Does the eosinophil have a protective role in amebiasis?

Abstract

Amebiasis is a major health problem in developing countries. Entamoeba histolytica infects 5 x 10 8 people worldwide, more than 90% of them living in West and South East Africa, China, SE Asia, México, the western portion of South America and India (Smyth 1994). Only 10% of all infected individuals eventually develop invasive amebiasis ranging from mild (i.e. self-limited) or serious intestinal amebiasis, to life-threatening hepatic invasion (Walsh 1986).It has been suggested that there are in fact two different species of Entamoeba. One, the classic pathogenic E. histolytica discovered by Schaudinn in 1903. The other, the non-pathogenic E. dispar described by Brumpt in 1925, based mainly on epidemiological considerations. The concept of two Entamoeba species began to be objectively established by functional in vitro studies (Martínez-Palomo 1982, Mirelman & Chayen 1990) and zymodeme patterns (Sargeaunt 1988), culminating now with molecular genetic data (Tannich & Burchard 1991, Tannich 1996.Thus, the majority of ameba infected individuals may actually harbour E. dispar, leaving the E. histolytica as the agent of the relatively rare invasive intestinal and extraintestinal disease. Amebic abscess of the liver (AAL) on the other hand, occurs in less than 1% of individuals with invasive intestinal amebiasis (Martínez-Palomo et al. 1993).Why the vast majority of individuals (≥99%) appear to be resistant to extraintestinal invasion remains unknown but some inroads have now been made: a significant increase in the SCO1 complotype and in HLA-DR3 was found in 160 Mexican mestizos (adults and children) with AAL when compared to healthy controls, to adult patients with amebic rectocolitis or to asymptomatic amebic carriers (Arellano et al. 1996). DNA subtyping is now in process to confirm these findings.Studies of human amebiasis and of experimental animal models of amebic disease have suggested that cell-mediated rather than humoral immune mechanisms, are responsible for acquired immunity to AAL (De León 1970, Salata & Radvin 1986, Kretschmer & López-Osuna 1990. Moreover, axenically grown trophozoites of E. histolytica kill in vitro normal human neutrophils and eosinophils (not-withstanding the aid by antibody and complement), normal monocytes and lymphocytes, without suffering changes in their own viability (Jarumilinta & Kradolfer 1964, Artigas et al. 1966, Guerrant et al. 1981, Salata et al. 1985, 1987, López-Osuna et al. 1986, López-Osuna & Kretschmer 1989 fectively destroying virulent amebas, even though finally succumbing in the process as well (Salata et al. 1985). In our laboratory we found that the same occurs with activated human peripheral blood eosinophils (López-Osuna et al. 1992).There is no circulating eosinophilia in most protozoan infections, yet this is not necessarily an argument against their possible participation in AAL, specially because eosinophils are regularly found in the early inflammatory stages of experimental amebic liver disease (Tsutsumi et al. 1984), and since the bulk of eosinophils in ...

CCR9+ T cells contribute to the resolution of the inflammatory response in a mouse model of intestinal amoebiasis

“…Also, in murine models of intestinal amoebiasis, an increase in PMN cells, particularly eosinophil, has been reported (Ghosh et al 2000). Nevertheless, controversy exists regarding a specific role for eosinophils in regulating E. histolytica infection (Lopez-Osuna et al 1997). In human, eosinophils are located in the fibrous zone that separates the floor of the ulcers from viable human tissue, in the lamina propria (LP) of amoebic colitis patients suggesting a potential role for these cells in the progression of infection and mucosal lesion development, although it remains to be elucidated (Prathap and Gilman 1970;Ventura-Juarez et al 2007).…”

Fulminant Amoebic Colitis: Role of the Innate and Adaptive Immune Responses

“…However, another study reported that NK cells activated by lipopeptidophosphoglicane from E. histolytica reduce the size of AHA (Lotter et al, 2009). Moreover, eosinophils and mast cells are also implicated in the cellular response and have been found to be involved in the reduction of amebic damage in various in vivo models (Houpt, 2002;Jarillo-Luna, 2002;López-Osuna et al, 1997. By using histochemical techniques in human intestinal tissue with FAC, eosinophils were stained with eritrosine B 1.5% (Benítez et al, 1987) and mast cells with toluidine blue 0.7% (Enerback, 1986;VenturaJuárez et al, 1990).…”

Role of Eosinophils and Tumor Necrosis Factor Alpha in Interleukin-25-Mediated Protection from Amebic Colitis

“…IL-25 is also a potent inducer of the antimicrobial peptide angiogenin-4 in an IL-13-dependent manner (23). IL-25 induces eosinophil infiltration in the gut (24), which is potentially relevant in amebiasis as eosinophilia was also associated with reduced size and number of amebic liver abscesses in the gerbil model (25). However, the role of IL-25 in amebic colitis remains unknown.…”