[BAD] EK9 - Abstracts



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Community Health Officer


Credits: None available.

ABSTRACT/PRESENTATION TITLE: THE ASTHMA NEW DISCOVERIES AND THERAPIES IN THE AGE OF COVID IN GHANA
CREDENTIALS: B.A /BSC MANAGEMENT /SOCIOLOGY/ACCOUNTING/PSYCHOLOGY
PRIMARY INSTITUTION: Global Sustainable Development Program NGO Ghana
Global Sustainable Development Program NGO Ghana .CO APPLICANTS: 1. Ahamed Iddrisu ahamed1958@hotmail.com male 2. Nawaratu Iddrisu nawaratuiddrisu@gmail.com Female 3. Hamidatu Iddrisu dobia1958@yahoo.co.uk Female.

ABSTRACT BODY
 THE Asthma: New Discoveries and Therapies in the Age of COVID; The topic is timely and urgent given the recent mechanistic insights into inflammatory airway disease, the current maturation of new biological therapies for this type of disease, and the overlap of this information with progressive lung disease after respiratory viral infections, including COVID-19. A new coronavirus (severe acute respiratory syndrome coronavirus 2; SARS-CoV-2) there are still no specific treatments or effective vaccines for coronavirus. Asthma was identified in 10.5% of all of the patients 13.5% in patients aged.
 Asthma: New Discoveries and Therapies.Moreover, this disease spectrum overlaps with inflammatory lung disease driven by respiratory viral infection, including COVID-19. Outcomes and Laboratory and Clinical Findings of Individual susceptibility and clinical outcome of Covid-19 are Outcomes and Laboratory and Clinical Findings of Asthma and Allergic Patients Admitted with Covid-19. This new pathogen was identified as an enveloped RNA.. Since all these drug therapies could be related to age.
Science Daily source of the latest research news Antibiotic Exposure in Children Under Age 2 Associated with Chronic Conditions. Nov. 16, 2020 — Children under age 2 who take antibiotics are at greater risk for childhood-onset asthma, respiratory allergies, eczema, celiac disease, obesity and Parasitic Worms Offer 'the Missing Link' on the Dual Nature of a Key Immune Regulator. Nov. 13, 2020 — By studying two models of parasite infection, researchers filled in crucial gaps about the activity of the signaling molecule IL-33 that is critical. Follow Your Gut: How Farms Protect from Childhood Asthma. Nov. 2, 2020 — Asthma impacts millions of children already at a young age. Children growing up on a farm have a lower risk of developing asthma than children not living on a farm. The mechanisms behind this Steroid Inhalers/pills for Asthma Linked to Heightened Risk of Brittle Bones and Fractures Oct. 20, 2020 — Taking steroid inhalers or tablets to treat asthma or control flare-ups is linked to a heightened risk of brittle bones (osteoporosis).
Heat Has Stronger Effect on Health in Less Developed Cities, Study Finds
Oct. 8, 2020 — Compared to high income cities, less developed cities in Brazil have a higher hospitalization rate associated with increased heat exposure, according to a new ...
Asthma Patients Given Risky Levels of Steroid Tablets
Sep. 13, 2020 — More than one quarter of asthma patients have been prescribed potentially dangerous amounts of steroid tablets, with researchers warning this puts them at greater risk of serious ...
Bronchitis as a Child Predicts Worse Lung Health in Middle Age
Sep. 4, 2020 — People who had bronchitis at least once before the age of seven are more likely to develop lung problems in later life, according to new research. However, the lung diseases they suffer from
Exposure to Cadmium in the Womb Linked to Childhood Asthma and Allergies
Sep. 2, 2020 — Babies born with higher levels of cadmium in their umbilical cord blood may be more likely to develop childhood asthma and allergies, according to new
Antibody Blockade Effective in Treatment of Severe COVID-19
Aug. 31, 2020 — Researchers find an overlap in the pathogenesis of cytokine release syndrome and COVID-19, and show that the symptoms of both can be alleviated by IL-6 signaling
Asthma May Not Be a Significant Risk Factor for Severe COVID-19
Aug. 31, 2020 — New research examines whether asthma is a significant risk factor for developing COVID-19 that is severe enough to warrant hospitalization and ...
Compared to Placebo, Vitamin D Has No Benefit for Severe Asthma Attacks, Study Finds
Aug. 25, 2020 — Contrary to earlier observational results, vitamin D supplements do not prevent severe asthma attacks in at-risk children, according to the first placebo-controlled clinical trial to test this ...
Electronic Alert Reduces Excessive Prescribing of Short-Acting Asthma Relievers
Aug. 23, 2020 — An automatic, electronic alert on general practitioners' computer screens can help to prevent excessive prescribing of short-acting asthma reliever medication, according to new ...
Air Pollution Linked to Higher Risk of Young Children Developing Asthma
Aug. 19, 2020 — Children exposed to higher levels of fine particles in the air (known as PM2.5) are more likely to develop asthma and persistent wheezing than children who are not exposed, finds a new ...
Protein Produced by the Nervous System May Help Treatments for Inflammatory Diseases
Aug. 17, 2020 — Researchers have discovered a protein produced by nervous system may be key to treating inflammatory diseases like asthma, allergies, chronic fibrosis and chronic obstructive pulmonary disease
Pregnant Mother's Immunity Tied to Behavioral, Emotional Challenges for Kids With Autism
Aug. 14, 2020 — Children with autism born to mothers who had immune conditions during their pregnancy are more likely to have behavioral and PRIMARY INSTITUTION: Ministry of Health/Ghana Health Service/ Global Sustainable Development Program NGO Ghana
Global Sustainable Development Program NGO Ghana .CO APPLICANTS: 1. Ahamed Iddrisu ahamed1958@hotmail.com male 2. Nawaratu Iddrisu nawaratuiddrisu@gmail.com Female 3. Hamidatu Iddrisu dobia1958@yahoo.co.uk Female.   emotional problems, a new study has found. Offspring sex may also interact 

Author(s):

Assistant Professor


Credits: None available.

Blimp-1 is essential for allergen-induced asthma and Th2 cell development in the lung

Kun He1,2,5, Angela Hettinga1,2,5, Sagar Laxman Kale2,3, Sanmei Hu2,3, Markus M. Xie4, Alexander L. Dent4, Anuradha Ray2,3 and Amanda C. Poholek1,2 *

1Division of Pediatric Rheumatology, Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.; 2Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.; 3Department of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, University of Pittsburgh, Pittsburgh PA, 15213, USA.; 4Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, 46202 USA.; 5These authors contributed equally: Kun He, Angela Hettinga
*Correspondence: poholeka@pitt.edu

A Th2 immune response is central to allergic airway inflammation, which afflicts millions worldwide. However, the mechanisms that augment GATA3 expression in an antigen-primed developing Th2 cell are not well understood. Here, we describe an unexpected role for Blimp-1, a transcriptional repressor that constrains autoimmunity, as an upstream promoter of GATA3 expression that is critical for Th2 cell development in the lung but is dispensable for TFH function and IgE production. Mechanistically, Blimp-1 acts through Bcl6, leading to increased GATA3 expression in lung Th2 cells. Using a murine model of house dust mite-mediated allergic asthma, we found Blimp-1 was required for inhaled but not systemically delivered allergens, suggesting a tissue-specific function for Blimp-1 to promote Th2 cells. Surprisingly, the anti-inflammatory cytokine IL-10, but not the pro-inflammatory cytokines IL-6 or IL-21, is required via STAT3 activation to upregulate Blimp-1 and promote Th2 cell development. These data reveal an unappreciated role for an IL-10-STAT3-Blimp-1 circuit as an initiator of an inflammatory Th2 response in the lung to allergens. Thus, Blimp-1 in a context-dependent fashion can drive inflammation by promoting rather than terminating effector T cell responses.

Author(s):

Lecturer 2


Credits: None available.

Inhibitory effects of lysophosphatidic acid on human lung mast cell function

Authors and Affiliations: 
Emeribe, A.U. 1, Peachell, P. 2, Kay, L. 2 1 Department of Medical Laboratory Science, University of Calabar,
Calabar-Nigeria.                       
2 Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield-United Kingdom

Background: Pulmonary fibrosis is an abnormal lung condition characterized by an inability to maintain regenerative processes in the lung. Although the pathological mechanisms that lead to lung fibrosis remain unclear, the activation of immune cells is almost certainly key. Recent studies in rodent cells have identified activation of the mast cell by lysophosphatidic acid (LPA) as central to the mediation of fibrosis. We hypothesized that similar processes might be operative in human mast cells so the aim of this study was to determine whether LPA activates human lung mast cells.
Methods: Mast cells were isolated and purified from human lung tissue. Expression of LPA receptor (LPAR) transcripts were evaluated using Taqman probe based qPCR. Mast cell activation was evaluated by monitoring the release of histamine using a spectrofluorometric technique. The effects of anti-IgE, and LPA on histamine release were evaluated.
Results: Data from this study revealed that LPAR1, 2 and 3 were highly expressed, LPAR5 was moderately expressed, while no expression was observed for LPAR4. LPA did not induce mediator release but unexpectedly was an effective inhibitor of anti-IgE-mediated histamine release. LPA inhibited histamine release in a concentration-dependent manner and with an EC50 of ~ 19 nM.
Conclusions and implications: This study demonstrates that human lung mast cells express LPA receptors. Moreover, the data indicate that, rather than activating mast cells, LPA was an effective inhibitor of mast cell secretion which was contrary to expectations. This suggests that targeting the relevant LPAR that mediates inhibition could be a novel mechanism to prevent unwanted mast cell activation.

Author(s):

PhD Student in Biomedical Sciences


Credits: None available.

Type 2 Immune Development Depends on MARCH1-mediated MHCII and CD86 Turnover in Lymph Node Resident Dendritic Cells

Authors: Carlos A. Castellanos (1), Xin Ren (2), Hong-Erh Liang (3), Brian J. Laidlaw (4), Satoshi Ishido (5), Jason G. Cyster (4), Richard M. Locksley (3), Xiaozhu Huang (2), and Jeoung-Sook Shin (1)

Affiliations:
(1) Department of Microbiology and Immunology, Sandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, CA 94143, USA.
(2) Department of Medicine, Lung Biology Center, University of California, San Francisco, San Francisco, CA 94158, USA.
(3) Department of Medicine, Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143, USA.
(4) Department of Microbiology and Immunology, Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143, USA.
(5) Department of Microbiology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya 663-8501, Japan.

Abstract: Th2 cells protect host from parasitic worm infection but also aggravate allergic inflammatory diseases including asthma. The role of dendritic cells (DCs) in Th2 cell development is well established, yet underlying mechanisms are unclear. We found that development of Th2 cells by DCs depends on membrane-associated RING-CH1 (MARCH1), an E3 ligase that mediates ubiquitination and endolysosomal degradation of MHCII and CD86. Mice lacking MARCH1 in DCs failed to develop Th2 cells against environmental allergens and parasitic worms although they remained competent at developing Th1 and cytotoxic T cells against influenza. While Th2 cell development often associates with DC migration to the draining lymph node, MARCH1 was barely expressed in migratory DCs, and the effect of MARCH1 in promoting Th2 cell development was not dependent on migratory DCs. Moreover, a DC migration blockade did not impair the expression of GATA3 in developing Th2 cells in the lymph node while MARCH1 deficiency did, suggesting MARCH1 promotes Th2 cell development through its expression in the lymph node-resident DCs. MARCH1 deficiency resulted in 7-10 fold increase in MHCII and CD86 in the lymph node-resident DCs. Mice with mutations in the ubiquitin acceptor amino acids of MHCII and CD86 also showed marked accumulation of these molecules in the lymph node-resident DCs and exhibited poor induction of GATA3 in developing Th2 cells and poor Th2 cell inflammation in allergen-exposed airway. Thus, development of Th2 cell immunity depends on ubiquitin-mediated control of antigen presenting and costimulatory molecules in lymph node-resident DCs.

Author(s):