The air passage epithelial tissue, while playing an of import function as a physical barrier, is now known to be cardinal to asthma pathogenesis. Bronchial biopsies in anything but the mildest signifiers of asthma show countries of epithelial metaplasia and harm, thickener of the subepithelial basal lamina, increased figure of myoi¬?broblasts, and other grounds of airway reconstructing such as hypertrophy and hyperplasia of airway smooth musculus, mucose secretory organ hyperplasia, angiogenesis and an altered deposition and composing of extracellular matrix proteins and proteoglycans ( Holgate et al. 2004 ) . While these diseased characteristics have been normally reported in asthma deceases and in bronchial biopsies from patients with asthma of changing badness, more late similar i¬?ndings have been found in the air passages of kids in relation to the oncoming of asthma ( Barbato et al. 2006 ) . Evidence of epithelial harm with upregulation of cuticular growing factor receptors ( EG FRs ) and characteristics of elf aired proliferation, e.g. , reduced look of proliferative markers such as Ki6 7 and proliferating cell atomic antigen ( PCNA ) and upregulation of the cell cyclin inhibitor, atomic p21, suggest that, as in grownup asthma ( Puddicombe et al. 2003 ) , the epithelial tissue is inveterate injured and unable to mend decently ( Kicic et al. 2006 ) . One of import characteristic of the wheezing epithelial tissue is its capacity to support itself against oxidant hurt, a characteristic that may partially explicate why wheezing topics are so sensitive to oxidant pollutants such as ozone, environmental baccy fume and ambient air particulates ( Truong-Tra n et Al. 2003 ) .


Asthma is a heterogenous upset ( Wenzel 2006 ) . Although different types of asthma have long been recognized, such as that triggered by exposure to allergens, occupational chemicals, non steroidal anti inflammatory drugs ( NSAIDs ) and non allergic ”intrinsic ” asthma, there has ne’er been a cellular or molecular footing for these different manifestations of intermittent airflow obstructor other than exposure to a peculiar environmental stimulation. With the coming of i¬?beroptic bronchoscopy and the ability to biopsy different parts of the bronchial tree, not invasive lung imaging such as HRCT and the development of therapeutics that target individual cells or tracts, it is now clear that asthma is non a individual disease but a broad rang vitamin E of different upset s that portion some common phenotypes such as reversible airflow obstructor and associated symptoms. Using noninvasive markers of airway redness suggests the presence of at least four distinguishable ”phenotypes ” : eosinophilic, neutrophilic, assorted inflammatory, and paucigranulocytic asthma ( Wenzel 2006 ) .

1.10.1. Eosinophilic asthma

Bronchial biopsy surveies of patients with mild asthma have shown that eosinophilic airway redness is extremely characteristic regardless of whether patients were atopic, non atopic, aspirin-sensitive, or had occupational asthma ( Bochner & A ; Busse 2005 ) . when eosinophils appear to be activated. With the coming of phlegm initiation it appears that there is a complex relationship between eosinophilic redness and other markers of asthma, including lung map and airway hyper reactivity. In contrast eosinophilic airway redness appears to be much more closely related to the hazard of terrible asthma aggravation ( Green et Al. 2002 ) .

1.10.2. Neutrophilic asthma

The usage of induced phlegm every bit good as lavage and i¬?beroptic bronchoscopy has revealed that some patients with asthma have a phlegm neutrophilia in the absence of eosinophils ( Tsoumakidou et a l. 2006 ) . Other surveies have noted neutrophilic redness in some patients with terrible asthma and during virus induced aggravations. In add-on, patients with terrible asthma treated with unwritten ( but non inhaled ) corticoids besides exhibit a preponderantly neutrophilic air passage redness and absence of eosinophils. Intense neutrophilic redness has besides been reported in patients ventilated for ague terrible asthma and in those who died all of a sudden of asthma ( Carroll et al. 1996 ) . In general, asthma associated with neutrophils tends to be a more aggressive disease perchance with more tissue devastation and airway reconstructing ( Holgate & A ; Polosa 2006 ) . Tobacco smoke is besides associated with a greater neutrophil constituent and, significantly, corticosteroid unmanageableness in both the air ways and systemically.

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1.10.3. Assorted eosinophilic and neutrophilic asthma

Mixed eosinophilic and neutrophilic asthma has besides been associated with Mycoplasma pneumoniae and/or Chlamydia pneumonia infection, with a good response to macrolide disinfectants ( John-ston et al. 2006 ; Kraft & A ; Hamid 2006 )

1.10.4. Paucigranulocytic asthma

Although sudden asthma decease has been recorded in the absence of airway redness, this is extremely unusual. Asthma in the absence of either neutrophils or eosinophils ( paucigranulocytic asthma ) has been described in which MMP-9 degrees in phlegm disease were normal as opposed to elevated degrees in patients with eosinophilic asthma ; ( Simpson et al. 2005 ) , proposing that an unnatural epithelial tissue or implicit in mesenchyme and /or smooth musculus may itself take to an asthma phenotype without the presence of obvious redness.

1.11. ASTHMA features

Asthma may be chronic or acute ( Rang et al. , 2006 ) .

In chronic asthma, the person has intermittent onslaughts of dyspnoea upset of take a breathing ) , wheezing, and cough, the dyspnea consisting of trouble in take a breathing out. Note that the term reversible as applied to chronic asthma demands to be qualified since it is merely the acute onslaught of dyspnea that is reversible-the implicit in pathological alteration may non be reversible and so can come on.

Acute terrible asthma ( besides known as position asthmaticus ) is non easy reversed. It can be fatal and requires prompt and energetic intervention. Hospitalization may be necessary.

It is presently recognized that the characteristic characteristics of most instances of asthma are:

inflammatory alterations in the air passages

bronchial hyper-reactivity

In allergic asthma, these are related to, and follow from, anterior sensitization.

The term bronchial hyper-reactivity ( or hyper-responsiveness ) refers to unnatural sensitiveness to a broad scope of stimulations such as irritant chemicals, cold air, stimulating drugs etc. , all of which can ensue in bronchoconstriction. Stimuli that cause the existent asthma onslaughts are many and varied and include allergens ( in sensitized persons ) , exercising ( in which the stimulation may be cold air ) , respiratory infections and atmospheric pollutants ( such as S dioxide. The non-steroidal anti-inflammatory drugs NSAIDs ) , particularly aspirin can precipitate asthma in sensitive persons.


In allergic asthma, there is prevailing activation of the T assistant ( Th2 ) type 2 cell. Sensitization involves exposure of genetically predisposed persons to allergens such as pollen or proteins of the house dust touch ; environmental factors ( e.g. atmospheric pollutants may lend to asthma ) . The allergens interact with dendritic cells and helper lymph cells giving rise to a ringer of Th2 lymph cells, which so:

Generate a cytokine environment that switches I? cells/plasma cells to the production and release of IgE

Generate cytokines such as interleukin-5 ( IL-5 ) , which promote distinction and activation of eosinophils.

1.13. Chronic clogging pneumonic disease ( COPD )

This is a disease characterized by a progressive air flow restriction caused by the unnatural inflammatory reaction to the chronic inspiration of atoms. COPD presently ranks as the 4th taking cause of decease in developing states. One of the most distressing facets of COPD is that is Under recognized by the patients and doctors and confused with that of asthma and lead to arguably undertreated. ( Kelly Sequeira et Al 2007 ) .

1.13.1. General characters of COPD

The pathophysiology is chiefly characterized by redness throughout the cardinal and peripheral air passages, lung parenchyma, and pneumonic vasculature. The usual cause of COPD is smoking. ( Hargreave FE et al- 2006 )

In the cardinal airways the redness caused by activation of centripetal nervus terminations by inhaled thorns consequences in increased mucous secretion production and impaired mucociliary clearance. It has been found that the mucose secretory organs become hypertrophied and the figure of globet cells increases, taking to mucus hypersecretion. ( Rodriguez-Roisin R et al- 2005 ) . Bacterial growing will happen in this country and things become more hazardous.

Repeated rhythms of redness and fix lead to structural narrowing of the air passages. This will take to airway remodeling, including collagen deposition and cicatrix tissue formation in the air passage wall that narrow the airway lms and leads to airway obstructor. Obstruction of the air passages leads to decrease in inspiratory capacity, consequences in dyspnoea and reduced exercising tolerance. Chronic bronchitis and emphysema are frequently present in COPD patients ( Rodriguez-Roisin R et al- 2005 ) . Chronic bronchitis

In COPD patients, chronic bronchitis is depicted by redness with mucous secretion production, and narrowing of the cardinal air passages. This will ensue in impaired muco-ciliary clearance and increased connective tissue deposition. ( Hogg J et Al. 2004 ) Emphysema

Emphysema is the lasting expansion of the air spaces distal to the terminal bronchioles, accompanied by devastation of their walls and without obvious fibrosis.

1.13.2. Comparison with COPD and ASTHMA



All air passages

Peripheral air passages

Hyperresponsiveness a†‘a†‘a†‘

Hyperresponsiveness a†‘


Epithelial casting

Epithelial mataplasia


Fibrosis a†‘a†‘a†‘

Fibrosis a†‘

No paranchymal alteration

Paranchymal devastation

Mucus secretiona†‘

Mucus secretiona†‘a†‘a†‘

Inflammatory cells

Mastcells, Eosinophils, , CD4+Lymphocytes,

Macrophages etc

Neutrophils, CD8+Lymphocytes,

Macrophages etc

Inflammatory go-betweens

Histamine, IL-4, IL-5, IL-13

Eotaxin, Rantes, oxidative


IL-8, IL-6, TNFI±

GRO-I± , MCP-1,

Oxidative emphasis.

Table.1. defferance between Asthma & A ; COPD


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