**2. Methodology**

*Rhinosinusitis*

allergic rhinitis.

Asthma is induced by an inflammatory response against usually manageable environmental inorganic and organic compounds in the respiratory tract. Indeed, asthma attacks can be triggered by exercise, viral illness, and allergens such as pollen. Other triggers include medications, extremes of weather, stress, smoke, and certain foods. Key indicators include a history of respiratory symptoms such as wheeze, shortness of breath, chest tightness, and cough that vary over time and in intensity, together with variable expiratory airflow limitation. It has variations in

Patients diagnosed with atopy have an increased likelihood to allergic responses mediated via IgE, mast cells, and CD4+ lymphocytes. In atopy, the allergic inflammatory responses are mainly due to cytokines (interleukins (IL-3, IL-4, and IL-5)) released from CD4+ lymphocytes. The interleukins increase the IgE production to neutralize the allergens. However, the binding of IgE-allergen complex formed further induces de novo synthesis and release of vasoactive substances that exacerbate the inflammatory reaction. This allergic inflammatory response occurs in two stages (early and late response) in both asthma and

The allergic immune response recognizes allergens via germ line or random encoding, which can be innate and adaptive. The innate allergic immune responses are the first line of defense against allergens that use germ-line encoding and phagocytic cells. In contrast, the adaptive allergic response is mainly designed against

According to the World Health Organization (WHO), the burden of asthma is estimated to have 300 million cases worldwide, making it one of the commonest noncommunicable diseases. Asthma is a serious global health problem affecting all age groups, with increasing prevalence in developing countries, treatment costs, and a burden for patients and the community. The WHO ranks asthma the highest among chronic illnesses afflicting the pediatric population worldwide. Of concern is that the majority of case fatalities attributed to asthma occur among populations in underdeveloped countries characterized with weak health systems for control and

Whereas allergic rhinitis results from activation of mucosal mast cells, asthma is triggered by allergen activation of submucosal mast cells in the lower airways. The nature and development airway inflammation may be driven by numerous factors, including pathogenic infections, pollution, or even relatively innocuous inhaled particles, such as allergens. International guidelines are available for the management of severe asthma by the European Respiratory Society and the American

Chronic allergen exposure leads to the continuous presence of increased number of lymphocytes, eosinophils, neutrophils, basophils, and other leukocytes causing airway hyper-reactivity and remodeling—a thickening of the airway walls due to hyperplasia and hypertrophy of the smooth muscle layer, with the eventual

It has become apparent that there are many phenotypic and endotype types of asthma. In patients with allergic asthma endotypes, allergen can cause activation of mast cells in an antigen-specific manner. Also allergens can stimulate the airway epithelium, through toll-like receptors (TLRs) and other damage receptors, to release IL-25, IL33, and thymic stromal lymphopoietin (TSLP). These cytokines can lead to the activation of submucosal type two innate lymphoid cells (ILC2), induc-

severity, natural history, and response to therapy [4].

infection and allergenic proteins from weed and pollen.

**1.1 Pathogenesis of allergic rhinitis and asthma**

management of the disease [4–7].

Thoracic Society [6].

development of fibrosis.

ing these to release IL-4, IL-5, IL-9, and IL-13.

**118**

A comprehensive review of all aspects of immunology, components of the immune system, immune responses to asthma and allergic rhinitis in children and adults, and airway epithelial cell mucosal immunology was done in a systematic and explicit search of PubMed and HINARI—identifying, selecting, and critically appraising relevant research and textbooks of Immunology from Europe and the United States of America used in undergraduate and postgraduate Medical Education (Cochrane Collaboration) [7–9].
