in the activity of protein kinases, and activation of cell proliferation signalling pathways, such as the MAP kinase pathway. Thus, the oxidative imbalance appears as a promising path for future investigations as a therapeutic target for the treatment of asthmatic patients, especially those resistant to currently available therapies.


2019 ◽  
Vol 4 (2) ◽  

Background: Bronchial asthma is a cause of significant morbidity and mortality with increasing prevalence worldwide. Although corticosteroids are routinely used in management of bronchial asthma either for long term therapy or control of acute attacks, but unfortunately they have limitations due to their diverse side effects. Resveratrol, a natural polyphenol, exhibits a wide range of biological and pharmacological activities, such as anticarcinogenesis, cardiovascular protection, and anti-inflammatory effects. Thus it is of much interest to investigate possible immunomodulatory effects of resveratrol in bronchial asthma representing a new mechanism that has not yet been fully elucidated. Methods: This experiment was performed on 50 albino mice divided in 5 equal groups. The normal control group (group I) received a veheicle of saline. The Ova-untreated group (group II); received ovalbumin (OVA) via two I.P. injections in days 0 and 14 in a dose of 100 µg and challenged with an intranasal (I.N.) dose of 50 µg OVA in days 14, 25, 26&27. The OVA- challenged group treated by Resveratrol (group III) in a dose of 30 mg/kg given by oral gavage 1 h. before challenge in days 14, 25, 26 & 27. The OVA- challenged group treated by Dexamethasone (group IV) in a dose of 2.5 mg/kg by intraperitoneal injection (I.P) 1 h. before challenge in days 14, 25, 26&27. OVA- challenged group treated by dexamethasone and resveratrol (group V) in the same dose regimen. At the end of experiment in the 28th day (24 hours after the last challenge in the 27thday), serum was analyzed for total IgE (TIgE) levels and bronchoalveolar lavage (BAL) was investigated for inflammatory cell count. The lung tissues were examined for histopathology score and immunohistochemistry for TLR2, CD4 and CD8. Results: The untreated group of asthma model showed a significant increase in serum level of TIgE, the number of total inflammatory cells, inflammatory score and the number of positive TLR2, CD4+ and CD8+ when compared to normal group. The treatment by both of resveratrol and dexamethasone was better than treatment with resveratrol alone as it showed significant decrease in the whole studied parameters. Conclusion:We demonstrated the immunomodulatory effect of resveratrol preclinical in bronchial asthma induced model via suppression of TLR2, CD4 and CD8 expression. We could suggest using resveratrol as add- on therapy with dexamethasone to achieve more efficacies in management of bronchial asthma. However, this should be verified in further clinical studies.


Author(s):  
I. А. Sinyakin ◽  
I. A. Andrievskaya ◽  
N. A. Ishutina ◽  
T. A. Batalova ◽  
N. R. Grigor'ev

Introduction. This review summarizes the available information on the role of Toll-like receptors (TLRs) in the pathogenesis of the novel coronavirus infection COVID-19 induced by SARS-CoV-2. The exact pathogenesis of COVID-19 and the role of each component of innate and adaptive immunity are still unknown. Aim. Discussion of the possible role of TLRs in the immune response in COVID-19 infection. Results. Analysis of the literature in the PubMed database showed that the mechanism of penetration of SARS-CoV-2 and lysis of type II alveolocytes is the binding of the spike S-glycoprotein or capsid protein M of the virus to the receptor-binding domain of ACE2 on the surface of epithelial cells. Migration and infiltration of inflammatory cells leads to overactivation of TLR4 on the surface of alveolocytes and bronchial epithelium, shifting the process to MyD88-dependent acute inflammatory signaling and hypersecretion of proinflammatory cytokines that cause a “cytokine storm” and the development of severe complications of COVID-19 infection, in particular, acute respiratory infections, respiratory distress syndrome, pathology of internal organs, and, in some cases, the death of the patient. Conclusion. It is possible to suggest that TLRs have an impact on the immune response in COVID19 infection. Both antagonists and agonists of TLRs, depending on their type, can be examined to determine the therapeutic and negative effects of COVID-19 infection. Further research is needed to investigate TLRs and pathways for activating cytokine expression, as they indicate a direct relationship with mortality and virus susceptibility. Bioinformatic research can also help to better understand the interaction of TLRs with proteins and RNA of the SARS-CoV-2.


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