Host susceptibility to Lernaea cyprinacea L. and its treatment in a large aquarium system

Background: During our lifetimes we develop a very complex set of interactions with the multitude of microorganisms colonizing our bodies. In the gastrointestinal system, the microbiota is highly important for morphological development, nutrition, and protection against infectious diseases. The gastrointestinal pathogens, enterohemorrhagic and enteropathogenic Escherichia coli (EHEC and EPEC) and Salmonella enterica serovar Typhimurium (ST) are food-borne pathogens that cause much morbidity and mortality worldwide. Citrobacter rodentium (Cr) is a mouse pathogen that is used in small animal models to mimic EHEC and EPEC infections. Methods: We began to characterize the contribution of intestinal microbiota to the progression of these infections. Two main phyla comprise the majority of mouse intestinal microbiota: Bacteroidetes and Firmicutes. Bacteria from a number of additional phyla are also present in smaller numbers; among them γ-Proteobacteria class, belonging to Proteobacteria phylum, is note-worthy as this class harbours many intestinal pathogens, such as ST and Cr. The mouse intestinal microbiota was perturbed using tetracycline (Tet) and streptomycin (Sm) to increase the proportion of Bacteroidetes in the colonic microbiota, and using vancomycin (Vanc) to create a predominance of Firmicutes. The mice with this perturbed microbiota were infected with ST to investigate the resultant pathology and virulence characteristics, and any additional shifts in microbiota as a result of infection. Results: Treatment of mice with Sm and Vanc was found to decrease the resistance of mice to colonization with ST, while Tet-treated mice exhibited unchanged colonization resistance. Treatment of mice with gradually increasing doses of Sm, which gradually augmented the proportion of CFB bacteria in the microbiota, resulted in progressively increasing colonization of mice by ST, as well as a step-wise increase in the ST-induced typhlitis, associated with higher levels of inflammatory markers IL-6 and KC. The increasing levels of ST colonization following both Sm and Vanc treatment were associated with an increase in the proportion of γ-Proteobacteria in the cecal and colonic microbiota, as well as a decrease in the total bacterial numbers in both organs. Conclusions: It is evident that the intestinal microbiota plays a significant role in the host’s response to infection with enteric pathogens, and its composition and numbers are also affected by the offending bacteria. Elucidation of the details regarding the contribution of the microbiota to infectious disease progression will offer novel targets for the future design of superior prevention and treatment methods.

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Faculty Opinions recommendation of Impact of the microbial derived short chain fatty acid propionate on host susceptibility to bacterial and fungal infections in vivo.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.727041630.793547980 ◽

2018 ◽

Author(s):

Dario Riccardo Valenzano

Keyword(s):

Fatty Acid ◽

Short Chain Fatty Acid ◽

Fungal Infections ◽

Chain Fatty Acid ◽

Host Susceptibility ◽

Short Chain

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Coordination of microbe–host homeostasis by crosstalk with plant innate immunity

Nature Plants ◽

10.1038/s41477-021-00920-2 ◽

2021 ◽

Author(s):

Ka-Wai Ma ◽

Yulong Niu ◽

Yong Jia ◽

Jana Ordon ◽

Charles Copeland ◽

...

Keyword(s):

Growth Inhibition ◽

Amplicon Sequencing ◽

Host Susceptibility ◽

16S Rrna Genes ◽

Rrna Genes ◽

Root Growth Inhibition ◽

Natural Soil ◽

Molecular Pattern ◽

Immune Related Genes ◽

Molecular Patterns

AbstractPlants grown in natural soil are colonized by phylogenetically structured communities of microbes known as the microbiota. Individual microbes can activate microbe-associated molecular pattern (MAMP)-triggered immunity (MTI), which limits pathogen proliferation but curtails plant growth, a phenomenon known as the growth–defence trade-off. Here, we report that, in monoassociations, 41% (62 out of 151) of taxonomically diverse root bacterial commensals suppress Arabidopsis thaliana root growth inhibition (RGI) triggered by immune-stimulating MAMPs or damage-associated molecular patterns. Amplicon sequencing of bacterial 16S rRNA genes reveals that immune activation alters the profile of synthetic communities (SynComs) comprising RGI-non-suppressive strains, whereas the presence of RGI-suppressive strains attenuates this effect. Root colonization by SynComs with different complexities and RGI-suppressive activities alters the expression of 174 core host genes, with functions related to root development and nutrient transport. Furthermore, RGI-suppressive SynComs specifically downregulate a subset of immune-related genes. Precolonization of plants with RGI-suppressive SynComs, or mutation of one commensal-downregulated transcription factor, MYB15, renders the plants more susceptible to opportunistic Pseudomonas pathogens. Our results suggest that RGI-non-suppressive and RGI-suppressive root commensals modulate host susceptibility to pathogens by either eliciting or dampening MTI responses, respectively. This interplay buffers the plant immune system against pathogen perturbation and defence-associated growth inhibition, ultimately leading to commensal–host homeostasis.

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Obesity-Induced Dysbiosis Exacerbates IFN-γ Production and Pulmonary Inflammation in the Mycobacterium tuberculosis Infection

Cells ◽

10.3390/cells10071732 ◽

2021 ◽

Vol 10 (7) ◽

pp. 1732

Author(s):

Sandra Patricia Palma Albornoz ◽

Thais Fernanda de Campos Fraga-Silva ◽

Ana Flávia Gembre ◽

Rômulo Silva de Oliveira ◽

Fernanda Mesquita de Souza ◽

...

Keyword(s):

Mycobacterium Tuberculosis ◽

Gut Microbiota ◽

Inflammatory Diseases ◽

Pulmonary Inflammation ◽

Host Susceptibility ◽

Chronic Infections ◽

Mycobacterium Tuberculosis Infection ◽

Pulmonary Damage ◽

Ifn Γ

The microbiota of the gut–lung axis affects local and far-reaching immune responses and might also trigger chronic and inflammatory diseases. We hypothesized that gut dysbiosis induced by obesity, which coexists in countries with a high tuberculosis burden, aggravates the host susceptibility and the pulmonary damage tolerance. To assess our hypothesis, we used a model of high-fat diet (HFD)-induced obesity, followed by infection of C57BL/6 mice with Mycobacterium tuberculosis. We showed that obesity increased the susceptibility, the pulmonary inflammation and IFN-γ levels in M. tuberculosis-infected mice. During the comorbidity obesity and tuberculosis, there is an increase of Bacteroidetes and Firmicutes in the lungs, and an increase of Firmicutes and butyrate in the feces. Depletion of gut microbiota by antibiotic treatment in the obese infected mice reduced the frequencies of CD4+IFN-γ+IL-17− cells and IFN-γ levels in the lungs, associated with an increase of Lactobacillus. Our findings reinforce the role of the gut–lung axis in chronic infections and suggest that the gut microbiota modulation may be a potential host-directed therapy as an adjuvant to treat TB in the context of IFN-γ-mediated immunopathology.

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Host Diversity and Potential Transmission Pathways of SARS-CoV-2 at the Human-Animal Interface

Pathogens ◽

10.3390/pathogens10020180 ◽

2021 ◽

Vol 10 (2) ◽

pp. 180 ◽

Cited By ~ 1

Author(s):

Hayden D. Hedman ◽

Eric Krawczyk ◽

Yosra A. Helmy ◽

Lixin Zhang ◽

Csaba Varga

Keyword(s):

Public Health ◽

Close Contact ◽

Natural Infection ◽

Emerging Infectious Diseases ◽

Reservoir Host ◽

Host Susceptibility ◽

Public Health Issue ◽

Severe Illness ◽

Host Diversity ◽

Transmission Pathways

Emerging infectious diseases present great risks to public health. The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), causing coronavirus disease 2019 (COVID-19), has become an urgent public health issue of global concern. It is speculated that the virus first emerged through a zoonotic spillover. Basic research studies have suggested that bats are likely the ancestral reservoir host. Nonetheless, the evolutionary history and host susceptibility of SARS-CoV-2 remains unclear as a multitude of animals has been proposed as potential intermediate or dead-end hosts. SARS-CoV-2 has been isolated from domestic animals, both companion and livestock, as well as in captive wildlife that were in close contact with human COVID-19 cases. Currently, domestic mink is the only known animal that is susceptible to a natural infection, develop severe illness, and can also transmit SARS-CoV-2 to other minks and humans. To improve foundational knowledge of SARS-CoV-2, we are conducting a synthesis review of its host diversity and transmission pathways. To mitigate this COVID-19 pandemic, we strongly advocate for a systems-oriented scientific approach that comprehensively evaluates the transmission of SARS-CoV-2 at the human and animal interface.

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MicroRNA319a regulates plant resistance to Sclerotinia stem rot

Journal of Experimental Botany ◽

10.1093/jxb/erab070 ◽

2021 ◽

Author(s):

Weiguo Dong ◽

Wenqing Ren ◽

Xuan Wang ◽

He Yuke

Keyword(s):

Plant Resistance ◽

Host Susceptibility ◽

Stem Rot ◽

Sclerotinia Stem Rot ◽

Sequencing Data ◽

Mobility Shift ◽

Expression Levels ◽

Affected Plant ◽

Mobility Shift Assay ◽

Rot Disease

Abstract MicroRNA319a (miR319a) controls cell division arrest in plant leaves by inhibiting the expression of TCP (TEOSINTE BRANCHED 1/CYCLOIDEA/PCF) family genes. However, it is unclear whether miR319a influences infections by necrotrophic pathogens and host susceptibility. In this study, we revealed that miR319a affected plant resistance to stem rot disease of Sclerotinia sclerotiorum. In the plants of Brassica rapa infected with S. sclerotiorum, miR319a levels increased while expression levels of several BraTCP genes significantly decreased compared with those of the uninfected plants. The overexpression of BraMIR319a in B. rapa increased the susceptibility of the plants to S. sclerotiorum and aggravated stem rot disease, whereas the overexpression of BraTCP4-1 promoted the plant resistance. Our RNA-sequencing data revealed a potential relationship between miR319a and pathogen-related WRKY genes. Chromatin immunoprecipitation (ChIP) assay, electrophoretic mobility shift assay (EMSA) and reporter transaction assay showed that BraTCP4-1 was bound to the promoters of WRKY75, WRKY70, and WRKY33 genes and directly activated these pathogen-related genes. Moreover, the expression levels of WRKY75, WRKY70, and WRKY33 in the plants overexpressing BraMIR319a declined significantly whereas those of the plants overexpressing BraTCP4-1 increased significantly. These results suggest that miR319a and its targeted gene BraTCP4 regulate stem rot resistance through pathways of WRKY genes.

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Antiparasitic potential of alternative treatments against larval stages of Lernaea cyprinacea

Journal of Parasitic Diseases ◽

10.1007/s12639-021-01400-2 ◽

2021 ◽

Author(s):

William Eduardo Furtado ◽

Lucas Cardoso ◽

Paula Brando de Medeiros ◽

Nicollas Breda Lehmann ◽

Elisabeth de Aguiar Bertaglia ◽

...

Keyword(s):

Alternative Treatments ◽

Larval Stages ◽

Lernaea Cyprinacea

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Mycobacterium tuberculosis Infection Up-Regulates Sialyl Lewis X Expression in the Lung Epithelium

Microorganisms ◽

10.3390/microorganisms9010099 ◽

2021 ◽

Vol 9 (1) ◽

pp. 99

Author(s):

Rita Matos ◽

Kaori L. Fonseca ◽

Stefan Mereiter ◽

Ana Raquel Maceiras ◽

Joana Gomes ◽

...

Keyword(s):

Mycobacterium Tuberculosis ◽

Biosynthetic Pathway ◽

Molecular Mechanisms ◽

Tuberculosis Infection ◽

Host Susceptibility ◽

Sialyl Lewis X ◽

Lung Pathology ◽

Lung Epithelium ◽

Lewis X ◽

Sialyl Lewis

Glycans display increasingly recognized roles in pathological contexts, however, their impact in the host-pathogen interplay in many infectious diseases remains largely unknown. This is the case for tuberculosis (TB), one of the ten most fatal diseases worldwide, caused by infection of the bacteria Mycobacterium tuberculosis. We have recently reported that perturbing the core-2 O-glycans biosynthetic pathway increases the host susceptibility to M. tuberculosis infection, by disrupting the neutrophil homeostasis and enhancing lung pathology. In the present study, we show an increased expression of the sialylated glycan structure Sialyl-Lewis X (SLeX) in the lung epithelium upon M. tuberculosis infection. This increase in SLeX glycan epitope is accompanied by an altered lung tissue transcriptomic signature, with up-regulation of genes codifying enzymes that are involved in the SLeX core-2 O-glycans biosynthetic pathway. This study provides novel insights into previously unappreciated molecular mechanisms involving glycosylation, which modulate the host response to M. tuberculosis infection, possibly contributing to shape TB disease outcome.

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Glochidial infection by the endangered Margaritifera margaritifera (Mollusca) increased survival of salmonid host (Pisces) during experimental Flavobacterium disease outbreak

Parasitology Research ◽

10.1007/s00436-021-07285-7 ◽

2021 ◽

Author(s):

M. Motiur R. Chowdhury ◽

Amitav Roy ◽

Kalle Auvinen ◽

Katja Pulkkinen ◽

Hanna Suonia ◽

...

Keyword(s):

Post Infection ◽

Current Knowledge ◽

Virulent Strain ◽

Freshwater Mussels ◽

Attachment Site ◽

Disease Outbreak ◽

Host Susceptibility ◽

Control Fish ◽

Margaritifera Margaritifera ◽

Past Infection

AbstractCo-infections are common in host-parasite interactions, but studies about their impact on the virulence of parasites/diseases are still scarce. The present study compared mortality induced by a fatal bacterial pathogen, Flavobacterium columnare between brown trout infected with glochidia from the endangered freshwater pearl mussel, Margaritifera margaritifera, and uninfected control fish during the parasitic period and after the parasitic period (i.e. glochidia detached) in a laboratory experiment. We hypothesised that glochidial infection would increase host susceptibility to and/or pathogenicity of the bacterial infection. We found that the highly virulent strain of F. columnare caused an intense disease outbreak, with mortality reaching 100% within 29 h. Opposite to the study hypothesis, both fresh ongoing and past infection (14 months post-infection) with glochidia prolonged the fish host’s survival statistically significantly by 1 h compared to the control fish (two-way ANOVA: fresh-infection, F1, 82 = 7.144, p = 0.009 and post-infection, F1, 51 = 4.227, p = 0.044). Furthermore, fish survival time increased with glochidia abundance (MLR: post-infection, t = 2.103, p = 0.045). The mechanism could be connected to an enhanced non-specific immunity or changed gill structure of the fish, as F. columnare enters the fish body mainly via the gills, which is also the glochidia’s attachment site. The results increase current knowledge about the interactions between freshwater mussels and their (commercially important) fish hosts and fish pathogens and also emphasise the importance of (unknown) ecosystem services (e.g., protection against pathogens) potentially associated with imperilled freshwater mussels.

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Monitoring and treatment of MDS in genetically susceptible persons

Hematology ◽

10.1182/hematology.2019000020 ◽

2019 ◽

Vol 2019 (1) ◽

pp. 105-109 ◽

Cited By ~ 1

Author(s):

Stella M. Davies

Keyword(s):

Bone Marrow ◽

Dna Damage ◽

Bone Marrow Failure ◽

Treatment Strategies ◽

Informed Choice ◽

Dyskeratosis Congenita ◽

Careful Consideration ◽

Host Susceptibility ◽

Bone Marrow Failure Syndromes ◽

Severe Infections

Abstract Genetic susceptibility to myelodysplastic syndrome (MDS) occurs in children with inherited bone marrow failure syndromes, including Fanconi anemia, Shwachman Diamond syndrome, and dyskeratosis congenita. Available evidence (although not perfect) supports annual surveillance of the blood count and bone marrow in affected persons. Optimal treatment of MDS in these persons is most commonly transplantation. Careful consideration must be given to host susceptibility to DNA damage when selecting a transplant strategy, because significant dose reductions and avoidance of radiation are necessary. Transplantation before evolution to acute myeloid leukemia (AML) is optimal, because outcomes of AML are extremely poor. Children and adults can present with germline mutations in GATA2 and RUNX1, both of which are associated with a 30% to 40% chance of evolution to MDS. GATA2 deficiency may be associated with a clinically important degree of immune suppression, which can cause severe infections that can complicate transplant strategies. GATA2 and RUNX1 deficiency is not associated with host susceptibility to DNA damage, and therefore, conventional treatment strategies for MDS and AML can be used. RUNX1 deficiency has a highly variable phenotype, and MDS can occur in childhood and later in adulthood within the same families, making annual surveillance with marrow examination burdensome; however, such strategies should be discussed with affected persons, allowing an informed choice.

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