Project Topic

Asthma in the Modern Age: Management Strategies,

Smoking Correlations, and Emerging Therapies

ID:18BGE047
 Asthma Definition

 Asthma is a disease that affects the airways in the lungs.

 The airways are tubes that carry air in and out of your lungs.
 If you have asthma, your airways can become inflamed and
narrowed at times. This makes it harder for air to flow out of your
airways when you breathe out.
 It’s a chronic (ongoing) condition, meaning it doesn’t go away and
needs ongoing medical management.
 Triggers

Irritants in the air: Different environment factors like pollen, dust, wood fire,
perfumes, chemical in the air, can also bring on an asthma episode. Although people
are not allergic to these items, they can bother inflamed, sensitive airways.

 Hereditary: If your family has history of asthma or allergic diseases, you have higher
risk of developing asthma.
 Triggers

 Weather condition: Inhaling cold and dry air can cause the
airways to tighten and produce mucus, leading to asthma
symptoms like coughing, wheezing, and shortness of breath.

 Physical exercise: Exercise-induced bronchoconstriction (EIB) is

the transient narrowing of the airways due to physical exertion.
Symptoms include wheezing, coughing, shortness of breath, and
chest tightness during or after exercise. It occurs due to increased
ventilation leading to airway cooling and drying
 Triggers

 Infection: Viral infections, such as those caused by common cold viruses like
rhinoviruses, can inflame and irritate the airways, often leading to asthma
exacerbations. In young children, respiratory syncytial virus (RSV) can cause
severe respiratory symptoms and is a significant risk factor for developing
asthma later in life.

 Psychological stress : Stress and anxiety, can significantly impact asthma

symptoms through various physiological and psychological mechanisms. Stress
can trigger hyperventilation, leading to rapid breathing and subsequent airway
constriction and narrowing, exacerbating asthma symptoms like wheezing and
shortness of breath.

 Tobacco smoke: If you or someone in your home smokes, you have a higher
risk of developing asthma.
 Pathophysiology

 Inhaled allergen taken up by dendritic cells that lie in the respiratory

epithelium.
 The interaction of the allergen with antigen presenting cell (APC) and
native T cell lead to the differentiation into T- helper ( Th-2) cells.
 T- helper-2 cell then release major cytokines like IL-4 and IL-5.
 IL-4 activates B cell which differentiate into plasma cell and release
IgE antibodies that attach to the surface of mast cells. The mast cell
then degranulate when the allergen bridges two IgE molecules on their
surface.
 As the mast cell degranulation, it release histamine, prostaglandins
(PGD2),leukotriene ( LTC4, LTD4, LTE4 etc.) which causes
bronchoconstriction, smooth muscle hyperplasia, vasodilation, mucus
secretion.
 Pathophysiology

 IL-5
activates eosinophils which release different inflammatory mediators like
Major binding protein (MBP), Eosinophil peroxidase (EPO), Eosinophil cationic
protein (ECP), Tumor necrosis factor (TNF) which causes damage of the lung
epithelial.

 Theseinflammatory mediators leads damage lung structural cells, smooth muscle

thickening, goblet cell metaplasia which cause airway remodeling.

 All of them cause bronchial airway narrowing, and asthma symptoms.

 Smoking & Asthma correlation

 A study of 4,000 adults initially aged 18–30 years, which was followed-up over 10 years
with serial spirometry measurements, found that
the decline in FEV1 was 8.5% in never smokers without asthma (n=2,393),
10.1% in non smokers with asthma (n=437) and 11.1% in smokers without
asthma(n=514).

The combination of asthma and smoking (n=101) had a synergistic effect on the decline in
lung function, and resulted in a 17.8% decline in FEV1 over 10 years.

 In 2007, a telephone survey of 11,962 asthmatic adults in the United States revealed that
those who currently smoked reported more asthma attacks (OR, 1.2; 95% CI, 1.0 –1.4) and
more nocturnal asthma symptoms (OR, 2.0; 95% CI, 1.4 –2.7) during the past 30 days than
those who did not smoke.
 Chances of Asthma in Children due to
Parental Smoking

 Studies carried out in the United States in the 1970s were the first to
provide evidence of the effects of Passive smoking on lung function in
children exposed to ETS.
 A wide-reaching prospective study in Germany, carried out on 7284
children between 9 and 11 years of age, found that children of parents
who smoked at home had lower peak expiratory flows and maximum
Expiratory flows at 75%, 50%, and 25%
 In a systematic review of 39 international studies, demonstrate a direct
relation between Parental smoking and increased respiratory risk in
Children OR=1.7; (95% CI, 1.6-1.9) if the smoker was the mother and
OR=1.3; (95% CI, 1.2-1.4) if the smoker was the father
Asthma management strategies

 Patient Education: Effective asthma management begins with educating patients about
their condition, including understanding their triggers and the proper use of
medications.

 Minimizing Exposure to Asthma Triggers: Identifying and reducing exposure to asthma

triggers like using air purifiers and avoiding known irritants, can significantly improve
asthma control.

 Monitoring Lung Function: Regular monitoring of asthma symptoms and lung function,
using tools like peak flow meters, allows for timely adjustments in treatment.

 Pharmacologic Therapy: Managing asthma effectively often necessitates pharmacologic

medications, like short-acting beta-agonists (SABAs), provide immediate relief during an
asthma attack, while long-term control medications, such as inhaled corticosteroids,
help reduce inflammation and prevent symptoms over time.
Emerging Treatment Approach

Anti IgE Antibody: Omalizumab is a humanized monoclonal antibody that targets the
high-affinity immunoglobulin E (IgE) receptor on mast cells, basophils, and dendritic
cells. This action reduces circulating IgE levels, preventing the release of mediators from
mast cells and basophils when exposed to allergens.

 Anti Interleukin -4 antibody: IL-4 play a crucial role for asthma development. IL-4
activate and promoting isotype class switching of B cells to IgE synthesis and recruiting
mast cells. IL-4 binds to the interleukin-4 receptor α (IL-4Rα) present on the B cell &
plasma cell.
 Dupilumab : An antibody that targets the IL-4 receptor alpha (IL-4Rα), inhibiting both
IL-4 and IL-13 signaling pathways. It is used to treat moderate to severe atopic asthma .
 Emerging Treatment Approach

Anti IL-5 Antibody: Anti-IL-5 antibodies are a class of

immunotherapeutic agents designed to target and neutralize
interleukin-5 (IL-5), a cytokine that plays a critical role in the growth,
differentiation, recruitment, activation, and survival of eosinophils.

Reslizumab , mepolizumab monoclonal antibody targeting IL-5, used

for the treatment of severe eosinophilic asthma.