Publications by authors named "Anne Rabes"

IL-22 plays a critical role in defending against mucosal infections, but how IL-22 production is regulated is incompletely understood. Here, we show that mice lacking IL-33 or its receptor ST2 (IL-1RL1) were more resistant to lung infection than wild-type animals and that single-nucleotide polymorphisms in and were associated with pneumococcal pneumonia in humans. The effect of IL-33 on infection was mediated by negative regulation of IL-22 production in innate lymphoid cells (ILCs) but independent of ILC2s as well as IL-4 and IL-13 signaling.

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In exhibiting gonochorism and phenotypic sexual dimorphism, spp. are unique among trematodes. Only females mating with male schistosomes can produce the highly immunogenic parasite eggs which determine the clinical picture of the disease schistosomiasis.

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Background: Schistosomiasis is a severe parasitic disease that is primarily driven by the host's immune response to schistosome eggs trapped in tissue and by the granulomatous inflammatory and fibrotic reaction they cause. Despite significant progress in understanding the complex immunological processes involved in the relationship between schistosomes and their host, neither an effective vaccine against the infection nor anti-fibrotic drugs currently exists, making the search for new targets for schistosome drugs and vaccine candidates even more important. In order to identify new molecular targets for defense against or elimination of the parasite, we investigate herein the interplay between the host and male or female schistosomes, clearly separating this from the action of the parasite eggs.

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Background: The current risk of infection with SARS-CoV-2 in schools continues to be a subject of controversy.

Methodology: "schugi-MV" collects data on the incidence of infection, hygiene management and other factors in structured inspections of schools in Mecklenburg-Western Pomerania. Recommendations for safe teaching are to be derived from the results.

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In recent decades, biofilm-associated infections have become a major problem in many medical fields, leading to a high burden on patients and enormous costs for the healthcare system. Microbial infestations are caused by opportunistic pathogens which often enter the incision already during implantation. In the subsequently formed biofilm bacteria are protected from the hosts immune system and antibiotic action.

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Schistosomiasis is one of the most devastating parasitic disease in the world. Schistosoma spp. survive for decades within the vasculature of their human hosts.

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As part of the parasite's excretory/secretory system, extracellular vesicles (EVs) represent a potent communication tool of schistosomes with their human host to strike the balance between their own survival in a hostile immunological environment and a minimal damage to the host tissue. Their cargo consists of functional proteins, lipids, and nucleic acids that facilitate biological processes like migration, nutrient acquisition, or reproduction. The most important impact of the vesicle-mediated communication, however, is the promotion of the parasite survival via mimicking host protein function and directly or indirectly modulating the immune response of the host.

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Background: Hepatic fibrosis and granuloma formation as a consequence of tissue entrapped eggs produced by female schistosomes characterize the pathology of infection. We have previously shown that single-sex infection with female schistosomes mitigates hepatic fibrosis after secondary infection. This was associated with an increased expression of cytotoxic T-lymphocyte-associated protein-4 (CTLA-4), known as a negative regulator of T cell activation.

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Background & Aims: We studied the role of interleukin 11 (IL11) signaling in the pathogenesis of nonalcoholic steatohepatitis (NASH) using hepatic stellate cells (HSCs), hepatocytes, and mouse models of NASH.

Methods: We stimulated mouse and human fibroblasts, HSCs, or hepatocytes with IL11 and other cytokines and analyzed them by imaging, immunoblot, and functional assays and enzyme-linked immunosorbent assays. Mice were given injections of IL11.

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Infection with the intravascular diecious trematode . remains a serious tropical disease and public health problem in the developing world, affecting over 258 million people worldwide. During chronic infection, complex immune responses to tissue-entrapped parasite eggs provoke granulomatous inflammation which leads to serious damage of the liver and intestine.

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Streptococcus pneumoniae frequently colonizes the upper respiratory tract of healthy individuals, but also commonly causes severe invasive infections such as community-acquired pneumonia and meningitis. One of the key virulence factors of pneumococci is the pore-forming toxin pneumolysin which stimulates cell death and is involved in the evasion of some defense mechanisms. The immune system, however, employs different inflammasomes to sense pneumolysin-induced pore formation, cellular membrane damage, and/or subsequent leakage of bacterial nucleic acid into the host cell cytosol.

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Article Synopsis
  • Streptococcus pneumoniae is a key pathogen linked to serious illnesses like pneumonia and meningitis, and its toxin pneumolysin plays a crucial role in its virulence.
  • Research indicates that different serotypes of S. pneumoniae activate the immune response differently, with serotype 1 and 8 being less effective at triggering IL-1β production in human lung cells compared to other serotypes like 2, 3, and 6B.
  • The findings suggest that serotype 1 pneumococci may evade immune responses, which could explain their significant role in causing invasive diseases globally.
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The innate immune system employs C-type lectin receptors (CLRs) to recognize carbohydrate structures on pathogens and self-antigens. The Macrophage-inducible C-type lectin (Mincle) is a FcRγ-coupled CLR that was shown to bind to mycobacterial cord factor as well as certain fungal species. However, since CLR functions during bacterial infections have not yet been investigated thoroughly, we aimed to examine their function in Streptococcus pneumonia infection.

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