Short-term consumption of a high-fat diet increases host susceptibility to Listeria monocytogenes infection

peer-reviewedBackground A westernized diet comprising a high caloric intake from animal fats is known to influence the development of pathological inflammatory conditions. However, there has been relatively little focus upon the implications of such diets for the progression of infectious disease. Here, we investigated the influence of a high-fat (HF) diet upon parameters that influence Listeria monocytogenes infection in mice. Results We determined that short-term administration of a HF diet increases the number of goblet cells, a known binding site for the pathogen, in the gut and also induces profound changes to the microbiota and promotes a pro-inflammatory gene expression profile in the host. Host physiological changes were concordant with significantly increased susceptibility to oral L. monocytogenes infection in mice fed a HF diet relative to low fat (LF)- or chow-fed animals. Prior to Listeria infection, short-term consumption of HF diet elevated levels of Firmicutes including Coprococcus, Butyricicoccus, Turicibacter and Clostridium XIVa species. During active infection with L. monocytogenes, microbiota changes were further exaggerated but host inflammatory responses were significantly downregulated relative to Listeria-infected LF- or chow-fed groups, suggestive of a profound tempering of the host response influenced by infection in the context of a HF diet. The effects of diet were seen beyond the gut, as a HF diet also increased the sensitivity of mice to systemic infection and altered gene expression profiles in the liver. Conclusions We adopted a systems approach to identify the effects of HF diet upon L. monocytogenes infection through analysis of host responses and microbiota changes (both pre- and post-infection). Overall, the results indicate that short-term consumption of a westernized diet has the capacity to significantly alter host susceptibility to L. monocytogenes infection concomitant with changes to the host physiological landscape. The findings suggest that diet should be a consideration when developing models that reflect human infectious disease.This research was funded by the European Union’s Horizon 2020 Research and Innovation Program under the Marie Skłodowska-Curie grant agreement No. 641984, through funding of the List_MAPS consortium. We also acknowledge funding and support from Science Foundation Ireland (SFI) in the form of a center grant (APC Microbiome Ireland grant SFI/12/RC/2273)

Determination of trace metals in seawater by ICP-MS after preconcentration and matrix separation by dithiocarbamate complexes

71-75A rapid single extraction procedure using dithiocarbamate complexing agent in methyl-isobutyl ketone (MIBK) organic phase and acid exchange back-extraction is described for the simultaneous quantitative preconcentration of Fe, Mn, V, Cr, Ni, Co, Cu, Zn, As, Mo, Cd, Pb and U in seawater followed by its determination by inductively coupled plasma mass spectrometry (ICP-MS). This method gives quantitative recoveries for all above metals at pH 4.1-6.4. A matrix matching seawater certified reference material (CRM), NASS-5, was used for calibration so as to minimize the matrix and other associated effects. Blanks and detection limits were in ng/l range. The method gives a recovery of 94-100% for 100 ml sample, facilitating the rapid and interference-free analysis of seawater samples. Excellent agreement was obtained with the certified values of another seawater CRM, CASS-4, when it was analyzed as an unknown. The major advantage of this procedure is that rapid analysis can be performed for a wide range of metals from relatively small samples

Magnetic studies in the northern Bay of Bengal

Total magnetic intensity and bathymetric surveys were carried out in the northern Bay of Bengal between 6° to 11°45' N latitudes and east of 84° to 93° 30' E longitudes. The hitherto known 85° E Ridge is characterised as a subsurface feature by a large amplitude, positive magnetic anomaly surrounded by Mesozoic crust. A newly identified NE to NNESSW trending magnetic anomaly between 7° N, 87° 30' E and 10° 30' N, 89-90° E may be one of the unidentified Mesozoic lineations in the northern Bay of Bengal. The Ninetyeast Ridge is not associated with any recognizable magnetic anomaly. The Sunda Trough to the east of the Ninetyeast Ridge is characterised by a positive magnetic anomaly. A combined interpretation, using Werner deconvolution and analytical signal methods, yields basement depths ~ 10 km below sea level. These depths are in agreement with the seismic results of Curray (1991)

Advanced Modeling of Surface Waves on Twisted Pair Cables: Surface Wave Stopbands

At the network access layer, optical fiber deployment continues at pace but copper cables containing twisted pairs (TWPs) will remain for some time and face an increasing bandwidth and data rate demand. Surface waves have been proposed to address these requirements. This article reports and investigates the existence of stopbands reaching over 50-dB insertion loss on 1-m-long, typical final drop cables under surface wave excitation at a few gigahertz. Coupled mode analysis shows that lack of helical symmetry enables the formation of a stopband in systems containing TWPs. A representative core model containing a single TWP alongside a straight wire is thoroughly studied. Numerical simulations and measurements confirm the crucial dependence of the stopband frequency on the twist rate of the TWP. Further investigation into the role of the dielectric coating and the distance of the straight wire is performed as well. Finally, in systems with multiple TWPs, we find that the twist rate associated with any pair can create a stopband effectively limiting surface wave propagation. Thus, careful design and deployment strategies are required for use of surface waves on legacy copper networks

Listeria adhesion protein orchestrates caveolae-mediated apical junctional remodeling of epithelial barrier for Listeria monocytogenes translocation

ABSTRACTThe cellular junctional architecture remodeling by Listeria adhesion protein-heat shock protein 60 (LAP-Hsp60) interaction for Listeria monocytogenes (Lm) passage through the epithelial barrier is incompletely understood. Here, using the gerbil model, permissive to internalin (Inl) A/B-mediated pathways like in humans, we demonstrate that Lm crosses the intestinal villi at 48 h post-infection. In contrast, the single isogenic (lap− or ΔinlA) or double (lap−ΔinlA) mutant strains show significant defects. LAP promotes Lm translocation via endocytosis of cell-cell junctional complex in enterocytes that do not display luminal E-cadherin. In comparison, InlA facilitates Lm translocation at cells displaying apical E-cadherin during cell extrusion and mucus expulsion from goblet cells. LAP hijacks caveolar endocytosis to traffic integral junctional proteins to the early and recycling endosomes. Pharmacological inhibition in a cell line and genetic knockout of caveolin-1 in mice prevents LAP-induced intestinal permeability, junctional endocytosis, and Lm translocation. Furthermore, LAP-Hsp60-dependent tight junction remodeling is also necessary for InlA access to E-cadherin for Lm intestinal barrier crossing in InlA-permissive hosts.IMPORTANCEListeria monocytogenes (Lm) is a foodborne pathogen with high mortality (20%–30%) and hospitalization rates (94%), particularly affecting vulnerable groups such as pregnant women, fetuses, newborns, seniors, and immunocompromised individuals. Invasive listeriosis involves Lm’s internalin (InlA) protein binding to E-cadherin to breach the intestinal barrier. However, non-functional InlA variants have been identified in Lm isolates, suggesting InlA-independent pathways for translocation. Our study reveals that Listeria adhesion protein (LAP) and InlA cooperatively assist Lm entry into the gut lamina propria in a gerbil model, mimicking human listeriosis in early infection stages. LAP triggers caveolin-1-mediated endocytosis of critical junctional proteins, transporting them to early and recycling endosomes, facilitating Lm passage through enterocytes. Furthermore, LAP-Hsp60-mediated junctional protein endocytosis precedes InlA’s interaction with basolateral E-cadherin, emphasizing LAP and InlA’s cooperation in enhancing Lm intestinal translocation. This understanding is vital in combating the severe consequences of Lm infection, including sepsis, meningitis, encephalitis, and brain abscess