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Aeroallergen pathways

An aeroallergen (pronounced aer·o·al·ler·gen) is any airborne substance, such as pollen or spores, which triggers an allergic reaction.


Aeroallergens include the pollens of specific seasonal plants is commonly known as "hay fever", because it is most prevalent during haying season, from late May to the end of June in the Northern Hemisphere; but it is possible to suffer from hay fever throughout the year.

The pollen which causes hay fever varies from person to person and from region to region; generally speaking, the tiny, hardly visible pollens of wind-pollinated plants are the predominant cause. Pollens of insect-pollinated plants are too large to remain airborne and pose no risk.

Examples of plant pollen commonly responsible for hay fever include:

  • Trees: such as birch (Betula), alder (Alnus), cedar (Cedrus), hazel (Corylus), hornbeam (Carpinus), horse chestnut (Aesculus), willow (Salix), poplar (Populus), plane (Platanus), linden/lime (Tilia) and olive (Olea). In northern latitudes birch is considered to be the most important allergenic tree pollen, with an estimated 15–20% of hay fever sufferers sensitive to birch pollen grains. Olive pollen is most predominant in Mediterranean regions.
  • Grasses (Family Poaceae): especially ryegrass (Lolium sp.) and timothy (Phleum pratense). An estimated 90% of hay fever sufferers are allergic to grass pollen.
  • Weeds: ragweed (Ambrosia), plantain (Plantago), nettles/parietaria (Urticaceae), mugwort (Artemisia), Fat hen (Chenopodium) and sorrel/dock (Rumex)

The time of year at which hay fever symptoms manifest themselves varies greatly depending on the types of pollen to which an allergic reaction is produced. The pollen count, in general, is highest from mid-spring to early summer. As most pollens are produced at fixed periods in the year, a long-term hay fever sufferer may also be able to anticipate when the symptoms are most likely to begin and end, although this may be complicated by an allergy to dust particles.


Spores being ejected by fungi

In fungi, both asexual and sexual spores or sporangiospores of many fungal species are actively dispersed by forcible ejection from their reproductive structures, which travel through the air over long distances. Many fungi thereby possess specialized mechanical and physiological mechanisms as well as spore-surface structures, such as hydrophobins, for spore ejection. These mechanisms include, for example, forcible discharge of ascospores enabled by the structure of the ascus and accumulation of osmolytes in the fluids of the ascus that lead to explosive discharge of the ascospores into the air.[1] The forcible discharge of single spores termed ballistospores involves formation of a small drop of water (Buller's drop), which upon contact with the spore leads to its projectile release with an initial acceleration of more than 10,000 g.[2] Other fungi rely on alternative mechanisms for spore release, such as external mechanical forces, exemplified by puffballs.


It is thought that peanuts and other allergic foodstuffs may become airborne, thus triggering allergic reactions in susceptible individuals, especially children.[3][4][5]

However, one report notes:

Recently concern has been raised that peanut protein in the air will trigger a full-blown anaphylaxis since respiratory exposure can occur in the school setting as food proteins aerosolize into vapors during cooking at high temperatures, even in well-ventilated cafeterias. When airborne peanut protein exposure and reactions of children with known peanut allergies were explored, no allergic symptoms or anaphylaxis were observed when peanut allergic children were not aware of the airborne exposure. Interestingly, when aware of the exposure, symptoms of itchy eyes, sneezing, and runny nose resulted. In a research article by Perry, et al. (2004), no peanut allergen was detected in the air after subjects consumed peanut butter, shelled peanuts, and unshelled peanuts. As Dr. Michael Young notes in his 2006 book, The Peanut Allergy Answer Book, predicting who will have a life-threatening anaphylactic response to airborne allergy is very unpredictable and the likelihood of it is very, very small. ... There remains no evidence that exposure to airborne peanut protein worsens allergy or results in anaphylaxis for the majority of peanut allergic individuals. There always remains the possibility that someone who is exceptionally sensitive will experience a severe reaction, however, protecting them from all possible exposures to peanut protein is extremely difficult.

— NetWellness website[6]

Eosinophilic gastroenteritis

Eosinophilic gastroenteritis (EG) is a rare and heterogeneous condition characterized by patchy or diffuse eosinophilic infiltration of gastrointestinal (GI) tissue, first described by Kaijser in 1937.[7][8] Aeroallergens can cause EG.[9][10]

The stomach is the organ most commonly affected, followed by the small intestine and the colon.[11][12]

As a part of host defense mechanism, eosinophil is normally present in gastrointestinal mucosa, though finding in deeper tissue is almost always pathologic.[13] What triggers such dense infiltration in EG is not clear. It is possible that different pathogenetic mechanisms of disease is involved in several subgroups of patients. Food allergy and variable IgE response to food substances has been observed in some patients which implies role of hypersensitive response in pathogenesis. Many patients indeed have history of other atopic conditions like eczema, asthma etc.

Eosinophil recruitment into inflammatory tissue is a complex process, regulated by a number of inflammatory cytokines. In EG cytokines IL-3, IL-5 and granulocyte macrophage colony stimulating factor (GM-CSF) may be behind the recruitment and activation. They have been observed immunohistochemically in diseased intestinal wall.[14] In addition eotaxin has been shown to have an integral role in regulating the homing of eosinophils into the lamina propria of stomach and small intestine.[10] In the allergic subtype of disease, it is thought that food allergens cross the intestinal mucosa and trigger an inflammatory response that includes mast cell degranulation and recruitment of eosinophils.[9]

EG is "managed" (treated) with corticosteroids, with a 90% response rate in some studies. Various steroid sparing agents e.g. sodium cromoglycate (a stabilizer of mast cell membranes), ketotifen (an antihistamine), and montelukast (a selective, competitive leukotriene receptor antagonist) have been proposed, centering on an allergic hypothesis, with mixed results.[9][15] An elimination diet may be successful if a limited number of food allergies are identified.[16]

Additional images

Induction and effector mechanisms in Type 1 hypersensitivity

See also


  1. Trail F. (2007). "Fungal cannons: explosive spore discharge in the Ascomycota". FEMS Microbiology Letters. 276 (1): 12–8. doi:10.1111/j.1574-6968.2007.00900.x. PMID 17784861.
  2. Pringle A, Patek SN, Fischer M, Stolze J, Money NP (2005). "The captured launch of a ballistospore". Mycologia. 97 (4): 866–71. doi:10.3852/mycologia.97.4.866. PMID 16457355.
  3. The Michael C. Young, M.D., "Common Beliefs About Peanut Allergy: Fact or Fiction?" (reprinted with permission of the Food Allergy & Anaphylaxis Network, in Anaphylaxis Canada, September newsletter) found at Archived December 27, 2006, at the Wayback Machine. (.pdf) Accessed March 19, 2009.
  4. "Passengers with the condition, which can be deadly, can try to ensure a peanut-free flight. But even the best plans sometimes don't work." See "Out of the Blue: Peanut allergies are a little-known danger." Elliott Hester, St. Petersburg Times, December 30, 2001, St. Petersburg Times Archived 2016-03-04 at the Wayback Machine. Accessed March 19, 2009.
  5. Constance Hays, "Ideas & Trends: Airborne Allergies; A New Fear of Flying: Peanuts", The New York Times, Sunday, May 10, 1998, found at NY Times archives Archived 2021-08-27 at the Wayback Machine. Accessed March 19, 2009.
  6. Jill F. Kilanowski & Ann Stalter (College of Nursing, The Ohio State University), "Children's Health: Peanut Allergy in the School Environment: Myths and Facts: Part 1 of a 2-Part Series", at NetWellness website Archived February 27, 2009, at the Wayback Machine, citing Perry, T., Conover-Walker, M., Pomes, A., Chapman, M., & Wood, R. (2004). "Distribution of peanut allergen in the environment." Journal of Allergy and Clinical Immunology, 113, 973-976. Accessed March 19, 2009.
  7. Kaijser R. Zur Kenntnis der allergischen Affektionen des Verdauugskanals vom Standpunkt des Chirurgen aus. Arch Klin Chir 1937; 188:36–64.
  8. Whitaker I, Gulati A, McDaid J, Bugajska-Carr U, Arends M (2004). "Eosinophilic gastroenteritis presenting as obstructive jaundice". European Journal of Gastroenterology & Hepatology. 16 (4): 407–9. doi:10.1097/00042737-200404000-00007. PMID 15028974.
  9. 9.0 9.1 9.2 Pérez-Millán A, Martín-Lorente J, López-Morante A, Yuguero L, Sáez-Royuela F (1997). "Subserosal eosinophilic gastroenteritis treated efficaciously with sodium cromoglycate". Dig. Dis. Sci. 42 (2): 342–4. doi:10.1023/A:1018818003002. PMID 9052516.
  10. 10.0 10.1 Mishra A, Hogan S, Brandt E, Rothenberg M (2001). "An etiological role for aeroallergens and eosinophils in experimental esophagitis". J. Clin. Invest. 107 (1): 83–90. doi:10.1172/JCI10224. PMC 198543. PMID 11134183.
  11. Naylor A (1990). "Eosinophilic gastroenteritis". Scottish Medical Journal. 35 (6): 163–5. doi:10.1177/003693309003500601. PMID 2077646.
  12. Jimenez-Saenz M, Villar-Rodriguez J, Torres Y, Carmona I, Salas-Herrero E, Gonzalez-Vilches J, Herrerias-Gutierrez J (2003). "Biliary tract disease: a rare manifestation of eosinophilic gastroenteritis". Dig. Dis. Sci. 48 (3): 624–7. doi:10.1023/A:1022521707420. PMID 12757181.
  13. Blackshaw A, Levison D (1986). "Eosinophilic infiltrates of the gastrointestinal tract". J. Clin. Pathol. 39 (1): 1–7. doi:10.1136/jcp.39.1.1. PMC 499605. PMID 2869055.
  14. Desreumaux P, Bloget F, Seguy D, Capron M, Cortot A, Colombel J, Janin A (1996). "Interleukin 3, granulocyte-macrophage colony-stimulating factor, and interleukin 5 in eosinophilic gastroenteritis". Gastroenterology. 110 (3): 768–74. doi:10.1053/gast.1996.v110.pm8608886. PMID 8608886.
  15. Barbie D, Mangi A, Lauwers G (2004). "Eosinophilic gastroenteritis associated with systemic lupus erythematosus". J. Clin. Gastroenterol. 38 (10): 883–6. doi:10.1097/00004836-200411000-00010. PMID 15492606.
  16. Katz A, Twarog F, Zeiger R, Falchuk Z (1984). "Milk-sensitive and eosinophilic gastroenteropathy: similar clinical features with contrasting mechanisms and clinical course". J. Allergy Clin. Immunol. 74 (1): 72–8. doi:10.1016/0091-6749(84)90090-3. PMID 6547462.