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CELLULAR AND MOLECULAR MECHANISM OF LISTERIA ADHESION PROTEIN-MEDIATED BACTERIAL CROSSING OF THE INTESTINAL BARRIERRishi Drolia (5929649) 14 January 2021 (has links)
<p>The
crossing of host barriers (intestinal, blood-brain, and placental) is a critical
step for systemic infections caused by entero-invasive pathogens. In the
intestine, the epithelial cells are the first line of defense against
enteric pathogens. <i>Listeria monocytogenes</i> is a
facultative-intracellular foodborne pathogen that first crosses the intestinal
barrier to cause a systemic infection. However, the underlying
mechanism is not well understood.</p><p><br></p>
<p>We
demonstrate that <i>Listeria</i> adhesion protein (LAP) promotes
the translocation of <i>L. monocytogenes </i>across the intestinal
barrier in mouse models (A/J and C57BL/6). Relative to the wild-type
(WT; serotype 4b) or the isogenic bacterial invasion protein
Internalin A mutant (Δ<i>inlA</i>) strain, the <i>lap<sup>─</sup></i>
strain showed significant defect in translocation across the intestinal
barrier and colonization of the mesenteric-lymph nodes, liver and
spleen in the early phase of infection (24 h and 48
h). LAP induces intestinal epithelial barrier dysfunction for
increased translocation as evidenced by increased permeability
to 4-kDa FITC-dextran (FD4), a marker of paracellular
permeability, in the serum and urine of WT and Δ<i>inlA</i>- infected
mice and across Caco-2 cell barrier, but not the <i>lap<sup>─</sup></i> mutant
strain. Microscopic examination confirmed localization of the WT
and Δ<i>inlA</i> strains in the tight junction, a crucial
barrier of intestinal paracellular permeability, in the mouse ileal tissue
but the <i>lap<sup>─</sup></i> strain remained confined in the
lumen. LAP also upregulates TNF-α and IL-6 in intestinal epithelia
of mice and in Caco-2 cells for increased permeability. </p><p><br></p>
<p>Investigation
of the underlying molecular mechanisms of LAP-mediated increase in intestinal
permeability by using <i>lap<sup>─</sup></i> mutant strain, purified
LAP and shRNA-mediated Hsp60 suppression, we demonstrate that LAP
interacts with its host receptor, Hsp60, and activates the canonical NF-κB
signaling, which in turn facilitates myosin light-chain
kinase (MLCK)-mediated opening of the epithelial barrier via the cellular
redistribution of major epithelial junctional proteins claudin-1, occludin, and
E-cadherin. Pharmacological inhibition of NF-κB or MLCK in cells or
genetic ablation of MLCK in mice (C57BL/6) prevents mislocalization of
epithelial junctional proteins, intestinal permeability and <i>L.
monocytogenes</i> translocation across the intestinal barrier.</p>
<p><br></p><p>Furthermore,
LAP also promotes <i>L. monocytogenes </i>translocation
across the intestinal barrier and systemic dissemination in a
Mongolian gerbil that are permissive to the bacterial invasion proteins;
InlA-and InlB-mediated pathways; similar to that in humans. We show
a direct LAP-dependent and InlA-independent pathway<i> </i>for <i>L.
monocytogenes</i> paracellular translocation across the intestinal
epithelial cells that do not express luminally accessible
E-cadherin. Additionally, we show a functional InlA/E-cadherin interaction
pathway that aids <i>L. monocytogenes</i> translocation by targeting
cells with luminally accessible E-cadherin such as cells at the site of
epithelial cell extrusion, epithelial folds and mucus-expelling goblet
cells. Thus, <i>L. monocytogenes</i> uses LAP to exploit
epithelial innate defense in the early phase of infection to cross the
intestinal epithelial barrier, independent of other invasion proteins.</p><p><br></p>
<p>This
work fills a critical gap in our understanding of <i>L.
monocytogenes </i>pathogenesis and sheds light to the complex interplay
between host-pathogen interactions for bacterial crossing of the crucial
intestinal barrier.</p>
<br>
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Effets d'une infection parasitaire sur la condition corporelle et les traits de comportement du crapet-soleil (Lepomis gibbosus)Gradito, Maryane 08 1900 (has links)
Le parasitisme est de plus en plus considéré comme un facteur écologique pouvant créer des variations dans le comportement des individus. Toutefois, la direction de causalité entre le comportement et le parasitisme reste incertaine. Les infections expérimentales sont le plus souvent réalisées en laboratoire, limitant les inférences écologiques. À l’aide d’une infection expérimentale semi-naturelle, nous avons infecté avec succès des crapets-soleils (Lepomis gibbosus) dans un lac où ils ont été exposés à une variété de vers parasites (trématodes, cestodes), permettant d’examiner les effets de la co-infection naturelle chez les hôtes. Nous avons mesuré la témérité, l’exploration et l’activité avant et après l’infection expérimentale. En utilisant une approche bayésienne, nous avons trouvé que les traits de comportement initiaux exercent une forte influence sur la susceptibilité à l’infection : les poissons les plus téméraires et/ou les moins actifs au départ ont acquis une plus grande densité de points noirs (c.-à-d. points noirs visibles sous la peau, les nageoires et dans les muscles du poisson) et de cestodes lors de l’infection. Par ailleurs, nous avons montré que la condition corporelle est réduite par la densité de cestodes, suggérant la débilitation de l’hôte. La condition corporelle était corrélée positivement avec la distance parcourue, quel que soit le statut d’infection individuel. Nous avons également trouvé une relation négative entre la distance parcourue après l’infection et la densité de trématodes, suggérant que l’infection causant la maladie des points noirs diminue le niveau d’activité des hôtes. La témérité et l'exploration n'étaient pas affectées par la densité parasitaire ou la condition corporelle. Nous suggérons que la diminution de l’activité est causée par une réponse adaptative de l’hôte, visant à rediriger son énergie pour combattre l’infection. Sachant que les points noirs ont un cycle de vie complexe et que le crapet-soleil est un hôte intermédiaire, ce changement dans le comportement de l’hôte pourrait aider le parasite à compléter sa transmission aux oiseaux-hôtes piscivores en augmentant la prédation sur les poissons infectés. Bien que nous ne puissions confirmer la direction de causalité, nos résultats montrent qu’il existe un lien étroit entre le comportement et le parasitisme. Nous suggérons que deux mécanismes peuvent simultanément agir : le comportement initial des individus influence le risque d’infection, et l’infection peut créer de la variation au niveau de la plasticité comportementale des individus. / Parasitism is increasingly seen as an ecological factor that can create variations in individual behaviour. However, the direction of causality between behaviour and parasitism remains uncertain. Experimental infections are most often conducted in laboratories, limiting ecological inferences. Using a semi-natural experimental infection, we successfully infected pumpkinseed sunfish (Lepomis gibbosus) in a lake where they were exposed to various parasitic worms (trematodes, cestodes), allowing us to examine the effects of natural co-infection in hosts. We measured boldness, exploration, and activity before and after the experimental infection. Using a Bayesian approach, we found that initial behavioural traits strongly influence infection susceptibility: initially bolder and/or less active fish acquired a higher density of black spots (i.e., visible black spots under the skin, fins, and in the fish's muscles) and cestodes during the infection. Additionally, we found that body condition was reduced by cestode density, suggesting host debilitation. Body condition was positively correlated with distance swam, regardless of individual infection status. We also found a negative relationship between distance swam after infection and trematode density, suggesting that infection causing black spot disease decreases host activity levels. Boldness and exploration were not affected by parasite density or body condition. We suggest that a decrease in activity is caused by an adaptive host response to redirect its energy to combat the infection. However, since trematode parasites have a complex life cycle and pumpkinseed sunfish are intermediate hosts, decreases in activity levels following infection may make infected fish more susceptible to predation by piscivorous birds, which is needed for trematodes to complete their life cycles. While we cannot confirm the direction of causality, our results show a close link between behaviour and parasitism. We propose that two mechanisms may simultaneously operate: the initial behaviour of individuals influences their risk of infection, and infection can create variation in behavioural plasticity of individuals.
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Investigations on the effects of dietary insoluble and soluble non-starch polysaccharides (NSP) on host-parasite interactions in laying hen chicks infected with Heterakis gallinarum or Ascaridia galli / Untersuchungen zum Einfluß löslicher und unlöslicher Nicht-Stärke-Polysaccharide (NSP) im Futter auf Parasit-Wirt-Interaktionen bei wachsenden JunghennenDaş, Gürbüz 16 November 2010 (has links)
No description available.
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Thousand Cankers Disease of Eastern Black Walnut: Ecological Interactions in the Holobiont of a Bark Beetle-Fungal DiseaseGeoffrey M Williams (11186766) 27 July 2021 (has links)
<p>Eastern black walnut (<i>Juglans
nigra</i> L.) ranks among the most highly valued timber species in the central
hardwood forest and across the world. This valuable tree fills a critical role
in native ecosystems as a mast bearing pioneer on mesic sites. Along with other
<i>Juglans</i> spp. (Juglandaceae), <i>J. nigra</i> is threatened by thousand
cankers disease (TCD), an insect-vectored disease first described in 2009. TCD
is caused by the bark beetle <i>Pityophthorus
juglandis</i> Blackman (Corthylini) and the phytopathogenic fungus <i>Geosmithia morbida</i> Kol. Free. Ut. &
Tiss. (Bionectriaceae). Together, the <i>P.
juglandis</i>-<i>G. morbida</i> complex has
expanded from its historical range in southwest North America throughout the
western United States (U.S.) and Europe. This range expansion has led to
widespread mortality among naïve hosts <i>J.
nigra</i> and <i>J. regia</i> planted
outside their native distributions.</p>
<p> The severity
of TCD was previously observed to be highest in urban and plantation
environments and outside of the host native range. Therefore, the objective of
this work was to provide information on biotic and abiotic environmental
factors that influence the severity and impact of TCD across the native and
non-native range of <i>J. nigra</i> and
across different climatic and management regimes. This knowledge would enable a
better assessment of the risk posed by TCD and a basis for developing
management activities that impart resilience to natural systems. Through a
series of greenhouse-, laboratory- and field-based experiments, environmental
factors that affect the pathogenicity and/or survival of <i>G. morbida</i> in <i>J. nigra</i>
were identified, with a focus on the microbiome, climate, and opportunistic
pathogens. A number of potentially important interactions among host, vector,
pathogen and the rest of the holobiont of TCD were characterized. The <i>holobiont</i> is defined as the whole
multitrophic community of organisms—including <i>J. nigra</i>, microinvertebrates, fungi and bacteria—that interact with
one another and with the host.</p>
<p>Our findings indicate that
interactions among host, vector, pathogen, secondary pathogens, novel microbial
communities, and novel abiotic environments modulate the severity of TCD in
native, non-native, and managed and unmanaged contexts. Prevailing climatic
conditions favor reproduction and spread of <i>G.
morbida</i> in the western United States due to the effect of wood moisture
content on fungal competition. The microbiome of soils, roots, and stems of
trees and seedlings grown outside the host native range harbor distinct,
lower-diversity communities of bacteria and fungi compared to the native range,
including different communities of beneficial or pathogenic functional groups
of fungi. The pathogen <i>G. morbida</i> was
also associated with a distinct community of microbes in stems compared to <i>G. morbida</i>-negative trees. The soil
microbiome from intensively-managed plantations facilitated positive feedback
between <i>G. morbida</i> and a
disease-promomting endophytic <i>Fusarium
solani</i> species complex sp. in roots of <i>J.
nigra</i> seedlings. Finally, the nematode species <i>Bursaphelenchus juglandis</i> associated with <i>P. juglandis</i> synergizes with <i>G.
morbida</i> to cause foliar symptoms in seedlings in a shadehouse; conversely,
experiments and observations indicated that the nematode species <i>Panagrolaimus</i> sp. and cf. <i>Ektaphelenchus</i> sp. could suppress WTB
populations and/or TCD outbreaks.</p>
<p>In conclusion, the composition,
function, and interactions within the <i>P.
juglandis</i> and <i>J. nigra</i> holobiont play
important roles in the TCD pathosystem. Managers and conservationists should be
aware that novel associations outside the host native range, or in monocultures,
intensive nursery production, and urban and low-humidity environments may favor
progression of the disease through the effects of associated phytobiomes,
nematodes, and climatic conditions on disease etiology. Trees in higher
diversity, less intensively managed growing environments within their native
range may be more resilient to disease. Moreover, expatriated, susceptible host
species (<i>i.e.</i>, <i>J. nigra</i>) growing in environments that are favorable to novel pests
or pest complexes (<i>i.e.</i>, the western
U.S.) may provide connectivity between emergent forest health threats (<i>i.e.</i>, TCD) and native host populations (<i>i.e.</i>, <i>J. nigra</i> in its native range).</p>
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