Review Elmer Press J Clin Med Res • 2010;2(6):247-255 Parasites Induced Skin Allergy: A Strategic Manipulation of the Host Immunity Alketa Hysni Bakiria, d, Ervin Cerciz Mingomataja, b, c, d Abstract The absence of a consistent link between parasitoses and skin al- lergic symptoms in the clinical investigations contrasts to the fact that some parasites are the most potent inducers of immunoglobulin E that exist in nature. To shed some light into this question, this review is focused on the actual knowledge regarding parasites life cycle, interactions with host immunity, the influence on host behav- ior, and finally the role of all these factors on the skin allergy. The collected data demonstrate that parasites could manipulate the host behavior for its own benefit in different ways, altering its (epi)ge- netic, biochemical, immunologic or physiologic functions as well as altering its behavior and activity. In this context, skin allergy may be associated with certain stages of the parasites’ life cycle and migration into biological barriers, but not necessarily with presence of the parasitosis in the host organism. As compared to T helper (Th) 1 response, the Th2 one, the eosinophilic infiltration and the complement inhibition could assure better conditions for the devel- opment of some parasites. Taken together, the suggested hypothe- ses could be a plausible explanation for the epidemiological puzzle regarding urticaria occurrence, Th2 response and parasitoses, but further studies are necessary to provide better-based conclusions. Keywords: Eosinophilic Infiltration; Host behavior; Parasites life cycle; Skin allergy; Th1/Th2 response Manuscript accepted for publication September 29, 2010 aUniversity of Tirana, Nursing Faculty, Dept. of Preclinical Disciplines, Albania b“Mother Theresa” School of Medicine, Department of Allergology and Clinical Immunology, Tirana, Albania cCorresponding author, Rruga Myslym Shyri, P. 47, Apt. 15, Tirana, Albania. Email: allergology@gmx.de dBoth authors contributed equally to this work doi:10.4021/jocmr456w Introduction Parasitic diseases are often considered as a classic cause of urticaria [1-3]. Potential urticaria-associated pathologies can be ascaridiosis, trichinellosis, fasciolosis, giardiosis, tox- ocarosis, anisakiasis, schistosomosis, strongyloidosis, hyda- tidosis, blastocytosis, filariasis, etc [2-6]. Nevertheless, laboratory and clinical investigations greatly vary from one centre to the other and the link be- tween these infections and skin signs does not rely on hard data. Thus, French studies have suggested a high prevalence of Toxocara canis markers in chronic urticaria, but anti-par- asitic treatment had only inconstant effects [7]. Similarly, there are only a few case reports about cutaneous manifesta- tions caused by giardiasis [8-10]. Many authors consider that such cutaneous manifestations as urticaria and itching were secondary to the associated gastrointestinal infection due to Giardia lamblia cysts and trophozoite forms, as they may disappear under specific treatment [10]. Also, the presence of urticaria associated with Blastocystic hominis infection has been described in very few studies [11]. The absence of a consistent link between parasitoses and skin allergic symptoms in the clinical investigations con- trasts to the fact that some parasites are possibly the most potent inducers of immunoglobulin (Ig) E that exist in na- ture [12-16]. In a previous review, we argued about the re- lationship between Helminth-induced IgE response and the decrease of respiratory symptoms during this pathology [16]. In effect, the immuno-inflammatory response to helminthic infections and allergic diseases have some similarities, the most profound being the increases in eosinophils and serum total IgE concentration [12-15, 17, 18]. Both entities, hel- minthic infections and atopic response are Th2/interleukin (IL)-4 inducers, but helminthic infections do not only stimu- late specific IgE responses against their own antigens, but also they induce a strong non-specific polyclonal synthesis of this Ig [12-16]. The experimental injection of the Ascaris- infected patients’ serum into the rats’ peritoneal is associated with an increase in mesentery mast cells and vascular con- gestion [16, 19]. In this paper we will focus in the aspect of relation- Articles © The authors | Journal compilation © J Clin Med Res and Elmer Press™ | www.jocmr.org 247