Allergic Rhinitis Essay

B.J.was exposed to cats, thus causing an acute asthma attack. Patient being exposed to cat fur is what caused his allergic reaction. IgE antibodies cause allergic reactions, these cells are mainly attached to mast cells that lie in the lung interstitium in close association with the bronchioles and small bronchi. Once BJ breathes in the fur, to which he is sensitive to, the pollen reacts with these mast cells and thus causing these cells to release histamine. Which causes localized edema in the bronchioles as well as thick mucus. This causes the spams in the bronchilar smooth muscle which cause airway resistance. In return causing an acute asthma attack.

The ironic thing about allergens is that most aren’t harmful to the body, but this doesn’t stop the immune system for mistaking them for foreign bodies, which is why it decides to fight back. Our immune systems are amazing things. They create proteins to fight disease, which are known as antibodies. These antibodies try to battle it out against the antigens. Once our immune system creates certain antibodies, they’ll recognize the same intruders again and protect our bodies automatically year in year

Allergies are very common and global chronic diseases which occurs when the people’s immune system overreacts a substance which is judged to be harmful to human body. It’s now becoming major public health problem in developed countries especially in Australia. In 2007, according to an ASCIA-Access Economics Report that 4.1 million Australians (19.6% of the population) had at least one allergic disease. Also specialists speculate if Australia’s ageing trend continues, there will be a 70% increase in the number of Australians with allergy, from 4.1 million in 2007 to 7.68 million by 2050 (26.1% of the population). In this article, three aspects which related to allergies in Australia will be discussed in turn: causes, symptoms

Steele, P. (2016) Clinical Immunology Module 3. Lecture 1: Hypersensitivity. (PowerPoint slides: Narration) Retrieved from University of Cincinnati Immunology Blackboard: https://canopy.uc.edu/bbcswebdav/courses/2168-F_35MLSC3053001/16US_MLSC3053001_ImportedContent_20160413040126/Handouts/Mod3_Lecture1_Hypersensitivity.pdf.

According to the fundamental burden of allergic rhinitis on global health, Allergic Rhinitis and its Impact on Asthma (ARIA) and Global Initiative for Asthma (GINA) guidelines have been developed to provide evidence based recommendations for the management of allergic rhinitis and asthma coexistence (2, 6). Physicians’ unawareness and unfamiliarity with guidelines and lack of positive attitude toward application of guidelines have key role in the mismanagement of this disorder (7).

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

Allergic rhinitis is an annoying condition. Your nose is stuffy and runny. You may sneeze a lot and have watery eyes. Your entire nose, eyes, and throat may itch and annoy you. Your sense of smell and taste can even be affected. And worse, even though the symptoms are caused by allergies, people may avoid you thinking you harbor cold germs. Here are some treatment options you may want to try so you get relief.

Asthma is a disease of the lungs that can be influenced by different genes or alleles. When the epithelial or mucosal barrier is exposed to pollens, allergens, microbes or pollutants, these can stimulate the underlying antigen presenting cells (APC) which causes an immune response to occur.17 This can cause a cell influx into the airway that is primarily eosinophilic or neutrophilic. When the allergens present themselves, they can initiate a breakdown in the physical barriers, causing further allergic, inflammatory responses.

Treatment of allergic diseases represents a vast source of global healthcare costs. Allergies affect hundreds of millions of people worldwide with the number of cases continuing to increase at an alarming rate. The study of allergies and how genes and environmental factors affect them are ongoing. Currently, allergen immunotherapy is one of the few viable forms of treatment recognized. However, an alternative method of therapy utilizing microbes may be on the horizon.

Endotyping asthma serves as a stepping stone toward the practice of personalized medicine for asthma. Targeting therapy based on asthma endotypes would at least allow the physicians to target treatment based on an individual's biology. Treatments that tailored to endotypes had achieved some success in clinical trial. For example, in the case of childhood onset allergic asthma, anti-IgE (omalizumab) has been effective in improving the clinical outcomes. As recently reviewed by Kuhl and Hanania, interleukin (IL)-4 and 13 signal pathways are probably the predominant underlying mechanism. For the treatment of severe

Allergic rhinitis (AR) is an inflammatory condition which affects the membrane lining of the nose; causing it to become sensitive to allergens such as pollen, dust and animal dander. During AR, antigens bind with immunoglobulin E (IgE) to form an antigen-antibody complex which then attach themselves to the surface of nasal mast cells; inducing a cascade of cellular events leading to mast cell degranulation and the release of histamine via exocytosis. The release of histamine and other inflammatory mediators on blood vessel and nerve endings results in the symptoms of AR such as sneezing, itching and nasal discharge (rhinorrhoea). AR which occurs the same time every year is known as seasonal AR or more commonly known as “hay fever”. Avoiding causative allergens is essential in the management of the symptoms of AR; however, drug treatment is used to alleviate and control its symptoms. This evaluation will focus on the use of H1 anti-histamines, corticosteroids and IgE therapy in the treatment and management of seasonal AR. (ARIA, 2008)

The histamine and its mast cell content remain central to the pathophysiology of the pruritic wheal and rashes are in the most forms of urticaria, and synthesis, storage, regulation of release of histamine as well as molecular characterization of its receptors are becoming well understood. (3). The challenge of the past fifty years has been to understand the causation of the in discriminated activation of mucosal mast cells and dermal in chronic urticaria and angioedema (4). In 1980 the discovery of auto reactivity in the serum of some patients with chronic urticaria (the autologous serum skin test) was a successful step to promote and forward the attempts to identify and characterize this activity (5). The subsequent finding in chronic urticaria of specific complement-dependent autoantibodies, which release histamine and other mediators from mast cells and basophils through dimerization of their high affinity IgE receptors, has stimulated deep interest in the multifactorial modes of activation of basophiles and mast cell in this disorder (6). Antihistamines, discovered in the 1940s, remain the main step for treatment of most types of urticaria. Although recent quotient (“second-generation”) compounds that manifest and refined with great properties, they are often only moderately effective

When an allergen enters the body, the immune system is alerted and reacts. It is attempting to protect the body from a substance believed to be harmful. Large amounts of immunoglobulin E antibodies are produced to the allergen. Histamine is released causing allergic symptoms, like itching skin or eyes and a runny nose.

In an immediate hypersensitivity reaction the primary immune cell involved is the mast cell, which becomes activated through an IgE/FcɛRl receptor interaction. These cells play a key role in the initial immune response known as the ‘immediate hypersensitivity reaction’ which involves release of granule contents as well as secreting cytokines that recruit other pro-inflammatory cells during the ‘late-phase reaction’ (1).

A cardinal feature of atopic disease (AD) is an inappropriate biological hypersensitivity to environmental stimuli mediated by the immune cells (i.e. T lymphocytes, eosinophils and mast cells) as well as neuropeptides, cytokines and chemokines [3]. Asthma is an atopic disease with the dominant pathophysiology being an inappropriate inflammation of the airways [2]. It is a well established fact that the immune system and the stress system communicate through avenues such as hormones, growth factors, and neurotransmitters [2]. This communication means that these two systems have