Asthma Is A Chronic Lung Disease Biology Essay

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Asthma is a chronic lung disease characterised by wheezing, coughing, breathlessness, and chest-tightness. Generally, asthmatic attacks constitute of bronchoconstriction, mucous hypersecretion, and inflammation[4].

Airway inflammation in asthma further instigates lungs to produce muscle tightening,mucous hypersecretion , and swelling in the breathing tubes of the lungs.[1]

Asthma is believed to be triggerred because of allergens like tobacco smoke,cat dander, dog dander, wood smoke, sulfur dioxide, high ozone levels, cold air, tree pollens, etc

incase of sensitive individuals.however, Medical Practitioners are of the view that viral infections like cold and flu damage the cells and hence sensitise the airways.environmental factors like cigarrette smoke also increases the risk of develop[ing asthma[4]

Asthma can also be 'exercise induced'.Running can trigger an asthma attack in over 80% of children with asthma.The act of running causesd swelling in airway and mucous hypersecretion.Emotional stress including laughs, yells, or cries may also trigger or worsen an asthma attack .[1]

Asthma is one of the most common chronic disease among children.Children most often affected by asthma are:

• Adolescents

• African American

• Males

• From low-income families

• From single-parent families

• From inner-city[1]

According to the World Health Organization, over 235 million people worldwide suffer from asthma and its prevalence increases by 50 % every decade. 10 % of human population in North America have asthma. Worldwide, approximately 180,000 deaths annually are attributable to asthma,however overall mortality rate has declined since 1980. [2]

Asthma is diagnosed on the basis of patient-history,physical examination, and pulmonary function tests.The treatment process involves control over triggering factors and drug therapy,which mostly comprises of inhaled β2 -agonists and corticosteroids.[3]

The National Asthma Education and Prevention Program (NAEPP) developed in 1988, defines following objectives with respect to asthma:

For Patients and the Public

• Increase public awareness of asthma as a significant public health problem.

• Increase public awareness of the signs and symptoms of asthma.

• Improve the knowledge, attitudes, and skills of patients regarding the detection, treatment, and control of asthma, particularly in high-risk populations.

• Define guidelines for effective asthma education programs.

• Promote development, dissemination, and use of patient and family education materials.

For Health Professionals

• Increase knowledge, attitudes, and skills of all health professionals regarding signs, symptoms, and management strategies for asthma.

• Encourage health professionals treating patients with asthma to adequately track and monitor patient status and to use objective measures of lung function.

• Assist and encourage health professional schools and continuing education programs to include up-to-date and accurate information on diagnosis, pathogenesis, and treatment of patients with asthma.

• Promote and encourage the concept of active patient participation with the physician in the management of asthma.

• Develop resources and materials for use by health professionals.

• Promote research to answer unresolved questions about underlying causes of asthma and appropriate asthma treatment and management practices.

With the implementation of these objectives, it is thought that the effect of asthma on our population can be minimized. The working objectives for respiratory diseases are outlined in the

West Virginia Healthy People 2010 Objectives for Respiratory Diseases.[4]

Asthma- pathophysiology

I. Airway inflammation

Airway inflammation in asthma involves cells like eosinophils, neutrophils, CD4 , T lymphocytes and mast cells.The inflammation is largely exhibited in conducting airways (large airways), however with the increase in the severity of the disease the inflammation spreads proximately as well as distally into small airways and adjacent alveoli.Inflammation in large airways resides in the submucosa, while that in the small airways is outside the airway smooth muscle[9].

THE IMMUNE RESPONSE -

Allergen induced asthma demonstrates the ability of airway to identify common enbvironmental allergens and subsequent generation of Th2 cytokine response.This immune response to allergens is initiated on the airway-surface.Dendritic cells uptake and process the allergens,the uptake is enhanced by IgE bound to high affinity receptors on tehese dendritic cells.After getting engaged with allergens,dendritic cells receive signals for migration into local lymphoid collections where it presents antigen.This presentation to the T-cell receptor instigates sensitization and the subsequent immune response to the specific allergen.Dendritic cells generate IL-12 which is capable of counter-attacking Th2 sensitization.Once sensitized, T cells migrate to airways and also become potent producers of range of cytokines including IL-3, IL-4, IL-5, IL-6, IL-9, IL-13 and granulocyte-macrophage colony stimulating factor[9].

Schemetic representation of the inflammatory cascade in allergic asthma[9].

THE IMMUNE RESPONSE -

Allergen induced asthma demonstrates the ability of airway to identify common enbvironmental allergens and subsequent generation of Th2 cytokine response.This immune response to allergens is initiated on the airway-surface.Dendritic cells uptake and process the allergens,the uptake is enhanced by IgE bound to high affinity receptors on tehese dendritic cells.After getting engaged with allergens,dendritic cells receive signals for migration into local lymphoid collections where it presents antigen.This presentation to the T-cell receptor instigates sensitization and the subsequent immune response to the specific allergen.Dendritic cells generate IL-12 which is capable of counter-attacking Th2 sensitization.Once sensitized, T cells migrate to airways and also become potent producers of range of cytokines including IL-3, IL-4, IL-5, IL-6, IL-9, IL-13 and granulocyte-macrophage colony stimulating factor[9].

Schemetic representation of the inflammatory cascade in allergic asthma[9].

MAST CELLS-

Allergens provocate asthmatic reaction which is mast-celkl dependent.Previously it was thought that the mast cells present in the epithelium of airway and sub-mucosa contribute to asthma.However, recent studies indicate that mast cells present deep in the airway walls also contribute towards the development of asthma.Mast cells are activated through the high affinity IgE receptor (FcεRI), thus causing release of cytokines including IL-4 and IL-5.Sodium cromoglycate and nedocromil sodium inhibits the secretion from mast cells[9].

EOSINOPHILS-

These cells are present in the airway wall and also in sputum and bronchoalveolar lavage fluid,in large amount.Eosinmophils have the capacity to generate eicosanoids such as prostacyclin, and cysteinyl leukotrienes, and also range of cytokines and chemokines.On treatment of asthma the level of eosinophils decreases in tissue and sputum, thus proving the fact that eosinophils contribute to airway dysfunction leading to asthma[9].

MONOCYTES AND MACROPHAGES-

Monocytes are capable of differentiating into macrophages and dendritic cells in the prtesence of GM-CSF (granulocyte-macrophage colony stimulating factor).They are an important source of cysteinyl leukotrienes but the exact mechanism in mediating asthma is still unknown[9].

II.Airway wall remodelling-

Airway smooth muscle increase in amount because of hypertrophy and hyperplasia, and also spread throught the airways.Increase in airway smooth muscles causes the thickening of airways and also accounts for hyper-responsiveness in asthma.Remodelling is more prominent in those with chronic astrhma rather than those who are hyper-reactive.Intensive studies initiated to study cell and molecular abnormalities in airway smooth muscles leading to asthma have failed to elucidate the exact cause of abnormalities[9].Some of the structural changes observed due to airway wall remodelling are as follows-

-Epithelial alteration

-Subepithelial fibrosis

-Increased smooth muscle mass

-Goblet and mucous gland hyperplasia

-Angiogenesis

-Loss of cartilage integrity.

The possible consequences of Airway remodelling are:-

1. Increased effect of smooth muscle contraction

2. Development of irreversible obstruction/increased decline in lung function

3. Increased risk of mucous plugs in severe exacerbations[10].

Schematic representation of the interactions between airway inflammation and remodelling in clinical asthma[9].

Asthma- Targets[6]

Asthma can be treated by targetting various receptors, enzymes and other physiological molecules.Following are the probable targets of asthma:-

I.RECEPTORS-

01. β2 receptors in bronchii (its activation treats asthma)

02. LT2 receptor, LTC4 & LTD4 [cys-leukotrienes] (its inhibition may treat asthma)

03. LT1 receptor, LTB4 (its inhibition may treat asthma)

04. TP receptor, TxA2 (its inhibition may treat asthma)

05. DP receptor, PGD2 (its inhibition may treat asthma)

06. EP receptor, PGE2 (its activation may treat asthma)

07. PF receptor, PGF2α (its inhibition may treat asthma)

08. 5-HT2A receptor (its inhibition may treat asthma)

09. Adenosine receptors [A1] (its inhibition may treat asthma)

10. Histamine receptors [H1, H4 ] (its inhibition may treat asthma)

II.ENZYMES-

11. COX-2 [cyclooxygenase-2] (its inhibition may treat asthma)

12. 5-LOX [5-lipooxygenase] (its inhibition may treat asthma)

13. PAF [platelet activating factor] (its inhibition may treat asthma)

14. Phosphodiesterase-IV (its inhibition may treat asthma)

15. Phospholipase A2 (its inhibition may treat asthma)

III. CELLS-

16. Mast Cells (inhibititon of degranulation of mast cells may treat asthma)

17. Eosinophils (its inactivation or prevention of its activation protects destruction of airway epithelium, hence hyper-responsiveness)

18. Th1 & Th2 cells (their inactivation may treat asthma)

IV. NOVEL TARGETS-

19. Neutralisation of IgE receptors present on Mast Cells.

20. Prevention of antigen : antibody reaction.

21. Modulation of RESPIRATORY CENTRE present in Medulla.

Asthma- Plants with proven activity[5]

PLANT

PARTS USED

EXTRACT/ACTIVE PRINCIPLE

M.O.A

A. aspera

Roots

Oily preparation

Decreased ESR and total eosinophil count

A. lebbec

Stem bark

Aqueous extract

Mast cell stabilization

B. serrata

Root

Boswellin, boswellic acids

Inhibits 5- LOX

C. gigantia, C. procera

Flower

Α & β vcalotropeol, β- amyrin, calotropin, giganteol

Bronchodilator, antiinflammatory

C. deodara

Wood

Himacholol

Mast cell stabilizer

C. minima

Whole plant

Pseudoguainolid, sesquiterpene, lactones, flavonoids

Inhibits passive cutaneous anaphylaxis in rats

P. kurroa

Roots

Picorrhizin

Inhibits release of histamine and SRS-A

S. xanthocarpum

Herb

Salasodin

Bronchodilator

S. brevistigma

Twigs

Alkaloid fraction

Inhibits passive cutaneous anaphylaxis in rats

T. purpurea

Whole plant

Ethanolic extract

Bronchodilator, anti-anaphylactic

V. negundo

Leaves

Alcoholic extract

Bronchodilatory, and membrane stabilizing

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