The Effects Of Peptide And Peptidomimetic Activation Of Par2 Dependent Ca2 + Signaling Essay

The effect of asthma can range from mild, irregular symptoms causing minor problems for an individual to severe and sudden asthma attacks. The extent of what causes asthma is not well known or fully understood but some common triggers include, cold temperatures, dust mites, cockroaches, pollen, sickness, mould and animal hair. When triggered, the airways in the lungs become inflamed and constricted causing shortness of breath, chest pain and wheezing [R]. Currently, there is no cure for asthma however symptoms can be managed with medication and improved living standards [R]. Asthma symptoms are commonly controlled with the use of inhalers, either preventers (taken to desensitizes airways to triggers) or relievers (provides instant relief by relaxing the muscles) [16].

Inhibitors of phosphodiesterase type 4 (PDE4) act by increasing intracellular concentrations of cyclic adenosine monophosphate, which has a broad range of anti-inflammatory effects on various key effector cells involved in asthma and chronic obstructive pulmonary disease (COPD)

Asthma is a “chronic inflammatory disease of the airways” and causes difficulties in breathing due to the widespread narrowing of the bronchial airways1. Asthma can occur in people of all ages and affects approximately 10.2% of Australians (2011-12) 2. Generally asthma is reversible with or without treatment however over time damage may occur3. Therefore it is important for patients to manage their asthma well in order to maintain a healthy and quality lifestyle. One of the most effective treatments used to control asthma is Salbutamol. Salbutamol is a short acting B2 adrenergic agonist and it is mainly used for quick relief or to prevent the onset of asthma3. This essay will explain the physiology of the respiratory system and the effect on the system when a person has asthma. It will also discuss the use of salbutamol as a treatment for asthma.

Asthma sufferers are among some of the most sensitive disease sufferers on the planet. The smallest thing can set off an attack such as dust,

the APCs will then migrate to bronchus associated lymphoid tissues and induce the type 2 helper (Th2) cytokines response. B cell proliferation are then stimulated by Th2 cells, leading to the plasma cells

Inflammation in allergic asthma occurs primarily in larger bronchi and larger airways and is marked by the influx of eosinophils. COPD involves the lung parenchyma and small airways and is marked by the influx of neutrophils. Current therapies like oral corticosteroids target these inflammatory processes. Anti-FAS, anti-IL-5 and corticosteroids treatment involves inducing eosinophil and neutrophils apoptosis and serve to counteract survival signals encountered by these same cells such as IL-5 and granulocyte macrophage-colony stimulating factor (GM-CSF). They all lack cell specificity and have a higher degree of cellular toxicity than required for use in a chronic disease state such as asthma and COPD. Sialic acid-binding immunoglobulin-type lectins (Siglecs) are immune regulatory molecules found on the surfaces of inflammatory cells. Siglec-8 is expressed on the surface of eosinophils, mast cells and Siglec-9 on neutrophils. Binding and crosslinking of these receptors to their ligand have proapoptotic effect on eosinophils and neutrophils and will help dampen immune responses and regulate

Asthma can best be described as a chronic inflammatory disease involving the pulmonary airways, and bronchial hyper responsiveness that results in lower airway obstruction (Kudo, Ishigatsubo, & Aoki, 2013). The pathophysiology of asthma involves airway inflammation, intermittent airflow obstruction, and bronchial hyper responsiveness (Kudo et al., 2013). It is now considered to be an assortment of several diseases that have similar characteristics and symptoms (London et al., 2017). Cells that were learned to be associated to airway inflammation include mast cells, eosinophils, epithelial cells, macrophages, and activated T lymphocytes (Mims, 2015). These cells influence smooth muscle tone and contribute to remodeling of the airway. Airway hyper responsiveness in asthma occurs from an overactive response to numerous organisms found from

Allergic asthma is considered to be autoimmune disease because immune system attacks allergen and releases immunoglobulin E (IgE) that induces inflammation and obstruction of the airway. In 2004, David Pritchard found that hookworm larvae infection can reduce airway responsiveness in patients with allergic asthma. In 2006, during his second clinical trial, there are 15 participants received a dose of10 hookworms, and the other15 participants received placebo. After six weeks, the result shown that 15 worm recipients experienced a low inflammatory response. This indicates that their immune system can be controlled and suppressed by

Scientists have for the first time identified the root cause of asthma and the importance CaSR’s in the treatment. As a result they have been able to produce a treatment that counteracts the many side effects associated with asthma. Although researchers have shown calcilytic are able to block the receptors, the longevity of the effect is still unknown. It’s still unclear how long the treatment will stop the lungs producing large numbers of receptors.

Asthma is characterized by reversible airway obstruction and airway hyper-responsiveness that is associated with airway inflammation and airway remodelling. Two prominent pathological features of asthma are the increase of airway smooth muscle (ASM) mass and the deposition of extracellular matrix (ECM) proteins, which contribute to the development of airway inflammation and remodelling. The deposition of increased ECM proteins such as fibronectin and collagen in ASM layer has been observed in asthma. Evidence suggests that increased ECM deposition could induce ASM phenotype switching from the contractile phenotype to the proliferative phenotype, accompanied by increased expression of cell adhesion receptors and costimulatory molecules as well

Immune cells in the respiratory system require contact with potentially dangerous organisms in order to differentiate between benign and lethal antigens. Without contact with these organisms, the immune system will not be able to fully develop. Stated in “Dear Earthtalk Gale”, “One theory is that better hygiene in developed countries means that Westerners have less exposure to bacteria, viruses and parasites, altering our immune response with the result being increased risk for allergic diseases like asthma. Indeed, Western asthma rates are 50 times higher than in rural Africa” (1). Those that have a lot of contact with pathogens, such as people living in developing countries, are easily able to protect themselves from asthma, unlike those

enzymes are released to destroy foreign microbes and irritants such as cigarette smoke, air pollution,

New findings that broaden the conventional definition of pharmacology demonstrate that ligands can concurrently behave as agonist and antagonists at the same receptor, depending on effector pathways or tissue type. Terms that describe this phenomenon are "functional selectivity", "protean agonism",[4][5] or selective receptor modulators.[6]

Irritant-induced asthma is described as asthma that is caused by exposure to more than one agent that could result to respiratory irritants when inhaled. It can occur during work or outside the workplace i.e. occur in an indoor and outdoor environment (Tarlo, 2013:1). There are currently no clinical diagnostic criteria that allow the acknowledgment of new-onset-asthma to low irritant exposure in each individual patient in the workplace. The recent publication thus suggest reconsideration of the role of irritants causing asthma, to include not only the very high exposures previously recognized to be able to cause asthma in a subset of exposed workers, likely from acute inflammatory responses, but also more chronic, lower exposures that may cause

The universal intracellular messenger, Calcium (Ca2+ ) regulates a wide range of cellular processes such as gene transcription, muscle contraction and cell proliferation. Ca2+ diffuses into organelles such as mitochondria and the nucleus as it is elevated in the cytosol (Martin D Bootman, 2006). Ca2+ is suited to this role as an intracellular messenger as it is a divalent cation and therefore it can form more stable complexes with other compounds compared to monovalent ions like magnesium and chloride. Moreover, Ca2+ has a larger radius and a stable electron configuration which provides flexibility that allows the formation of bonds with coordination sites that have irregular geometry (Bading, 2013).