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Gutworms and similar parasites are present in untreated drinking water in developing countries, and were present in the water of developed countries until the routine [[chlorination]] and purification of drinking water supplies.<ref>{{cite journal |author=Macpherson CN, Gottstein B, Geerts S |title=Parasitic food-borne and water-borne zoonoses |journal=Rev. - Off. Int. Epizoot. |volume=19 |issue=1 |pages=240–58 |year=2000 |pmid=11189719 |doi=}}</ref> Recent research has shown that some common [[parasite]]s, such as [[Intestinal parasite|intestinal worm]]s (e.g. [[hookworm]]s), secrete chemicals into the gut wall (and hence the bloodstream) that [[immunosuppressant|suppress]] the immune system and prevent the body from attacking the parasite.<ref>{{cite journal |author=Carvalho EM, Bastos LS, Araújo MI |title=Worms and allergy |journal=Parasite Immunol. |volume=28 |issue=10 |pages=525–34 |year=2006 |pmid=16965288 |doi=10.1111/j.1365-3024.2006.00894.x}}</ref> This gives rise to a new slant on the hygiene hypothesis theory — that co-evolution of man and parasites has led to an immune system that only functions correctly in the presence of the parasites. Without them, the immune system becomes unbalanced and oversensitive.<ref>{{cite journal |author=Yazdanbakhsh M, Kremsner PG, van Ree R |title=Allergy, parasites, and the hygiene hypothesis |journal=Science |volume=296 |issue=5567 |pages=490–4 |year=2002 |pmid=11964470 |doi=10.1126/science.296.5567.490}}</ref> In particular, research suggests that allergies may coincide with the delayed establishment of [[gut flora]] in [[infant]]s.<ref name="pmid17382394">{{cite journal |author=Emanuelsson C, Spangfort MD |title=Allergens as eukaryotic proteins lacking bacterial homologues |journal=Mol. Immunol. |volume=44 |issue=12 |pages=3256–60 |year=2007 |pmid=17382394 |doi=10.1016/j.molimm.2007.01.019}}</ref> However, the research to support this theory is conflicting, with some studies performed in China and Ethiopia showing an increase in allergy in people infected with intestinal worms.<ref name = cooper04/> Clinical trials have been initiated to test the effectiveness of certain worms in treating some allergies.<ref name = falcone05>{{cite journal |author=Falcone FH, Pritchard DI |title=Parasite role reversal: worms on trial |journal=Trends Parasitol. |volume=21 |issue=4 |pages=157–60 |year=2005 |pmid=15780835 |doi=10.1016/j.pt.2005.02.002}}</ref> It may be that the term 'parasite' could turn out to be inappropriate, and in fact a hitherto unsuspected [[symbiosis]] is at work.<ref name = falcone05/>
Gutworms and similar parasites are present in untreated drinking water in developing countries, and were present in the water of developed countries until the routine [[chlorination]] and purification of drinking water supplies.<ref>{{cite journal |author=Macpherson CN, Gottstein B, Geerts S |title=Parasitic food-borne and water-borne zoonoses |journal=Rev. - Off. Int. Epizoot. |volume=19 |issue=1 |pages=240–58 |year=2000 |pmid=11189719 |doi=}}</ref> Recent research has shown that some common [[parasite]]s, such as [[Intestinal parasite|intestinal worm]]s (e.g. [[hookworm]]s), secrete chemicals into the gut wall (and hence the bloodstream) that [[immunosuppressant|suppress]] the immune system and prevent the body from attacking the parasite.<ref>{{cite journal |author=Carvalho EM, Bastos LS, Araújo MI |title=Worms and allergy |journal=Parasite Immunol. |volume=28 |issue=10 |pages=525–34 |year=2006 |pmid=16965288 |doi=10.1111/j.1365-3024.2006.00894.x}}</ref> This gives rise to a new slant on the hygiene hypothesis theory — that co-evolution of man and parasites has led to an immune system that only functions correctly in the presence of the parasites. Without them, the immune system becomes unbalanced and oversensitive.<ref>{{cite journal |author=Yazdanbakhsh M, Kremsner PG, van Ree R |title=Allergy, parasites, and the hygiene hypothesis |journal=Science |volume=296 |issue=5567 |pages=490–4 |year=2002 |pmid=11964470 |doi=10.1126/science.296.5567.490}}</ref> In particular, research suggests that allergies may coincide with the delayed establishment of [[gut flora]] in [[infant]]s.<ref name="pmid17382394">{{cite journal |author=Emanuelsson C, Spangfort MD |title=Allergens as eukaryotic proteins lacking bacterial homologues |journal=Mol. Immunol. |volume=44 |issue=12 |pages=3256–60 |year=2007 |pmid=17382394 |doi=10.1016/j.molimm.2007.01.019}}</ref> However, the research to support this theory is conflicting, with some studies performed in China and Ethiopia showing an increase in allergy in people infected with intestinal worms.<ref name = cooper04/> Clinical trials have been initiated to test the effectiveness of certain worms in treating some allergies.<ref name = falcone05>{{cite journal |author=Falcone FH, Pritchard DI |title=Parasite role reversal: worms on trial |journal=Trends Parasitol. |volume=21 |issue=4 |pages=157–60 |year=2005 |pmid=15780835 |doi=10.1016/j.pt.2005.02.002}}</ref> It may be that the term 'parasite' could turn out to be inappropriate, and in fact a hitherto unsuspected [[symbiosis]] is at work.<ref name = falcone05/>
For more information on this topic, see [[Helminthic therapy]].
For more information on this topic, see [[Helminthic therapy]].
==Pathophysiology==
The [[pathophysiology]] of allergic responses can be divided into two phases. The first is an [[Acute (medical)|acute response]] that occurs immediately after exposure to an allergen. This phase can either subside or progress into a "late phase reaction" which can substantially prolong the symptoms of a response, and result in tissue damage.
===Acute response===
[[Image:Allergy degranulation processes 01.svg|thumb|Degranulation process in allergy.'''1''' - antigen; '''2''' - IgE antibody; '''3''' - FcεRI receptor; '''4''' - preformed mediators (histamine, proteases, chemokines, heparine); '''5''' - [[granules]]; '''6''' - [[mast cell]]; '''7''' - newly formed mediators (prostaglandins, leukotrienes, thromboxanes, PAF)]]
In the early stages of allergy, a type I hypersensitivity reaction against an allergen, encountered for the first time, causes a response in a type of immune cell called a [[T helper cell|T<sub>H</sub>2 lymphocyte]], which belongs to a subset of [[T cell]]s that produce a [[cytokine]] called [[interleukin-4]] (IL-4).  These T<sub>H</sub>2 cells interact with other [[lymphocytes]] called [[B cell]]s, whose role is production of antibodies.  Coupled with signals provided by IL-4, this interaction stimulates the B cell to begin production of a large amount of a particular type of antibody known as IgE.  Secreted IgE circulates in the blood and binds to an IgE-specific receptor (a kind of [[Fc receptor]] called [[FcεRI]]) on the surface of other kinds of immune cells called [[mast cell]]s and [[basophil]]s, which are both involved in the acute inflammatory response.  The IgE-coated cells, at this stage are sensitized to the allergen.<ref name=Janeway/>
If later exposure to the same allergen occurs, the allergen can bind to the IgE molecules held on the surface of the mast cells or basophils.  Cross-linking of the IgE and Fc receptors occurs when more than one IgE-receptor complex interacts with the same allergenic molecule, and activates the sensitized cell.  Activated mast cells and basophils undergo a process called [[degranulation]], during which they release [[histamine]] and other inflammatory chemical mediators ([[cytokine]]s, [[interleukin]]s, [[leukotriene]]s, and [[prostaglandin]]s) from their [[granule]]s into the surrounding tissue causing several systemic effects, such as [[vasodilation]], [[mucous]] secretion, [[nerve]] stimulation and [[smooth muscle]] contraction. This results in [[rhinorrhea]], itchiness, dyspnea, and anaphylaxis. Depending on the individual, allergen, and mode of introduction, the symptoms can be system-wide (classical anaphylaxis), or localized to particular body systems; asthma is localized to the respiratory system and eczema is localized to the [[dermis]].<ref name=Janeway/>
===Late-phase response===
After the chemical mediators of the acute response subside, late phase responses can often occur. This is due to the migration of other [[leukocyte]]s such as [[neutrophil]]s, [[lymphocyte]]s, [[eosinophil]]s and [[macrophage]]s to the initial site. The reaction is usually seen 2-24 hours after the original reaction.<ref>{{cite journal |author=Grimbaldeston MA, Metz M, Yu M, Tsai M, Galli SJ |title=Effector and potential immunoregulatory roles of mast cells in IgE-associated acquired immune responses |journal=Curr. Opin. Immunol. |volume=18 |issue=6 |pages=751–60 |year=2006 |pmid=17011762 |doi=10.1016/j.coi.2006.09.011}}</ref> Cytokines from mast cells may also play a role in the persistence of long-term effects. Late phase responses seen in [[asthma]] are slightly different from those seen in other allergic responses, although they are still caused by release of mediators from eosinophils, and are still dependent on activity of T<sub>H</sub>2 cells.<ref>{{cite journal |author=Holt PG, Sly PD |title=Th2 cytokines in the asthma late-phase response |journal=Lancet |volume=370 |issue=9596 |pages=1396–8 |year=2007 |pmid=17950849 |doi=10.1016/S0140-6736(07)61587-6}}</ref>


==References==
==References==

Revision as of 14:49, 22 September 2011

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Overview

Allergy causation can be placed in two general categories, namely host and environmental factors. Biological factors are strongly familial whereas environmental factors very largely on the type of living environment. More common in industrialized countries than in countries that are more traditional or agricultural, and there is a higher rate of allergic disease in urban populations versus rural populations.

Cause

Allergy causation can be placed in two general categories, namely host and environmental factors. Host factors include heredity, sex, race and age, with heredity being by far the most important. There are recent increases in the incidence of allergic disorders, however, that cannot be explained by genetic factors alone. The four main candidate environmental factors are alterations in exposure to infectious diseases during early childhood, environmental pollution, allergen levels, and dietary changes.[1]

Genetic basis

Allergic diseases are strongly familial: identical twins are likely to have the same allergic diseases about 70% of the time; the same allergy occurs about 40% of the time in non-identical twins.[2] Allergic parents are more likely to have allergic children,[3] and their allergies are likely to be stronger than those from non-allergic parents. However some allergies are not consistent along genealogies; parents who are allergic to peanuts, may have children who are allergic to ragweed, or siblings that are allergic to different things. It seems that the likelihood of developing allergies is inherited and due to some irregularity in the way the immune system works, but the specific allergen, which causes the development of an allergy, is not.[3]

The risk of allergic sensitization and the development of allergies varies with age, with young children most at risk.[4] Several studies have shown that IgE levels are highest in childhood and fall rapidly between the ages of 10 and 30 years.[4] The peak prevalence of hay fever is highest in children and young adults and the incidence of asthma is highest in children under 10.[5] Overall, boys have a higher risk of developing allergy than girls,[3] although for some diseases, namely asthma in young adults, females are more likely to be affected.[6] Sex differences tend to decrease in adulthood.[3] Ethnicity may play a role in some allergies, however racial factors have been difficult to separate from environmental influences and changes due to migration.[3] Interestingly, with regards to asthma, it has been suggested that different genetic loci are responsible for asthma in people of Caucasian, Hispanic, Asian, and African origins.[7]

Environmental factors

International differences have been associated with the number of individuals within a population that suffer from allergy. Allergic diseases are more common in industrialized countries than in countries that are more traditional or agricultural, and there is a higher rate of allergic disease in urban populations versus rural populations, although these differences are becoming less defined.[8]

Exposure to allergens, especially in early life, is an important risk factor for allergy. Alterations in exposure to microorganisms is the most plausible explanation, at present, for the increase in atopic allergy.[1] Since children that live in large families or overcrowded households, or attend day care, have a reduced incidence of allergic disease, a relationship has been proposed between exposures to bacteria and viruses during childhood, and protection against the development of allergy, which has been called – the "hygiene hypothesis".[8] Exposure to endotoxin and other components of bacteria may reduce atopic diseases.[9] Endotoxin exposure reduces release of inflammatory cytokines such as TNF-α, IFNγ, interleukin-10, and interleukin-12 from white blood cells (leukocytes) that circulate in the blood.[10] Certain microbe-sensing proteins, known as Toll-like receptors, found on the surface of cells in the body are also thought to be involved in these processes.[11]

Gutworms and similar parasites are present in untreated drinking water in developing countries, and were present in the water of developed countries until the routine chlorination and purification of drinking water supplies.[12] Recent research has shown that some common parasites, such as intestinal worms (e.g. hookworms), secrete chemicals into the gut wall (and hence the bloodstream) that suppress the immune system and prevent the body from attacking the parasite.[13] This gives rise to a new slant on the hygiene hypothesis theory — that co-evolution of man and parasites has led to an immune system that only functions correctly in the presence of the parasites. Without them, the immune system becomes unbalanced and oversensitive.[14] In particular, research suggests that allergies may coincide with the delayed establishment of gut flora in infants.[15] However, the research to support this theory is conflicting, with some studies performed in China and Ethiopia showing an increase in allergy in people infected with intestinal worms.[8] Clinical trials have been initiated to test the effectiveness of certain worms in treating some allergies.[16] It may be that the term 'parasite' could turn out to be inappropriate, and in fact a hitherto unsuspected symbiosis is at work.[16] For more information on this topic, see Helminthic therapy.

References

  1. 1.0 1.1 Janeway, Charles (2001). Immunobiology; Fifth Edition. New York and London: Garland Science. pp. e–book. ISBN 0-8153-4101-6. Unknown parameter |coauthors= ignored (help).
  2. Galli SJ (2000). "Allergy". Curr. Biol. 10 (3): R93–5. PMID 10679332.
  3. 3.0 3.1 3.2 3.3 3.4 De Swert LF (1999). "Risk factors for allergy". Eur. J. Pediatr. 158 (2): 89–94. PMID 10048601.
  4. 4.0 4.1 Croner S (1992). "Prediction and detection of allergy development: influence of genetic and environmental factors". J. Pediatr. 121 (5 Pt 2): S58–63. PMID 1447635.
  5. Jarvis D, Burney P (1997) Epidemiology of atopy and atopic disease In: Kay AB (ed) Allergy and allergic diseases, vol 2. Blackwell Science London, pp 1208–1224
  6. Anderson HR, Pottier AC, Strachan DP (1992). "Asthma from birth to age 23: incidence and relation to prior and concurrent atopic disease". Thorax. 47 (7): 537–42. PMID 1412098.
  7. Barnes KC, Grant AV, Hansel NN, Gao P, Dunston GM (2007). "African Americans with asthma: genetic insights". Proc Am Thorac Soc. 4 (1): 58–68. doi:10.1513/pats.200607-146JG. PMID 17202293.
  8. 8.0 8.1 8.2 Cooper PJ (2004). "Intestinal worms and human allergy". Parasite Immunol. 26 (11–12): 455–67. doi:10.1111/j.0141-9838.2004.00728.x. PMID 15771681.
  9. von Mutius E (2002). "Environmental factors influencing the development and progression of pediatric asthma". J. Allergy Clin. Immunol. 109 (6 Suppl): S525–32. PMID 12063508.
  10. Braun-Fahrländer C, Riedler J, Herz U; et al. (2002). "Environmental exposure to endotoxin and its relation to asthma in school-age children". N. Engl. J. Med. 347 (12): 869–77. doi:10.1056/NEJMoa020057. PMID 12239255.
  11. Garn H, Renz H (2007). "Epidemiological and immunological evidence for the hygiene hypothesis". Immunobiology. 212 (6): 441–52. doi:10.1016/j.imbio.2007.03.006. PMID 17544829.
  12. Macpherson CN, Gottstein B, Geerts S (2000). "Parasitic food-borne and water-borne zoonoses". Rev. - Off. Int. Epizoot. 19 (1): 240–58. PMID 11189719.
  13. Carvalho EM, Bastos LS, Araújo MI (2006). "Worms and allergy". Parasite Immunol. 28 (10): 525–34. doi:10.1111/j.1365-3024.2006.00894.x. PMID 16965288.
  14. Yazdanbakhsh M, Kremsner PG, van Ree R (2002). "Allergy, parasites, and the hygiene hypothesis". Science. 296 (5567): 490–4. doi:10.1126/science.296.5567.490. PMID 11964470.
  15. Emanuelsson C, Spangfort MD (2007). "Allergens as eukaryotic proteins lacking bacterial homologues". Mol. Immunol. 44 (12): 3256–60. doi:10.1016/j.molimm.2007.01.019. PMID 17382394.
  16. 16.0 16.1 Falcone FH, Pritchard DI (2005). "Parasite role reversal: worms on trial". Trends Parasitol. 21 (4): 157–60. doi:10.1016/j.pt.2005.02.002. PMID 15780835.


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