scholarly journals Mycobacterium-Induced Th1, Helminths-Induced Th2 Cells and the Potential Vaccine Candidates for Allergic Asthma: Imitation of Natural Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Mohamed Hamed Abdelaziz ◽  
Xiaoyun Ji ◽  
Jie Wan ◽  
Fatma A. Abouelnazar ◽  
Sayed F. Abdelwahab ◽  
...  
Keyword(s):  
Allergic Asthma ◽  
Natural Infection ◽  
Hygiene Hypothesis ◽  
Developed Countries ◽  
Th2 Cells ◽  
Early Age ◽  
General Strategy ◽  
Helminth Infections ◽  
Chronic Pulmonary Diseases ◽  
Potential Vaccine

Bronchial asthma is one of the most chronic pulmonary diseases and major public health problems. In general, asthma prevails in developed countries than developing countries, and its prevalence is increasing in the latter. For instance, the hygiene hypothesis demonstrated that this phenomenon resulted from higher household hygienic standards that decreased the chances of infections, which would subsequently increase the occurrence of allergy. In this review, we attempted to integrate our knowledge with the hygiene hypothesis into beneficial preventive approaches for allergic asthma. Therefore, we highlighted the studies that investigated the correlation between allergic asthma and the two different types of infections that induce the two major antagonizing arms of T cells. This elucidation reflects the association between various types of natural infections and the immune system, which is predicted to support the main objective of the current research on investigating of the benefits of natural infections, regardless their immune pathways for the prevention of allergic asthma. We demonstrated that natural infection with Mycobacterium tuberculosis (Mtb) prevents the development of allergic asthma, thus Bacille Calmette-Guérin (BCG) vaccine is suggested at early age to mediate the same prevention particularly with increasing its efficiency through genetic engineering-based modifications. Likewise, natural helminth infections might inhabit the allergic asthma development. Therefore, helminth-derived proteins at early age are good candidates for designing vaccines for allergic asthma and it requires further investigation. Finally, we recommend imitation of natural infections as a general strategy for preventing allergic asthma that increased dramatically over the past decades.

scholarly journals SERPINB10 contributes to asthma by inhibiting the apoptosis of allergenic Th2 cells

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Yuqing Mo ◽  
Ling Ye ◽  
Hui Cai ◽  
Guiping Zhu ◽  
Jian Wang ◽  
...  
Keyword(s):  
T Cells ◽  
Allergic Asthma ◽  
Cd4 T Cells ◽  
Quantitative Polymerase Chain Reaction ◽  
Allergic Inflammation ◽  
Specific Ige ◽  
Th2 Cells ◽  
Th1 Cells ◽  
Th2 Response ◽  
Th1 And Th2

Abstract Background Serine peptidase inhibitor, clade B, member 10 (SERPINB10) contributes to allergic inflammation in asthma. However, its role in the T-helper type 2 (Th2) response of allergic asthma is not known. The goal of this study was to unveil the function of SERPINB10 in the Th2 response of allergic asthma and the mechanism by which SERPINB10 affects the viability of Th2 cells. Methods Th2 cytokines and serum levels of house dust mite (HDM)-specific IgE in bronchoalveolar lavage fluid were examined by ELISA in an HDM-induced asthma model. The number and apoptosis of Th1 and Th2 cells in mouse lungs were measured by flow cytometry. Naïve CD4 T cells from patients with asthma were cultured under appropriate polarizing conditions to generate Th1 and Th2 cells. SERPINB10 expression in polarized Th1 and Th2 cells was quantified by real-time reverse transcription-quantitative polymerase chain reaction. SERPINB10 expression was knocked down in human CD4 T cells with lentivirus. Results Knockdown of SERPINB10 expression significantly diminished HDM-induced Th2 cytokine secretion and level of HDM-specific IgE. After HDM exposure, SERPINB10-knockdown mice had diminished numbers of Th2 cells, but similar numbers of Th1 cells, compared with those in negative-control mice. Th2 cells of SERPINB10-knockdown mice were more susceptible to apoptosis than that of control mice. Stimulating T-cell receptors (TCRs) with anti-CD3 antibody caused upregulation of SERPINB10 expression in polarized Th2 cells, but not polarized Th1 cells. Knockdown of SERPINB10 expression resulted in fewer numbers and greater apoptosis of polarized Th2 cells. Conclusion Our results suggest that SERPINB10 may contribute to allergic inflammation and the Th2 response of asthma by inhibiting the apoptosis of Th2 cells.

scholarly journals Positive Design for Children with Atopic Dermatitis—Enhanced Problem-Solving and Possibility-Driven Approach in the Context of Chronic Disease

2020 ◽  
Vol 4 (4) ◽  
pp. 69
Author(s):  
Veronika Weiß ◽  
Michael Minge ◽  
Bernhard Preim ◽  
Steffi Hußlein
Keyword(s):  
Atopic Dermatitis ◽  
Problem Solving ◽  
Developed Countries ◽  
Research Area ◽  
Steady Increase ◽  
Early Age ◽  
Human Flourishing ◽  
Very Young Children ◽  
The 1960S ◽  
Design For Children

Since the 1960s, atopic dermatitis has seen a steady increase in prevalence in developed countries. Most often, the onset begins at an early age and many patients are very young children. Due to their young age, their parents are forced to take over handling of the disease. As a consequence, atopic dermatitis places a high burden not only on affected children, but also on their parents and siblings, limiting human flourishing of a whole family. Therefore, the described research area calls for a possibility-driven approach that looks beyond mere problem-solving while building on existing support possibilities and creating new ones. This paper presents atopi as a result of such a possibility-driven approach. It incorporates existing patient education and severity scoring into an extensive service, adding new elements to turn necessary practices into joyful experiences, to create feelings of relatedness and to increase perceived self-efficacy, thus is suitable to enable human flourishing.

scholarly journals Global Distribution, Public Health and Clinical Impact of the Protozoan PathogenCryptosporidium

2010 ◽  
Vol 2010 ◽  
pp. 1-39 ◽  
Author(s):  
Lorenza Putignani ◽  
Donato Menichella
Keyword(s):  
Public Health ◽  
Immunological Response ◽  
Developed Countries ◽  
Clinical Impact ◽  
Early Age ◽  
Underdeveloped Countries ◽  
Detection Systems ◽  
Immunological Status ◽  
Host Determinants ◽  
Key Indicators

Cryptosporidiumspp. are coccidians, oocysts-forming apicomplexan protozoa, which complete their life cycle both in humans and animals, through zoonotic and anthroponotic transmission, causing cryptosporidiosis. The global burden of this disease is still underascertained, due to a conundrum transmission modality, only partially unveiled, and on a plethora of detection systems still inadequate or only partially applied for worldwide surveillance. In children, cryptosporidiosis encumber is even less recorded and often misidentified due to physiological reasons such as early-age unpaired immunological response. Furthermore, malnutrition in underdeveloped countries or clinical underestimation of protozoan etiology in developed countries contribute to the underestimation of the worldwide burden. Principal key indicators of the parasite distribution were associated to environmental (e.g., geographic and temporal clusters, etc.) and host determinants of the infection (e.g., age, immunological status, travels, community behaviours). The distribution was geographically mapped to provide an updated picture of the global parasite ecosystems. The present paper aims to provide, by a critical analysis of existing literature, a link between observational epidemiological records and new insights on public health, and diagnostic and clinical impact of cryptosporidiosis.

scholarly journals Potential of Immunoglobulin A to Prevent Allergic Asthma

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Anouk K. Gloudemans ◽  
Bart N. Lambrecht ◽  
Hermelijn H. Smits
Keyword(s):  
Allergic Asthma ◽  
Immunoglobulin A ◽  
Bronchial Hyperresponsiveness ◽  
Airway Disease ◽  
Epidemiological Studies ◽  
Allergic Airway Disease ◽  
Secretory Iga ◽  
Th2 Cells ◽  
Lower Airway

Allergic asthma is characterized by bronchial hyperresponsiveness, a defective barrier function, and eosinophilic lower airway inflammation in response to allergens. The inflammation is dominated by Th2 cells and IgE molecules and supplemented with Th17 cells in severe asthma. In contrast, in healthy individuals, allergen-specific IgA and IgG4 molecules are found but no IgE, and their T cells fail to proliferate in response to allergens, probably because of the development of regulatory processes that actively suppress responses to allergens. The presence of allergen-specific secretory IgA has drawn little attention so far, although a few epidemiological studies point at a reverse association between IgA levels and the incidence of allergic airway disease. This review highlights the latest literature on the role of mucosal IgA in protection against allergic airway disease, the mechanisms described to induce secretory IgA, and the role of (mucosal) dendritic cells in this process. Finally, we discuss how this information can be used to translate into the development of new therapies for allergic diseases based on, or supplemented with, IgA boosting strategies.

scholarly journals Immunological and Pathophysiological Outcomes of Helminth Infections and Type 2 Diabetes Comorbidity Studies in Humans and Experimental Animals—A Scoping Review

2021 ◽  
Vol 11 (17) ◽  
pp. 8079
Author(s):  
Ekuyikeno Silas ◽  
Siyanda Ndlovu ◽  
Selaelo Ivy Tshilwane ◽  
Samson Mukaratirwa
Keyword(s):  
Type 2 Diabetes ◽  
Immune Modulation ◽  
Animal Studies ◽  
Developed Countries ◽  
Laboratory Animals ◽  
Future Research ◽  
Protective Effects ◽  
Degree Of Protection ◽  
Helminth Infections

Animal and human studies have demonstrated that helminth infections are associated with a decreased prevalence of type 2 diabetes mellitus (T2DM). Lack of exposure to helminth infections has been postulated to be one mechanism to explain the markedly increased prevalence of T2DM in developed countries. However, there is still paucity of information regarding the immunological interactions between helminth infections and T2DM. The study aimed at reviewing peer-reviewed articles on host immune and pathophysiological outcomes from human and laboratory animal studies of helminth infections and T2DM comorbidity. A literature search was carried out in Google Scholar, PubMed, and EBSCOhost databases using the following keywords; immune responses OR immune modulation of helminth infections OR parasites infections AND Type 2 diabetes comorbidity in humans AND experimental/laboratory animals. Results showed that helminth infections provided some degree of protection from the pathology associated with T2DM by modulating the surrounding cytokine and chemokine milieu in humans and animals. Whilst there is some evidence regarding the protective effects of helminth infections to T2DM in cases of comorbidity, there is paucity of research in both laboratory animals and humans, with reference to the immunological and pathophysiological mechanisms which occur during comorbidity, and these constitute gaps for future research.

scholarly journals IgM regulates airway hyperresponsiveness via modulation of actin associated genes.

2021 ◽  
Author(s):  
SABELO HADEBE ◽  
Anca Flavia Savulescu ◽  
Jermaine Khumalo ◽  
Katelyn Jones ◽  
Sandisiwe Mangali ◽  
...  
Keyword(s):  
B Cells ◽  
Allergic Asthma ◽  
Airway Hyperresponsiveness ◽  
Angiogenesis Inhibitor ◽  
Erythroid Differentiation ◽  
Immunoglobulin M ◽  
Th2 Cells ◽  
T Helper 2 ◽  
Current Therapies ◽  
Cell Force

Abstract Allergic asthma is a disease driven by T helper 2 (Th2) cells, eosinophilia, airway hyperresponsiveness (AHR) and IgE-secreting B cells. Asthma is largely controlled by corticosteroids and β2 adregenic receptor agonists that target and relax airway smooth muscle (ASM). Immunoglobulin M (IgM) isotype secreted by naïve B cells is important for class switching but may have other undefined functions. We investigated the role of IgM in a house dust mite (HDM)-induced Th2 allergic asthma model by sensitising wild type (WT) and IgM-deficient (IgM-/-) mice with HDM. We validated our findings using CRISPR and single cell force cytometry in human ASM. We found IgM to be essential in AHR but not Th2 airway inflammation or eosinophilia. RNA sequencing of lung tissue suggested that IgM regulated AHR through modulating brain-specific angiogenesis inhibitor 1-associated protein 2-like protein 1 (Baiap2l1) and erythroid differentiation regulator 1 (Erdr1). Deletion of BAIAP2L1 and ERDR1 reduced human ASM contraction when stimulated with TNF-α. These are unprecedented findings and have implications in future treatment of asthma beyond current therapies.

scholarly journals Distinct functions of tissue-resident and circulating memory Th2 cells in allergic airway disease

2020 ◽  
Author(s):  
Rod A. Rahimi ◽  
Keshav Nepal ◽  
Murat Cetinbas ◽  
Ruslan I. Sadreyev ◽  
Andrew D. Luster
Keyword(s):  
Allergic Asthma ◽  
Allergic Airway Inflammation ◽  
Lung Parenchyma ◽  
Airway Disease ◽  
Gene Signature ◽  
Allergic Airway Disease ◽  
Transcriptional Analysis ◽  
Th2 Cells ◽  
Redundant Functions

ABSTRACTMemory CD4+ T helper type 2 (Th2) cells are critical in driving allergic asthma pathogenesis, yet the mechanisms whereby tissue-resident memory Th2 cells (Th2 Trm) and circulating memory Th2 cells collaborate in vivo remain unclear. Here, using a house dust mite (HDM) model of allergic asthma and parabiosis, we demonstrate that Th2 Trm and circulating memory Th2 cells perform non-redundant functions in vivo. Upon HDM re-challenge, circulating memory Th2 cells trafficked into the lung parenchyma and ignited perivascular inflammation to promote eosinophil and CD4+ T cell recruitment. In contrast, Th2 Trm proliferated near airways and promoted mucus metaplasia, airway hyper-responsiveness, and airway eosinophil activation. Transcriptional analysis revealed that Th2 Trm and circulating memory Th2 cells share a core Th2 gene signature, but also exhibit distinct transcriptional profiles. Specifically, Th2 Trm express a tissue adaptation signature, including genes involved in regulating and interacting with extracellular matrix. Our findings demonstrate that Th2 Trm and circulating memory Th2 cells are functionally and transcriptionally distinct subsets with unique roles in promoting allergic airway disease.SUMMARYHow memory Th2 cell subsets orchestrate allergic airway inflammation remains unclear. Rahimi et al. use a murine model of allergic asthma and parabiosis to demonstrate that tissue-resident and circulating memory Th2 cells are functionally distinct subsets with unique roles in promoting allergic airway disease.

scholarly journals Inhaled house dust programs pulmonary dendritic cells to promote type 2 T-cell responses by an indirect mechanism

2015 ◽  
Vol 309 (10) ◽  
pp. L1208-L1218 ◽  
Author(s):  
Timothy P. Moran ◽  
Keiko Nakano ◽  
Gregory S. Whitehead ◽  
Seddon Y. Thomas ◽  
Donald N. Cook ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Allergic Asthma ◽  
House Dust ◽  
Lavage Fluid ◽  
Th2 Cells ◽  
T Helper 2 ◽  
Cell Responses ◽  
Th2 Responses ◽  
Th2 Differentiation

The induction of allergen-specific T helper 2 (Th2) cells by lung dendritic cells (DCs) is a critical step in allergic asthma development. Airway delivery of purified allergens or microbial products can promote Th2 priming by lung DCs, but how environmentally relevant quantities and combinations of these factors affect lung DC function is unclear. Here, we investigated the ability of house dust extract (HDE), which contains a mixture of environmental adjuvants, to prime Th2 responses against an innocuous inhaled antigen. Inhalational exposure to HDE conditioned lung conventional DCs, but not monocyte-derived DCs, to induce antigen-specific Th2 differentiation. Conditioning of DCs by HDE was independent of Toll-like receptor 4 signaling, indicating that environmental endotoxin is dispensable for programming DCs to induce Th2 responses. DCs directly treated with HDE underwent maturation but were poor stimulators of Th2 differentiation. In contrast, DCs treated with bronchoalveolar lavage fluid (BALF) from HDE-exposed mice induced robust Th2 differentiation. DC conditioning by BALF was independent of the proallergic cytokines IL-25, IL-33, and thymic stromal lymphopoietin. BALF treatment of DCs resulted in upregulation of CD80 but low expression of CD40, CD86, and IL-12p40, which was associated with Th2 induction. These findings support a model whereby environmental adjuvants in house dust indirectly program DCs to prime Th2 responses by triggering the release of endogenous soluble factor(s) by airway cells. Identifying these factors could lead to novel therapeutic targets for allergic asthma.

scholarly journals Risk Factors of Cardiovascular Disease in Developing Countries

2016 ◽  
Vol 5 (8) ◽  
pp. 69-72 ◽  
Author(s):  
Farah Rehan ◽  
Alina Qadeer ◽  
Irfan Bashir ◽  
Mohammed Jamshaid
Keyword(s):  
Risk Factors ◽  
Developing Countries ◽  
Salt Intake ◽  
Pharmaceutical Journal ◽  
Developed Countries ◽  
Dietary Factors ◽  
Anxiety And Depression ◽  
Early Age ◽  
Strategic Implementation ◽  
As Stress

Cardiovascular diseases (CVDs) have increased the mortality rate both in developing as well as developed countries, however a lower trend in death rates have been seen in developed and high income countries like USA, UK, Australia, Japan and other European countries due to improved life style, better strategic implementation, control of disease both in young and adults and especially reduced smoking habits. In developing countries CVD become an alarming situation due to prevalence of disease in early age that later on become chronic and difficult to control. Various risk factors that can contribute toward CVD in developing countries include smoking, high alcohol and salt intake, dietary factors, diabetes, high blood pressure and psychosocial aspects such as stress, anxiety and depression. Various other factors such as family history and the gender difference also contributing towards the high risk of developing CVD.Rehan et al., International Current Pharmaceutical Journal, July 2016, 5(8): 69-72http://www.icpjonline.com/documents/Vol5Issue8/02.pdf

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