Immune responses of IL-5 transgenic mice to parasites and aeroallergens

Abstract

Eosinophils have long been thought to be effectors of immunity to helminths but have also been implicated in the pathogenesis of asthma. Patterns of cytokine production in the host

FVB/N mice are highly resistant to primary infection withNippostrongylus brasiliensis

“…Mice with constitutive eosinophilia due to expression of an interleukin (IL)-5 transgene (Dent et al . 1990) are highly resistant to infections with Nippostrongylus brasiliensis , and entrapment of infective larvae in the skin is associated with the rapid recruitment of eosinophils (Dent et al . 1997 b ; Daly, 1999; Dent et al .…”

Inactivation of the complement anaphylatoxin C5a by secreted products of parasitic nematodes

“…Although N. brasiliensis L3s are trapped in the skin of IL-5 transgenic mice for extended periods, indicative of susceptibility to eosinophil-mediated attack (Daly et al, 1999), other nematodes such as T. spiralis and Toxocara canis appear unaffected (Sugane et al, 1996; Hokibara et al, 1997; Dent et al, 1999), and eosinophilia may actually impair host resistance to T. spiralis (Dent et al, 1997). More recent work suggests that eosinophils promote survival of T. spiralis by skewing cytokine production and thereby inhibiting nitric oxide synthesis (Fabre et al, 2009).…”

Murine nematode immunology in Australasia

“…These animals, originally produced on a CBA/Ca background and later also backcrossed into the BALB/c and C57BL/6 backgrounds (51), have constitutive eosinophilia in the peripheral blood, spleen and bone marrow. Early experiments initiated at NIMR suggested that IL‐5 Tg mice do not have enhanced resistance to primary peritoneal infection with the cestode Mesocestoides corti (52), or primary or vaccine‐induced resistance to the trematode Schistosoma mansoni (53) and also develop only modest lung inflammation and pathology in response to the aeroallergen chicken ovalbumin (OVA) (54). As with infections with S. mansoni (53), IL‐5 Tg mice are also actually more susceptible than wild‐type (WT) littermates to T. spiralis (54) and Plasmodium chabaudi (Dent and Brown, unpublished).…”

“…Early experiments initiated at NIMR suggested that IL‐5 Tg mice do not have enhanced resistance to primary peritoneal infection with the cestode Mesocestoides corti (52), or primary or vaccine‐induced resistance to the trematode Schistosoma mansoni (53) and also develop only modest lung inflammation and pathology in response to the aeroallergen chicken ovalbumin (OVA) (54). As with infections with S. mansoni (53), IL‐5 Tg mice are also actually more susceptible than wild‐type (WT) littermates to T. spiralis (54) and Plasmodium chabaudi (Dent and Brown, unpublished). Our findings with primary T. spiralis infections have been confirmed recently using an independently generated IL‐5 Tg line, in which eosinophils enhance parasite survival by influencing the balance of interferon‐γ and IL‐4 and consequentially, the generation of larvicidal nitric oxide (55).…”