Allergic rhinitis - disorder of the nasal cavity
Introduction
1 in 5 adults in Australia, 40% of children and
30% of adults in the United Kingdom, and
approximately 60 million Americans have been
affected by Allergic rhinitis at some point in
their life. It usually goes undetected in the
primary case setting. Allergic-rhinitis, also
known as hay fever, is the inflammation of
mucous membrane lining the nasal cavity. It is considered
as an allergic reaction causing sneezing, itching, nasal
congestion and a runny nose, in response to indoor and
outdoor allergens.[1] Examples of these allergens include pollen, ragweed, dust mites, cats,
smoke and mold. When an individual inhales these allergens through their mouth or nose, their
body responds by generating histamine - a natural molecule.[1]
Types
Allergic rhinitis is of two types. It can either be seasonal or perennial.
a) Seasonal pollination occurs just during the time of year when particular plants pollinate.
Outdoor molds and pollen in the air from grass, trees, and weeds are usually what cause
seasonal allergic rhinitis in the spring, summer, and fall. For instance, if an individual
gets allergic rhinitis in the spring, they are most likely allergic to tree pollen. On the other
hand, during summer, grass and weed pollens may be the source of the allergic response.
Finally, ragweed pollen may cause the symptoms in autumn, while fungal spores cause
issues largely from late March to November, but they can be present all year. When the
temperature becomes colder, particularly after a strong frost, symptoms usually improve.
b) Perennial pollination occurs all year. People who suffer from a year-round (perennial)
allergic rhinitis are frequently sensitive to one or more indoor allergens. Feathers, dust
mites in the house, and the skin flakes of pets such as cats and dogs (animal dander)are
all examples of these contaminants. These contaminants may be found in bedding,
pillows, heavy-draperies, carpetin and upholstery. Mold, another frequent allergy, thrives
in wet environments like bathrooms and basements.
Causes
As a result of allergens being so small, they can be readily inhaled by the individual and can
enter the oral or nasal cavity. When the allergen is inhaled, the immune system reacts to it, and
allergic rhinitis is caused.[1] This causes the entry of several inflammatory-cells, such as B-cells,
T-cells, mast-cells, CD4-positive, macrophages, and eosinophils into the nasal cavity upon
exposure to the inciting allergen. T-cells (mostly T helper 2) infiltrating the nasal mucosa in
allergic persons produce cytokines (e.g., interleukin [IL]-3, IL-4, IL-5, and IL-13) that increase
the synthesis of immunoglobulin E (IgE) by plasma-cells. This causes allergens and IgE to
crosslink, in turn resulting in the release of leukotriene and most importantly histamines which
are essentially mediators causing-dilatation of the arteries, increase in thee vascular-permeability,
itching, rhinorrhea, mucous production, and finally smooth-muscle contraction in the lungs. The
mediators and cytokines generated during the early-phase of an immune response to an
Introduction
1 in 5 adults in Australia, 40% of children and
30% of adults in the United Kingdom, and
approximately 60 million Americans have been
affected by Allergic rhinitis at some point in
their life. It usually goes undetected in the
primary case setting. Allergic-rhinitis, also
known as hay fever, is the inflammation of
mucous membrane lining the nasal cavity. It is considered
as an allergic reaction causing sneezing, itching, nasal
congestion and a runny nose, in response to indoor and
outdoor allergens.[1] Examples of these allergens include pollen, ragweed, dust mites, cats,
smoke and mold. When an individual inhales these allergens through their mouth or nose, their
body responds by generating histamine - a natural molecule.[1]
Types
Allergic rhinitis is of two types. It can either be seasonal or perennial.
a) Seasonal pollination occurs just during the time of year when particular plants pollinate.
Outdoor molds and pollen in the air from grass, trees, and weeds are usually what cause
seasonal allergic rhinitis in the spring, summer, and fall. For instance, if an individual
gets allergic rhinitis in the spring, they are most likely allergic to tree pollen. On the other
hand, during summer, grass and weed pollens may be the source of the allergic response.
Finally, ragweed pollen may cause the symptoms in autumn, while fungal spores cause
issues largely from late March to November, but they can be present all year. When the
temperature becomes colder, particularly after a strong frost, symptoms usually improve.
b) Perennial pollination occurs all year. People who suffer from a year-round (perennial)
allergic rhinitis are frequently sensitive to one or more indoor allergens. Feathers, dust
mites in the house, and the skin flakes of pets such as cats and dogs (animal dander)are
all examples of these contaminants. These contaminants may be found in bedding,
pillows, heavy-draperies, carpetin and upholstery. Mold, another frequent allergy, thrives
in wet environments like bathrooms and basements.
Causes
As a result of allergens being so small, they can be readily inhaled by the individual and can
enter the oral or nasal cavity. When the allergen is inhaled, the immune system reacts to it, and
allergic rhinitis is caused.[1] This causes the entry of several inflammatory-cells, such as B-cells,
T-cells, mast-cells, CD4-positive, macrophages, and eosinophils into the nasal cavity upon
exposure to the inciting allergen. T-cells (mostly T helper 2) infiltrating the nasal mucosa in
allergic persons produce cytokines (e.g., interleukin [IL]-3, IL-4, IL-5, and IL-13) that increase
the synthesis of immunoglobulin E (IgE) by plasma-cells. This causes allergens and IgE to
crosslink, in turn resulting in the release of leukotriene and most importantly histamines which
are essentially mediators causing-dilatation of the arteries, increase in thee vascular-permeability,
itching, rhinorrhea, mucous production, and finally smooth-muscle contraction in the lungs. The
mediators and cytokines generated during the early-phase of an immune response to an
