Anisakis simplex: Histopathological changes in experimentally infected CBA/J mice

Jones, Richard E.; Deardorff, Thomas L.; Kayes, Stephen G.

doi:10.1016/0014-4894(90)90112-p

Cited by 31 publications

(26 citation statements)

References 17 publications

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“…Several research groups have investigated the kinetics of specific antibody production in mice and rabbits (118,119,133,149), but these results cannot be directly extrapolated to allergic responses in humans. In 2006, Cho et al described the specific antibody response in rats that were infected orally with L3 on two occasions at intervals of 9 weeks.…”

Section: Innate Immune Responsesmentioning

confidence: 99%

Anisakis simplex: from Obscure Infectious Worm to Inducer of Immune Hypersensitivity

2008

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SUMMARY Infection of humans with the nematode worm parasite Anisakis simplex was first described in the 1960s in association with the consumption of raw or undercooked fish. During the 1990s it was realized that even the ingestion of dead worms in food fish can cause severe hypersensitivity reactions, that these may be more prevalent than infection itself, and that this outcome could be associated with food preparations previously considered safe. Not only may allergic symptoms arise from infection by the parasites (“gastroallergic anisakiasis”), but true anaphylactic reactions can also occur following exposure to allergens from dead worms by food-borne, airborne, or skin contact routes. This review discusses A. simplex pathogenesis in humans, covering immune hypersensitivity reactions both in the context of a living infection and in terms of exposure to its allergens by other routes. Over the last 20 years, several studies have concentrated on A. simplex antigen characterization and innate as well as adaptive immune response to this parasite. Molecular characterization of Anisakis allergens and isolation of their encoding cDNAs is now an active field of research that should provide improved diagnostic tools in addition to tools with which to enhance our understanding of pathogenesis and controversial aspects of A. simplex allergy. We also discuss the potential relevance of parasite products such as allergens, proteinases, and proteinase inhibitors and the activation of basophils, eosinophils, and mast cells in the induction of A. simplex-related immune hypersensitivity states induced by exposure to the parasite, dead or alive.

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Section: Innate Immune Responsesmentioning

confidence: 99%

Anisakis simplex: from Obscure Infectious Worm to Inducer of Immune Hypersensitivity

2008

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“…Although the ability of these parasites to infect humans has been known for more than 40 years (28,36), their relevance as etiologic agents of systemic allergic reactions (i.e., urticaria, angioedema, and anaphylaxis), including gastroallergic anisakiasis, was not recognized until the end of the last century (5,10). Unlike nematodes that complete their biological cycle in humans, Anisakis organisms do not develop beyond the L4 stage, and it is believed that most of the larvae are either expelled in the first 24 h (2) or die within 3 weeks of infecting the host (19). However, the IgE immune response, induced against some allergens released by the Anisakis larvae while they are still alive, can be detected in sera from infected patients over long periods (11), which may be prolonged when patients suffer one or more reinfections.…”

mentioning

confidence: 99%

Diagnosing Human Anisakiasis: Recombinant Ani s 1 and Ani s 7 Allergens versus the UniCAP 100 Fluorescence Enzyme Immunoassay

Anadón

Rodríguez

Gárate

et al. 2010

Clin Vaccine Immunol

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“…Indeed the question of whether host innate cells bear "danger" receptors for parasite products has barely been explored. In parasitic infections, there can be phenomenal intensity and selectivity of granulocyte recruitment, such as the eosinophilic phlegmons (large granulomatous infiltrations of eosinophils with marked submucosal oedema) caused by Anisakis simplex (anisakiasis or eosinophilic gastroenteritis) (17,28,30,31) and Ancylostoma caninum (eosinophilic enteritis) (52,70). Since most of the damage caused by tissue-invading parasites can be attributed to the recruited inflammatory cells, a clear picture of the mechanisms mediating granulocyte recruitment and activation is of pivotal importance to the understanding and management of pathology.…”

mentioning

confidence: 99%

Ascaris suum-Derived Products Induce Human Neutrophil Activation via a G Protein-Coupled Receptor That Interacts with the Interleukin-8 Receptor Pathway

et al. 2001

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Infection with tissue-migrating helminths is frequently associated with intense granulocyte infiltrations. Several host-derived factors are known to mediate granulocyte recruitment to the tissues, but less attention has been paid to how parasite-derived products trigger this process. Parasite-derived chemotactic factors which selectively recruit granulocytes have been described, but nothing is known about which cellular receptors respond to these agents. The effect of products from the nematodes Ascaris suum, Toxocara canis, and Anisakis simplex on human neutrophils were studied. We monitored four parameters of activation: chemotaxis, cell polarization, intracellular Ca 2؉ transients, and priming of superoxide anion production. Body fluids of A. suum (ABF) and T. canis (TcBF) induced strong directional migration, shape change, and intracellular Ca 2؉ transients. ABF also primed neutrophils for production of superoxide anions. Calcium mobilization in response to A. suum-derived products was completely abrogated by pretreatment with pertussis toxin, implicating a classical G protein-coupled receptor mechanism in the response to ABF. Moreover, pretreatment with interleukin-8 (IL-8) completely abrogated the response to ABF, demonstrating desensitization of a common pathway. However, ABF was unable to fully desensitize the response to IL-8, and binding to CXCR1 or CXCR2 was excluded in experiments using RBL-2H3 cells transfected with the two human IL-8 receptors. Our results provide the first evidence for a direct interaction between a parasite-derived chemotactic factor and the host's chemotactic network, via a novel G protein-coupled receptor which interacts with the IL-8 receptor pathway.Neutrophilic and eosinophilic granulocytes have evolved in the immune system as a first line of defense against invading pathogens. Remarkable numbers of eosinophils or neutrophils infiltrate lesions caused by tissue-invading parasites, as seen, e.g., in anisakiasis (57) and schistosomiasis. A series of chemokines and low-molecular-weight attractants are known to mediate recruitment of granulocytes to the site of infection (56), but less attention has been paid to the role of parasite-derived products in inflammatory infiltration. Indeed the question of whether host innate cells bear "danger" receptors for parasite products has barely been explored. In parasitic infections, there can be phenomenal intensity and selectivity of granulocyte recruitment, such as the eosinophilic phlegmons (large granulomatous infiltrations of eosinophils with marked submucosal oedema) caused by Anisakis simplex (anisakiasis or eosinophilic gastroenteritis) (17,28,30,31) and Ancylostoma caninum (eosinophilic enteritis) (52,70). Since most of the damage caused by tissue-invading parasites can be attributed to the recruited inflammatory cells, a clear picture of the mechanisms mediating granulocyte recruitment and activation is of pivotal importance to the understanding and management of pathology.The intensity and selectivity of inflammatory recruitment...

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Anisakis simplex: Histopathological changes in experimentally infected CBA/J mice

Cited by 31 publications

References 17 publications

Anisakis simplex: from Obscure Infectious Worm to Inducer of Immune Hypersensitivity

Anisakis simplex: from Obscure Infectious Worm to Inducer of Immune Hypersensitivity

Diagnosing Human Anisakiasis: Recombinant Ani s 1 and Ani s 7 Allergens versus the UniCAP 100 Fluorescence Enzyme Immunoassay

Ascaris suum-Derived Products Induce Human Neutrophil Activation via a G Protein-Coupled Receptor That Interacts with the Interleukin-8 Receptor Pathway

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