Effects of parasitic worms on the immune system

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The effects of parasitic worms, or

helminths, on the immune system is a recently emerging topic of study among immunologists and other biologists. Experiments have involved a wide range of parasites, diseases, and hosts. The effects on humans have been of special interest. The tendency of many parasitic worms to pacify the host's immune response allows them to mollify some diseases, while worsening others.[1]

Immune response hypothesis

Mechanisms of immune regulation

Extensive research shows that parasitic worms have the ability to deactivate certain immune system cells, leading to a gentler immune response.

gut flora, and the body itself.[9]

cytokines
and activate other immune cells. Parasitic worms influence what kinds of T helper cells are activated.

In the past, helminths were thought to simply suppress

autoimmune diseases caused by Th1 cells.[10] However, helminths also regulate Th2-caused diseases, such as allergy and asthma.[10] Rook postulates that different parasitic worms suppress different Th types, but always in favor of regulatory T (Treg) cells.[10]

Rook explains that these regulatory T cells release

immunoglobulin E (IgE) response.[12] All these fight a hyperactive immune response, reduce the inflammation throughout the body, and thus lead to less severe autoimmune diseases.[12]

Osada et al. state that because parasitic worms may and often do consist of allergens themselves, the degree to which they pacify or agitate the immune response against allergens is a balance of their regulating effects and their allergenic components.[11] Therefore, depending on both of these variables, some parasitic worms may worsen allergies.[11]

In their Parasite Immunology article on worms and

viral infections, Kamal et al. explain why some parasitic worms aggravate the immune response.[13] Because parasitic worms often induce Th2 cells and lead to suppressed Th1 cells, problems arise when Th1 cells are needed.[13] Such cases occur with viral diseases.[13]
Several examples of viral infections worsened by parasitic worms are described below in the Negative Effects section.

Evolutionary theory

The positive effects of parasitic worms are theorized to be a result of millions of years of evolution, when humans and human ancestors would have been constantly inhabited by parasitic worms.[9] In the journal EMBO Reports, Rook says that such helminths "are all either things that really do us no harm, or things where the immune system is forced to give in and avoid a fight because it's just a waste of time.[14]" In the journal Immunology, Rook states that, because parasitic worms were almost always present, the human immune system developed a way to treat them that didn't cause tissue damage.[9]

The immune system extends this response to its treatments of

developing world, where parasites are more common.[9]

Comparison with the hygiene hypothesis

The

microorganisms results in an increase of autoimmune diseases, according to Rook.[17] This theory and the theory that certain parasitic worms pacify the immune response are similar in that both theories attribute the recent rise of autoimmune diseases to the decreased levels of pathogens in developed countries. However, the Hygiene Hypothesis claims that the absence of pathogenic organisms in general has led to this.[17] In contrast, the parasitic worm theory only analyzes helminths, and specifically ones found to have a regulating effect.[17]

Positive effects

Experimental and also some clinical work has demonstrated the protective benefits of helminth therapy against the wide spectrum of

age-related diseases promoted by inflammaging.[18]

Type 1 diabetes

pancreatic beta cells.[2]
In an experiment with mice, infection with parasitic worms or helminth-products generally inhibited the spontaneous development of T1D, according to Anne Cook in the journal Immunology.
Salmonella typhimurium was successful even when administered late in the development of T1D.[2]

filarial nematodes

Allergy and asthma

According to Hopkin, asthma involves

filarial nematodes and ES-62, a protein that nematodes secrete in their host.[3] They discovered that pure ES-62 prevents the release of allergenic inflammatory mediators in mice, resulting in weaker allergic and asthmatic symptoms.[3] In the Journal of Immunology, Bashir et al. describe their experimental findings that an allergic response against peanuts is inhibited in mice infected with an intestinal parasite.[4]

Inflammatory bowel disease

whipworm.[6]

blood fluke

Arthritis

In 2003, Iain McInnes et al. found that

arthritic-induced mice experienced less inflammation and other arthritic effects when infected with ES-62, a protein derived from filarial nematodes, a kind of parasitic worm.[19] Similarly, in the International Journal for Parasitology, Osada et al. published their experimental findings that arthritis-induced mice infected with the parasitic worm Schistosoma mansoni had down-regulated immune systems.[20] This led to resistance to arthritis.[20]

Multiple sclerosis

In 2007, Jorge Correale et al. studied the effects of parasitic infection on multiple sclerosis (MS). Correale evaluated several MS patients infected with parasites, comparable MS patients without parasites, and similar healthy subjects over the course of 4.6 years.[8] During the study, the MS patients that were infected with parasites experienced far less effects of MS than the non-infected MS patients.[8]

Negative effects

Vaccination

In the journal Parasite Immunology, Kamal et al. explains that parasitic worms often weaken the immune system's ability to effectively respond to a vaccine because such worms induce a Th2-based immune response that is less responsive than normal to antigens.[21] This is a major concern in developing countries where parasitic worms and the need for vaccinations exist in large number.[21] It may explain why vaccines are often ineffective in developing countries.[21]

Hepatitis

human whipworm
, a parasitic worm

Because

CD4+ T-cells, and so a much higher percentage of those infected with bloodflukes are unable to combat HCV effectively and develop chronic HCV.[22] Parasitic effects of Hepatitis B virus, however, are contested—some studies show little association, while others show exacerbation of the disease.[23]

HIV

Because the two diseases are abundant in developing countries, there are many patients with both HIV (Human immunodeficiency virus) and parasites, and specifically bloodflukes.[24] In his article, Kamal relates the findings that those infected with parasites are more likely to be infected by HIV.[24] However, it is disputed whether or not the viral infection is more severe because of the parasites.[24]

Tuberculosis

According to Kamal, the human immune system needs Th1 cells to effectively fight TB.[25] Since the immune system often responds to parasitic worms by inhibiting Th1 cells, parasitic worms generally worsen tuberculosis.[25] In fact, Tuberculosis patients who receive successful parasitic therapy experience major improvement.[25]

Malaria

Malaria distribution map. Most countries with a high distribution of malaria also have a high distribution of parasitic worm infections.

In 2004, Sokhna et al. performed a study of Senegalese children.[26] Those infected with blood flukes had significantly higher rates of malaria attacks than those who were not.[26] Furthermore, children with the highest counts of blood flukes also had the most malaria attacks.[26] Based on this study, Hartgers et al. drew a "cautious conclusion" that helminths make humans more susceptible to contracting malaria and experiencing some of its lighter symptoms, while actually protecting them from the worst symptoms.[27] Hartgers reasons that a Th2-skewed immune system resulting from helminth infection would lower the immune system's ability to counter an initial malarial infection.[27] However, it would also prevent a hyperimmune response resulting in severe inflammation, reducing morbidity and pathology.[27]

See also

References

  1. ^ Kamal 2006, pp. 484-491
  2. ^ a b c d e f Cooke 2008, pp. 12-14
  3. ^ a b c Melendez 2007, p. 1375
  4. ^ a b Bashir 2002, p. 3284
  5. ^ a b c Moreels 2004, p. 99
  6. ^ a b c d Weinstock 2005, pp. 249-251
  7. ^ Osada 2010, pp. 2-3
  8. ^ a b c Correale 2007, pp. 98-99
  9. ^ a b c d e f g h Rook 2008, pp. 3-4
  10. ^ a b c d Rook 2008, pp. 4-5
  11. ^ a b c Osada 2010, pp. 1-2
  12. ^ a b c Hopkin 2009, pp. 267-270
  13. ^ a b c Kamal 2006, pp. 483-484
  14. ^ Hadley 2004, p. 1124
  15. ^ Hadley 2004, pp. 1122-1124
  16. ^ Weinstock 2004, p. 7
  17. ^ a b c Hadley 2004, pp. 1122-1123
  18. doi:10.7554/eLife.65180
  19. ^ McInnes 2003, pp. 2127-2129
  20. ^ a b Osada 2008, p. 457
  21. ^ a b c Kamal 2006, pp. 484-485
  22. ^ a b c d Kamal 2006, pp. 485-487
  23. ^ Kamal 2006, pp. 487-489
  24. ^ a b c Kamal 2006, pp. 489-491
  25. ^ a b c Kamal 2006, p. 485
  26. ^ a b c Sokhna 2004, p. 43
  27. ^ a b c Hartgers 2006, p. 502-503

Bibliography

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