Hepatitis E, Schistosomiasis and Echinococcosis-Prevalence in a Cohort of Pregnant Migrants in Germany and Their Influence on Fetal Growth Restriction.

Background: Infections, as well as adverse birth outcomes, may be more frequent in migrant women. Schistosomiasis, echinococcosis, and hepatitis E virus (HEV) seropositivity are associated with the adverse pregnancy outcomes of fetal growth restriction and premature delivery.

Methods: A cohort study of 82 pregnant women with a history of migration and corresponding delivery of newborns in Germany was conducted.

Dynamic, Helminth-Induced Immune Modulation Influences the Outcome of Acute and Chronic Hepatitis B Virus Infection.

Background: Chronic hepatitis B develops more frequently in countries with high prevalence of helminth infections. The crosstalk between these 2 major liver-residing pathogens, Schistosoma mansoni and hepatitis B virus (HBV), is barely understood.

Methods: We used state-of-the-art models for both acute and chronic HBV infection to study the pathogen-crosstalk during the different immune phases of schistosome infection.

Maternal Schistosomiasis: Immunomodulatory Effects With Lasting Impact on Allergy and Vaccine Responses.

Early exposure to immune stimuli, including maternal infection during the perinatal period, is increasingly recognized to affect immune predisposition during later life. This includes exposure to not only viral and bacterial infection but also parasitic helminths which remain widespread. Noted effects of helminth infection, including altered incidence of atopic inflammation and vaccine responsiveness, support further research into the impact these infections have for skewing immune responses.

Maternal immune response to helminth infection during pregnancy determines offspring susceptibility to allergic airway inflammation.

Background: Schistosomiasis, a chronic helminth infection, elicits distinct immune responses within the host, ranging from an initial TH1 and subsequent TH2 phase to a regulatory state, and is associated with dampened allergic reactions within the host.

Objective: We sought to evaluate whether non-transplacental helminth infection during pregnancy alters the offspring's susceptibility to allergy.

Methods: Ovalbumin-induced allergic airway inflammation was analyzed in offspring from Schistosoma mansoni-infected mothers mated during the TH1, TH2, or regulatory phase of infection.

Pronounced phenotype in activated regulatory T cells during a chronic helminth infection.

Although several markers have been associated with the characterization of regulatory T cells (Tregs) and their function, no studies have investigated the dynamics of their phenotype during infection. Since the necessity of Tregs to control immunopathology has been demonstrated, we used the chronic helminth infection model Schistosoma mansoni to address the impact on the Treg gene repertoire. Before gene expression profiling, we first studied the localization and Ag-specific suppressive nature of classically defined Tregs during infection.

Immunopathology in schistosomiasis is controlled by antigen-specific regulatory T cells primed in the presence of TLR2.

Regulatory T cells (Treg) are vital in maintaining the homeostasis of immune reactions. In chronic infections, such as schistosomiasis, it remains unclear whether engagement of the TLR family is required to induce Treg activity. Thus, we performed in vivo studies using TLR2-/- mice infected with Schistosoma mansoni and found elevated immunopathology, decreased egg burden and extended antigen-specific Th1 responses.

Lack of antigen-specific Th1 response alters granuloma formation and composition in Schistosoma mansoni-infected MyD88-/- mice.

To evaluate the role of the innate immune system during schistosomiasis in vivo, we infected myeloid differentiation factor 88 (MyD88)-deficient mice with Schistosoma mansoni and analyzed their pathognomonic formation of hepatic granulomas and T cell responses. Even though the differences between knockout and wild-type mice in terms of mortality, liver damage, serum IgE and parasite burden were insignificant, the liver granulomas in the MyD88-deficient mice were significantly smaller, less cellular and contained a reduced percentage of eosinophils. Histologically, these granulomas revealed stronger fibrosis, confirmed also by increased levels of soluble collagen and IL-13, implying a Th2 bias.

Polymorphonuclear neutrophils improve replication of Chlamydia pneumoniae in vivo upon MyD88-dependent attraction.

Chlamydia pneumoniae, an obligate intracellular bacterium, causes pneumonia in humans and mice. In this study, we show that GR1+/CD45+ polymorphonuclear neutrophils (PMN) surprisingly increase the bacterial load of C. pneumoniae in vivo.

Heat shock protein 60 from Chlamydia pneumoniae elicits an unusual set of inflammatory responses via Toll-like receptor 2 and 4 in vivo.

Heat shock protein 60 (HSP60) from Chlamydia pneumoniae was described to trigger in vitro inflammatory and cytokine responses including TNF and IL-12p40. Although it can be found in atherosclerotic plaques of patients, the stimulatory potential of chlamydial and other HSP60 in vivo is unclear. We now report that chlamydial HSP60 fails to induce TNF expression in vivo, and significant serum levels of IL-12p40 are only found upon intraperitoneal injection of high doses of HSP60 or after intravenous application.