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Superimposed visceral leishmanial infection aggravates response to Heligmosomoides polygyrus.
Parasites & Vectors 2018 July 12
BACKGROUND: Polyparasitism is the rule in all animal species, including humans, and has an important role in pathogenicity, diagnosis and control measures. Among them, co-infections by gastrointestinal helminths and protists are very prevalent under natural conditions but experimental infections are relatively scarce. Thus, despite the frequent association of visceral Leishmania infections and intestinal helminth parasitism the experimental co-infection has not been addressed. Heligmosomoides polygyrus, an intestinal nematode of mice, is related to other helminths causing important pathologies and is a model species for immunological studies. Mice are valuable experimental model for visceral leishmaniasis.
METHODS: BALB/c mice infected with H. polygyrus (200 third-stage larvae, L3) were subsequently infected seven days later with Leishmania infantum (107 promastigotes) with the aim of determining the effect of the overinfection on the host response to the primary infection with the helminth.
RESULTS: Overinfection with the protist did not affect the establishment rate of the nematode but induced a higher fecal egg output. Helminth burdens in co-infected animals were significant at the end of the experiment. Early unspecific immune suppression induced by the nematode in mesenteric lymph nodes was not switched by L. infantum infection. Co-infection elicited a higher serum antibody (IgG1 ) response against the helminth.
CONCLUSIONS: Visceral leishmanial overinfection aggravated the early host response against primary infections with the intestinal helminth. This effect was evidenced by an increased longevity and higher production of non-protective antibodies.
METHODS: BALB/c mice infected with H. polygyrus (200 third-stage larvae, L3) were subsequently infected seven days later with Leishmania infantum (107 promastigotes) with the aim of determining the effect of the overinfection on the host response to the primary infection with the helminth.
RESULTS: Overinfection with the protist did not affect the establishment rate of the nematode but induced a higher fecal egg output. Helminth burdens in co-infected animals were significant at the end of the experiment. Early unspecific immune suppression induced by the nematode in mesenteric lymph nodes was not switched by L. infantum infection. Co-infection elicited a higher serum antibody (IgG1 ) response against the helminth.
CONCLUSIONS: Visceral leishmanial overinfection aggravated the early host response against primary infections with the intestinal helminth. This effect was evidenced by an increased longevity and higher production of non-protective antibodies.
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