Predisposition to Brugia Malayi Microfilaremia in Progeny of Infected Gerbils *

Af, Schrater; Spielman, Andrew; Wf, Piessens

doi:10.4269/ajtmh.1983.32.1306

Cited by 24 publications

(10 citation statements)

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“…Women commonly harbor filarial infections during their childbearing years, raising the possibility that the developing fetus may be exposed to filarial antigens in utero and thereby have altered immunity and susceptibility to infection during early childhood. Animal models of intravascular helminthic infections support this hypothesis, as these have shown that offspring of infected pregnant rodents are immunologically less responsive to parasite antigens, have less pathology, and are more susceptible than offspring of uninfected mothers (9,17,21,32,36). Analogous studies of humans are inherently more complex and difficult to interpret because of heterogeneities in exposure to infectivestage parasites, genetic differences among various study populations, and prior treatment with antifilarial drugs.…”

mentioning

confidence: 55%

Influence of Maternal Filariasis on Childhood Infection and Immunity toWuchereria bancroftiin Kenya

et al. 2003

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To determine whether maternal filariasis influences the risk of infection by and immunity to Wuchereria bancrofti in children, we performed a cross-sectional study in an area of Kenya where filariasis is endemic. Residents of 211 households were enrolled; 376 parents and 938 of their offspring between the ages of 2 and 17 years were examined for filarial infection status as determined by blood-borne microfilariae and filarial antigenemia. Children of infected mothers had a three-to fourfold increased risk of filarial infection, as ascertained by circulating filarial antigen, relative to children of uninfected mothers (P < 0.001). Paternal infection did not correlate with childhood infection status, indicating a specific maternal effect. Peripheral blood mononuclear cells from children of filaria-infected mothers (n ‫؍‬ 33) had higher levels of constitutive interleukin-5 (IL-5) and IL-10, increased microfilarial antigen-specific IL-5 production, and diminished microfilarial antigen-driven lymphocyte proliferation than cells from children of uninfected mothers (n ‫؍‬ 46; P < 0.05). In contrast, there were no differences between the two groups in adult worm antigen-driven gamma interferon, IL-2, IL-4, IL-5, and IL-10 production and lymphocyte proliferation. These data indicate that maternal filarial infection increases childhood susceptibility to W. bancrofti and skews filaria-specific immunity toward a Th2-type cytokine response. The results support the notion that in utero exposure to filarial antigens affects the natural history of filariasis during childhood.

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confidence: 55%

Influence of Maternal Filariasis on Childhood Infection and Immunity toWuchereria bancroftiin Kenya

et al. 2003

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“…Animal models suggest that exposure to parasites in utero may be either beneficial (by accelerating the development of protective antibodies and cellular immune responses) or detrimental (by impairing the acquisition of a protective immune response and inducing immune tolerance) [71]–[74].…”

Section: Proposed Mechanismsmentioning

confidence: 99%

Do Antenatal Parasite Infections Devalue Childhood Vaccination?

et al. 2009

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On a global basis, both potent vaccine efficacy and high vaccine coverage are necessary to control and eliminate vaccine-preventable diseases. Emerging evidence from animal and human studies suggest that neglected tropical diseases (NTDs) significantly impair response to standard childhood immunizations. A review of efficacy and effectiveness studies of vaccination among individuals with chronic parasitic infections was conducted, using PUBMED database searches and analysis of data from the authors' published and unpublished studies. Both animal models and human studies suggest that chronic trematode, nematode, and protozoan infections can result in decreased vaccine efficacy. Among pregnant women, who in developing countries are often infected with multiple parasites, soluble parasite antigens have been shown to cross the placenta and prime or tolerize fetal immune responses. As a result, antenatal infections can have a significant impact on later vaccine responses. Acquired childhood parasitic infections, most commonly malaria, can also affect subsequent immune response to vaccination. Additional data suggest that antiparasite therapy can improve the effectiveness of several human vaccines. Emerging evidence demonstrates that both antenatal and childhood parasitic infections alter levels of protective immune response to routine vaccinations. Successful antiparasite treatment may prevent immunomodulation caused by parasitic antigens during pregnancy and early childhood and may improve vaccine efficacy. Future research should highlight the varied effects that different parasites (alone and in combination) can have on human vaccine-related immunity. To optimize vaccine effectiveness in developing countries, better control of chronic NTDs may prove imperative.

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“…In utero exposure to the nematode parasites Dipetalonema viteae , Brugia malayi , or Acanthocheilonema viteae enhanced the offspring's susceptibility to subsequent infection by these parasites and produce impaired spleen cell responsiveness to T cell mitogens and filarial antigens (15)(16)(17). In murine models of schistosomiasis or filariasis, offspring of infected mothers developed smaller granulomas (1,18) or reduced gross lymphatic pathology (2) compared with newborns of uninfected mothers.…”

Section: Introductionmentioning

confidence: 99%

In utero exposure to helminth and mycobacterial antigens generates cytokine responses similar to that observed in adults.

et al. 1997

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Neonates exposed to parasite antigens (Ags) in utero may develop altered fetal immunity that could affect subsequent responses to infection. We hypothesized that cord blood lymphocytes (CBL) from offspring of mothers residing in an area highly endemic for schistosomiasis, filariasis, and tuberculosis in Kenya would either fail to respond or generate a predominantly Th2-associated cytokine response to helminth and mycobacterial antigens (PPD) in vitro compared to maternal PBMC. Kenyan CBL generated helminth Ag-

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Predisposition to Brugia Malayi Microfilaremia in Progeny of Infected Gerbils *

Cited by 24 publications

References 0 publications

Influence of Maternal Filariasis on Childhood Infection and Immunity toWuchereria bancroftiin Kenya

Influence of Maternal Filariasis on Childhood Infection and Immunity toWuchereria bancroftiin Kenya

Do Antenatal Parasite Infections Devalue Childhood Vaccination?

In utero exposure to helminth and mycobacterial antigens generates cytokine responses similar to that observed in adults.

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