Schistosoma mansoni Modulation of Phagocytosis in Biomphalaria glabrata

Abstract

Both short-term (3 hr) exposure of Biomphalaria glabrata snails (M-line and 13-16-R1) to Schistosoma mansoni (PR1) miracidia and in vitro incubation of parasite sporocysts with host hemolymph components altered host phagocytic ability. Hemocytes obtained from susceptible (M-line) snails that had been exposed to parasite miracidia for 3 hr showed reduced levels of phagocytosis of yeast cells in vitro compared to hemocytes from unexposed individuals. Incubation of whole hemolymph with sporocysts in vitro also reduced yeast phagocytosis in this susceptible strain. In contrast, resistant (13-16-R1) hemocytes showed increased levels of yeast phagocytosis after in vitro incubation with the parasite, and the opsonic properties of 13-16-R1 plasma were greater after exposure of snails to miracidia. These strain-specific effects of S. mansoni on host hemocyte phagocytosis and plasma opsonization were seen only when both plasma and hemocytes were present at the time of exposure to the parasite.

Modificación de los parámetros inmunitarios hemolinfáticos en el ostión del norte (Argopecten purpuratus Lamarck, 1819) afectados por el cuadro de retracción del manto

“…La disminución en el número de hemocitos circulantes que se observan en los ostiones con RM, responde al patrón determinado para otros moluscos parasitados (Fryer & Bayne, 1990;Noda & Sato, 1990;Ford et al, 1993), lo que se explicaría por su infiltración a los tejidos y/o a su agregación en la hemolinfa.…”

“…Estas células circulantes están presentes en la hemolinfa, pero también son capaces de salir de la circulación y migrar a otros tejidos del animal donde pueden agregarse para restringir la infección o alguna lesión tisular (Bachère et al, 2004). Su ca-pacidad de fagocitosis es una de las funciones esenciales de los hemocitos para eliminar agentes exó-genos como bacterias o protozoos (Bayne, 1990), en este caso se induce la producción de especies reactivas de oxígeno (Nappi & Ottaviani, 2000;Lambert et al, 2003). En bivalvos pectínidos la capacidad fagocítica se ha evaluado en Pecten maximus con diversos tipos de bacterias y levaduras (Lambert & Nicolas, 1998).…”

“…La formación de cápsulas de origen hemocitario frente a protozoos parásitos ha sido estudiada en detalle en la ostra C. virginica (Cheng, 1996) y en las almejas Tapes semidecussatus (Montes et al, 1995) y Mercenaria mercenaria (Smolowitz et al, 1998). El modelo más estudiado en la respuesta inmune innata de hemocitos frente a las larvas de tremátodos de Schistosoma mansoni ha sido el molusco gastrópo-do Biomphalaria glabrata (Mollusca: Pulmonata) (Bayne et al, 2001), donde se ha demostrado que el parásito tiene un efecto modulador sobre varios parámetros hemocitarios, como la supresión de la fagocitosis, cambio de la movilidad, variación en el número de hemocitos, citoadherencia y capacidad metabólica (Noda & Loker, 1989;Fryer & Bayne, 1990;Noda & Sato, 1990).…”

Interaction between primary and secondary sporocysts of Schistosoma mansoni and the internal defence system of Biomphalaria resistant and susceptible to the parasite

“…In addition, it has been demonstrated that sporocysts release glycoproteins (excreted/secreted products) that bind to carbohydrate-binding receptors on the haemocyte cell surface to attenuate the initial cellular recognition of the parasite (Johnston & Yoshino 2001). These molecules can inhibit IDS mechanisms (Adema & Loker 1997) by suppressing the synthesis of many haemocyte molecules (Lodes et al 1991) or by reducing haemocyte motility and phagocytic activity (Fryer & Bayne 1990, Lodes & Yoshino 1990). Other important parasite escape mechanisms include the use of molecular mimicry, likely through the production of sporocyst surface membrane molecules similar to those present on the host, and the ability of the parasite to absorb host antigens (Yoshino & Bayne 1983, Damian 1987, Salzet et al 2000, Lehr et al 2008, Peterson et al 2009, van Die & Cummings 2010.…”

“…Parasite escape mechanisms that respond to the host IDS can assure the survival and adaptability of the parasite (Yoshino & Bayne 1983, Adema & Loker 1997. Previous studies have demonstrated that success of the infection depends on the parasite interfering with the mollusc IDS (Fryer & Bayne 1990). The parasite can disturb the IDS by producing proteases (Yoshino et al 1993) and by the action of enzymes that neutralise reactive oxygen species (Connors & Yoshino 1990).…”