With the blooming of spring flowers and sprouting of fresh
green leaves and grasses, we are reminded that life is all around us. Quite
literally, too, as windborne plant pollen is small enough to enter our eyes,
nose, and mouth. Pollen, the primary cause of seasonal allergies, contains the
male gametophytes of seed-bearing grasses and trees. Each pollen grain contains
a generative cell, or sperm, which fertilizes the egg of the female plant, and
a vegetative cell, which develops into a pollen tube and delivers the sperm to
the ovule. Many trees and grasses rely on wind to spread their pollen and
fertilize the female plant. So although your college roommate may have been
discrete while attempting to procreate, wind-pollinated plants uphold no such
personal boundaries.
So which plants are responsible for producing the powdered cheese-like substance that coats our houses, bicycles, and cars? Although thousands of plant species produce pollen that makes the Holderness family cough and gag, only a handful are responsible for their allergic wheezing and sneezing.
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| Next time you smell a flower, realize you are sniffing a plant’s “naughty bits”. |
So which plants are responsible for producing the powdered cheese-like substance that coats our houses, bicycles, and cars? Although thousands of plant species produce pollen that makes the Holderness family cough and gag, only a handful are responsible for their allergic wheezing and sneezing.
The exact timing of seasonal allergies can vary depending
on region and climate. You can blame your early spring allergies on tree pollen,
particularly that from birch trees. From March to May, many other trees
including beech, ash, pine, box elder, cottonwood, oak, mulberry, elm, alder,
cedar, hazel, willow, poplar, linden, olive, hornbeam, and plane contribute to
early spring allergies. By June, grass pollen becomes predominant, especially
timothy and ryegrass. Other grasses such as Bermuda, Johnson, Kentucky
bluegrass, orchard, redtop, sweet vernal, and rye contribute to allergies. As
the heat and humidity rises during July and August, your hair and electricity
bill aren’t the only things that grow. Molds can thrive in grass, grains and
leaves; airborne spores can cause hay fever.
The warm days and cool nights of late summer and autumn
are perfect conditions for weeds, particularly ragweed, which is the primary
cause of autumn-onset seasonal allergies. Ragweed can produce metric tons of
pollen per square mile of plant. Other weeds that produce allergenic pollen are
cocklebur, burning bush, lamb’s quarters, pigweed, plaintain, Russian thistle,
sagebrush, mugwort, and sheep sorrel.
The heavy vegetation towards the end of the growing
season provides a perfect breeding ground for additional outdoor mold. Mold
grows in fallen autumn leaves, hay, and straw, and can be stirred up during
raking or baling. In general, mold spores are considered perennial allergens
because mold has the potential to grow outdoors and indoors, especially in
kitchens, bathrooms, and basements throughout the entire year. However, growth
conditions are optimal during different seasons, potentially resulting in a
seasonal effect with mold allergies.
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| Even in winter, mold spores on indoor live pine trees can cause an allergic reaction. So even though the pine tree isn’t releasing pollen, it can still aggravate hay fever symptoms. |
Other perennial allergens besides mold spores include dust mites, pet hair dander, and cockroach droppings. Dust mites are always present, but have been shown to increase with installation and use of central heating and insulated windows in apartment buildings. And although we may not even know cockroaches are present, the proteins in their droppings can cause hay fever. Cat dander is the most common cause of pet allergies, but thankfully The Big Bang Theory writers conveniently overlooked Sheldon’s alleged cat dander allergy so he could adopt this zazzy guy.
What is it about allergens that trigger the allergic response? Although scientists have worked to understand the molecular details of allergens and how they interact with components of our immune system, there is no clear answer as to what specifically makes something allergenic. However, within many of the most common allergens, the primary antigen has been identified. The antigen is the specific molecule that is recognized by our immune system. Antigens can be different components of a bacterial cell or viral particle; in the case of allergens, it is a protein derived from pollen, dander, mold, etc.
Pollen from birch trees is one of the largest
contributors to hay fever in spring and early summer in North America The
primary antigen from birch tree pollen, Betula
verrucosa is called Bet v 1.
The Bet v 1 antigen exists as a mixture of 14 isoforms that share ≥ 96.5%
sequence identity; these isoforms possess different binding capabilities for
the antibody immunoglobulin E (IgE). In fact, only 1 of the 14 isoforms, Bet v
1.0101, induces an immune response in an individual with birch tree allergy,
and the two other isoforms tested, Bet v 1.0401 and Bet v 1.1001 induced no
response (PMID: 20005001). Immune cells
isolated from patients with no birch tree allergy did not react to any of the
isoforms. The difference in the antigens is their affinity for the IgE, but precisely
what makes one antigen more reactive than the other is unclear. On a basic
level, the protein sequence and structure influence the binding to antibodies.
One complication with diagnosing and treating allergies
is the potential for cross-reactivity between different antigens. In some parts
of the world, allergic patients are double-sensitized to ragweed and mugwort, Artemisia vulgaris. The flowering season
of these two plants overlaps, making it difficult to diagnose the primary
sensitizer. In addition to increasing the number of allergies a patient may
have, cross-reactivity also complicates prescription of the correct
immunotherapy to combat the primary allergy. The primary antigen of mugwort is
Art v 1 and up to 95% of people are sensitized to Art v 1. However, a minor
mugwort antigen, Art v 6 shares high homology with and commonly cross-reacts
with the primary ragweed antigen, Amb a 1. At least 90% of ragweed-allergen
sufferers are sensitized to Amb a 1. This means that patients who are allergic
to ragweed may be sensitive to mugwort and vice versa. New proteomic
technologies allow for more accurate diagnoses of the primary sensitizer so
that the proper immunotherapy can be prescribed. Treatment of allergies will be
discussed in article 4 of this series.
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Birch pollen primary antigen Bet v 1 (wikipedia.org)
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With so many potential allergens bombarding us more or
less year-round, it’s almost surprising that more of us don’t suffer from hay
fever. As mentioned above, 1 in 5 people are afflicted and, unfortunately, that
number is increasing, particularly in suburban areas of North America. Perhaps
the reason allergies are not more common is because they are not hardwired into
us, as is the immune response to infectious agents such as bacteria, viruses,
and parasites. Hay fever is considered an atopy, a genetic predisposition to
mount inappropriate immune responses to harmless environmental allergens. The
immune response mounted against allergens will be described in detail in
article 2 of this series.
The tendency to have seasonal allergies is hereditary,
but does not follow Mendelian principles, like inheritance of eye or hair
color. In addition to genes, the environment contributes to allergy
susceptibility. Understanding the genetic and environmental factors involved in
allergy development is complex and requires sound knowledge of the actual
allergic response. A more complete discussion of genetic and environmental
factors that influence allergy susceptibility will be presented in the third
article of this series. We hope you’ll tune in for the remaining articles in
this ongoing series.
Hirsch T, Hering M, Bürkner K, Hirsch D, Leupold W, Kerkmann ML, Kuhlisch E, & Jatzwauk L (2000). House-dust-mite allergen concentrations (Der f 1) and mold spores in apartment bedrooms before and after installation of insulated windows and central heating systems. Allergy, 55 (1), 79-83 PMID: 10696861
Leb VM, Jahn-Schmid B, Schmetterer KG, Kueng HJ, Haiderer D, Neunkirchner A, Fischer GF, Nissler K, Hartl A, Thalhamer J, Bohle B, Seed B, & Pickl WF (2008). Molecular and functional analysis of the antigen receptor of Art v 1-specific helper T lymphocytes. The Journal of allergy and clinical immunology, 121 (1), 64-71 PMID: 18037161
Jahn-Schmid B, Hauser M, Wopfner N, Briza P, Berger UE, Asero R, Ebner C, Ferreira F, & Bohle B (2012). Humoral and cellular cross-reactivity between Amb a 1, the major ragweed pollen allergen, and its mugwort homolog Art v 6. Journal of immunology (Baltimore, Md. : 1950), 188 (3), 1559-67 PMID: 22205029
Wopfner N, Bauer R, Thalhamer J, Ferreira F, & Chapman M (2008). Immunologic analysis of monoclonal and immunoglobulin E antibody epitopes on natural and recombinant Amb a 1. Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 38 (1), 219-26 PMID: 18028463
Asero R, Bellotto E, Ghiani A, Aina R, Villalta D, & Citterio S (2014). Concomitant sensitization to ragweed and mugwort pollen: who is who in clinical allergy? Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology, 113 (3), 307-13 PMID: 25053399
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