Association of angiitis of central nervous system, cerebral amyloid angiopathy, and Alzheimer’s disease: Report of an autopsy case

The association of angiitis of central nervous system (ACNS) with cerebral amyloid angiopathy (CAA) suggests a physiopathological relationship between these two affections. Few cases are reported in patients with Alzheimer’s disease (AD). We describe here a clinicopathological case associating ACNS, CAA, and AD. We discuss the aetiology of ACNS and its relationship with cerebral deposition of beta A4 amyloid protein (βA4)

Schistosomiasis Coinfection in Children Influences Acquired Immune Response against Plasmodium falciparum Malaria Antigens

Background: Malaria and schistosomiasis coinfection frequently occurs in tropical countries. This study evaluates the influence of Schistosoma haematobium infection on specific antibody responses and cytokine production to recombinant merozoite surface protein-1-19 (MSP1-19) and schizont extract of Plasmodium falciparum in malaria-infected children. Methodology: Specific IgG1 to MSP1- 19, as well as IgG1 and IgG3 to schizont extract were significantly increased in coinfected children compared to P. falciparum mono-infected children. Stimulation with MSP1- 19 lead to a specific production of both interleukin-10 (IL-10) and interferon-c (IFN-c), whereas the stimulation with schizont extract produced an IL-10 response only in the coinfected group. Conclusions: Our study suggests that schistosomiasis coinfection favours anti-malarial protective antibody responses, which could be associated with the regulation of IL-10 and IFN-c production and seems to be antigen-dependent. This study demonstrates the importance of infectious status of the population in the evaluation of acquired immunity against malari

New reactor dedicated to in operando studies of model catalysts by means of surface x-ray diffraction and grazing incidence small angle x-ray scattering

International audienceA new experimental setup has been developed to enable in situ studies of catalyst surfaces during chemical reactions by means of surface x-ray diffraction (SXRD) and grazing incidence small angle x-ray scattering. The x-ray reactor chamber was designed for both ultrahigh-vacuum (UHV) and reactive gas environments. A laser beam heating of the sample was implemented; the sample temperature reaches 1100 K in UHV and 600 K in the presence of reactive gases. The reactor equipment allows dynamical observations of the surface with various, perfectly mixed gases at controlled partial pressures. It can run in two modes: as a bath reactor in the pressure range of 1-1000 mbars and as a continuous flow cell for pressure lower than 10−3 mbar. The reactor is connected to an UHV preparation chamber also equipped with low energy electron diffraction and Auger spectroscopy. This setup is thus perfectly well suited to extend in situ studies to more complex surfaces, such as epitaxial films or supported nanoparticles. It offers the possibility to follow the chemically induced changes of the morphology, the structure, the composition, and growth processes of the model catalyst surface during exposure to reactive gases. As an example the Pd8Ni92(110) surface structure was followed by SXRD under a few millibars of hydrogen and during butadiene hydrogenation while the reaction was monitored by quadrupole mass spectrometry. This experiment evidenced the great sensitivity of the diffracted intensity to the subtle interaction between the surface atoms and the gas molecules

Impact of Mycobacterium ulcerans Biofilm on Transmissibility to Ecological Niches and Buruli Ulcer Pathogenesis

The role of biofilms in the pathogenesis of mycobacterial diseases remains largely unknown. Mycobacterium ulcerans, the etiological agent of Buruli ulcer, a disfiguring disease in humans, adopts a biofilm-like structure in vitro and in vivo, displaying an abundant extracellular matrix (ECM) that harbors vesicles. The composition and structure of the ECM differs from that of the classical matrix found in other bacterial biofilms. More than 80 proteins are present within this extracellular compartment and appear to be involved in stress responses, respiration, and intermediary metabolism. In addition to a large amount of carbohydrates and lipids, ECM is the reservoir of the polyketide toxin mycolactone, the sole virulence factor of M. ulcerans identified to date, and purified vesicles extracted from ECM are highly cytotoxic. ECM confers to the mycobacterium increased resistance to antimicrobial agents, and enhances colonization of insect vectors and mammalian hosts. The results of this study support a model whereby biofilm changes confer selective advantages to M. ulcerans in colonizing various ecological niches successfully, with repercussions for Buruli ulcer pathogenesis

Protection against Mycobacterium ulcerans Lesion Development by Exposure to Aquatic Insect Saliva

BACKGROUND: Buruli ulcer is a severe human skin disease caused by Mycobacterium ulcerans. This disease is primarily diagnosed in West Africa with increasing incidence. Antimycobacterial drug therapy is relatively effective during the preulcerative stage of the disease, but surgical excision of lesions with skin grafting is often the ultimate treatment. The mode of transmission of this Mycobacterium species remains a matter of debate, and relevant interventions to prevent this disease lack (i) the proper understanding of the M. ulcerans life history traits in its natural aquatic ecosystem and (ii) immune signatures that could be correlates of protection. We previously set up a laboratory ecosystem with predatory aquatic insects of the family Naucoridae and laboratory mice and showed that (i) M. ulcerans-carrying aquatic insects can transmit the mycobacterium through bites and (ii) that their salivary glands are the only tissues hosting replicative M. ulcerans. Further investigation in natural settings revealed that 5%–10% of these aquatic insects captured in endemic areas have M. ulcerans–loaded salivary glands. In search of novel epidemiological features we noticed that individuals working close to aquatic environments inhabited by insect predators were less prone to developing Buruli ulcers than their relatives. Thus we set out to investigate whether those individuals might display any immune signatures of exposure to M. ulcerans-free insect predator bites, and whether those could correlate with protection. METHODS AND FINDINGS: We took a two-pronged approach in this study, first investigating whether the insect bites are protective in a mouse model, and subsequently looking for possibly protective immune signatures in humans. We found that, in contrast to control BALB/c mice, BALB/c mice exposed to Naucoris aquatic insect bites or sensitized to Naucoris salivary gland homogenates (SGHs) displayed no lesion at the site of inoculation of M. ulcerans coated with Naucoris SGH components. Then using human serum samples collected in a Buruli ulcer–endemic area (in the Republic of Benin, West Africa), we assayed sera collected from either ulcer-free individuals or patients with Buruli ulcers for the titre of IgGs that bind to insect predator SGH, focusing on those molecules otherwise shown to be retained by M. ulcerans colonies. IgG titres were lower in the Buruli ulcer patient group than in the ulcer-free group. CONCLUSIONS: These data will help structure future investigations in Buruli ulcer–endemic areas, providing a rationale for research into human immune signatures of exposure to predatory aquatic insects, with special attention to those insect saliva molecules that bind to M. ulcerans