Bacterial Invasion on Spontaneous Gingivitis in SUS Rats

AbstractThe variant virulent porcine epidemic diarrhea virus (PEDV) strain (YN15) can cause severe porcine epidemic diarrhea (PED); however, the attenuated vaccine-like PEDV strain (YN144) can induce immunity in piglets. To investigate the differences in pathogenesis and epigenetic mechanisms between the two strains, differential expression and correlation analyses of the microRNA (miRNA) and mRNA in swine testicular (ST) cells infected with YN15, YN144, and mock were performed on three comparison groups (YN15 vs Control, YN144 vs Control, and YN15 vs YN144). The mRNA and miRNA expression profiles were obtained using next-generation sequencing (NGS), and the differentially expressed (DE) (p-value < 0.05) mRNA and miRNA were obtained using DESeq R package. mRNAs targeted by DE miRNAs were predicted using the miRanda algortithm. 8039, 8631 and 3310 DE mRNAs, and 36, 36, and 22 DE miRNAs were identified in the three comparison groups, respectively. 14,140, 15,367 and 3771 DE miRNA–mRNA (targeted by DE miRNAs) interaction pairs with negatively correlated expression patterns were identified, and interaction networks were constructed using Cytoscape. Six DE miRNAs and six DE mRNAs were randomly selected to verify the sequencing data by real-time relative quantitative reverse transcription polymerase chain reaction (qRT-PCR). Based on bioinformatics analysis, we discovered the differences were mostly involved in host immune responses and viral pathogenicity, including NF-κB signaling pathway and bacterial invasion of epithelial cells, etc. This is the first comprehensive comparison of DE miRNA–mRNA pairs in YN15 and YN144 infection in vitro, which could provide novel strategies for the prevention and control of PED.

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The Gb3-enriched CD59/flotillin plasma membrane domain regulates host cell invasion by Pseudomonas aeruginosa

Cellular and Molecular Life Sciences ◽

10.1007/s00018-021-03766-1 ◽

2021 ◽

Author(s):

Annette Brandel ◽

Sahaja Aigal ◽

Simon Lagies ◽

Manuel Schlimpert ◽

Ana Valeria Meléndez ◽

...

Keyword(s):

Pseudomonas Aeruginosa ◽

Plasma Membrane ◽

Host Cell ◽

Acyl Chain ◽

Mass Spectrometry Analysis ◽

Bacterial Invasion ◽

Fatty Acyl Chain ◽

Membrane Domain ◽

Host Cell Membrane ◽

Plasma Membrane Domain

AbstractThe opportunistic pathogen Pseudomonas aeruginosa has gained precedence over the years due to its ability to develop resistance to existing antibiotics, thereby necessitating alternative strategies to understand and combat the bacterium. Our previous work identified the interaction between the bacterial lectin LecA and its host cell glycosphingolipid receptor globotriaosylceramide (Gb3) as a crucial step for the engulfment of P. aeruginosa via the lipid zipper mechanism. In this study, we define the LecA-associated host cell membrane domain by pull-down and mass spectrometry analysis. We unraveled a predilection of LecA for binding to saturated, long fatty acyl chain-containing Gb3 species in the extracellular membrane leaflet and an induction of dynamic phosphatidylinositol (3,4,5)-trisphosphate (PIP3) clusters at the intracellular leaflet co-localizing with sites of LecA binding. We found flotillins and the GPI-anchored protein CD59 not only to be an integral part of the LecA-interacting membrane domain, but also majorly influencing bacterial invasion as depletion of either of these host cell proteins resulted in about 50% reduced invasiveness of the P. aeruginosa strain PAO1. In summary, we report that the LecA-Gb3 interaction at the extracellular leaflet induces the formation of a plasma membrane domain enriched in saturated Gb3 species, CD59, PIP3 and flotillin thereby facilitating efficient uptake of PAO1.

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MicroRNA expression profile in bovine mammary gland parenchyma infected by coagulase-positive or coagulase-negative staphylococci

Veterinary Research ◽

10.1186/s13567-021-00912-2 ◽

2021 ◽

Vol 52 (1) ◽

Author(s):

Emilia Bagnicka ◽

Ewelina Kawecka-Grochocka ◽

Klaudia Pawlina-Tyszko ◽

Magdalena Zalewska ◽

Aleksandra Kapusta ◽

...

Keyword(s):

Mammary Gland ◽

Immune System ◽

Differentially Expressed ◽

Bacterial Invasion ◽

Coagulase Negative Staphylococci ◽

Cellular Processes ◽

Differentially Expressed Mirnas ◽

Non Coding Rnas ◽

Coagulase Positive Staphylococci ◽

Generation Sequencing

AbstractMicroRNAs (miRNAs) are short, non-coding RNAs, 21–23 nucleotides in length which are known to regulate biological processes that greatly impact immune system activity. The aim of the study was to compare the miRNA expression in non-infected (H) mammary gland parenchyma samples with that of glands infected with coagulase-positive staphylococci (CoPS) or coagulase-negative staphylococci (CoNS) using next-generation sequencing. The miRNA profile of the parenchyma was found to change during mastitis, with its profile depending on the type of pathogen. Comparing the CoPS and H groups, 256 known and 260 potentially new miRNAs were identified, including 32 that were differentially expressed (p ≤ 0.05), of which 27 were upregulated and 5 downregulated. Comparing the CoNS and H groups, 242 known and 171 new unique miRNAs were identified: 10 were upregulated (p ≤ 0.05), and 2 downregulated (p ≤ 0.05). In addition, comparing CoPS with H and CoNS with H, 5 Kyoto Encyclopedia of Genes and Genomes pathways were identified; in both comparisons, differentially-expressed miRNAs were associated with the bacterial invasion of epithelial cells and focal adhesion pathways. Four gene ontology terms were identified in each comparison, with 2 being common to both immune system processes and signal transduction. Our results indicate that miRNAs, especially miR-99 and miR-182, play an essential role in the epigenetic regulation of a range of cellular processes, including immunological systems bacterial growth in dendritic cells and disease pathogenesis (miR-99), DNA repair and tumor progression (miR-182).

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Identification of SopE2, a SalmonellaSecreted Protein Which Is Highly Homologous to SopE and Involved in Bacterial Invasion of Epithelial Cells

Journal of Bacteriology ◽

10.1128/jb.182.8.2341-2344.2000 ◽

2000 ◽

Vol 182 (8) ◽

pp. 2341-2344 ◽

Cited By ~ 116

Author(s):

C. S. Bakshi ◽

V. P. Singh ◽

M. W. Wood ◽

P. W. Jones ◽

T. S. Wallis ◽

...

Keyword(s):

Epithelial Cells ◽

Cellular Responses ◽

Eukaryotic Cells ◽

Bacterial Invasion ◽

Secreted Protein ◽

Temperate Bacteriophage ◽

Type Iii

ABSTRACT Type III secreted Sop protein effectors are delivered into target eukaryotic cells and elicit cellular responses underlyingSalmonella pathogenicity. In this work, we have identified another secreted protein, SopE2, and showed that SopE2 is an important invasion-associated effector. SopE2 is encoded by the sopE2gene which is present and conserved in pathogenic strains ofSalmonella. SopE2 is highly homologous to SopE, a protein encoded by a gene within a temperate bacteriophage and present in only some pathogenic strains.

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Human Lung Tissue Explants Reveal Novel Interactions during Legionella pneumophila Infections

Infection and Immunity ◽

10.1128/iai.00703-13 ◽

2013 ◽

Vol 82 (1) ◽

pp. 275-285 ◽

Cited By ~ 35

Author(s):

Jens Jäger ◽

Sebastian Marwitz ◽

Jana Tiefenau ◽

Janine Rasch ◽

Olga Shevchuk ◽

...

Keyword(s):

Lung Tissue ◽

Legionella Pneumophila ◽

Human Lung ◽

Transcriptional Response ◽

Human Infection ◽

Bacterial Invasion ◽

Human Lung Tissue ◽

Content Type ◽

Tissue Explants ◽

Legionnaires Disease

ABSTRACTHistological and clinical investigations describe late stages of Legionnaires' disease but cannot characterize early events of human infection. Cellular or rodent infection models lack the complexity of tissue or have nonhuman backgrounds. Therefore, we developed and applied a novel model forLegionella pneumophilainfection comprising living human lung tissue. We stimulated lung explants withL. pneumophilastrains and outer membrane vesicles (OMVs) to analyze tissue damage, bacterial replication, and localization as well as the transcriptional response of infected tissue. Interestingly, we found that extracellular adhesion ofL. pneumophilato the entire alveolar lining precedes bacterial invasion and replication in recruited macrophages. In contrast, OMVs predominantly bound to alveolar macrophages. Specific damage to septa and epithelia increased over 48 h and was stronger in wild-type-infected and OMV-treated samples than in samples infected with the replication-deficient, type IVB secretion-deficient DotA−strain. Transcriptome analysis of lung tissue explants revealed a differential regulation of 2,499 genes after infection. The transcriptional response included the upregulation of uteroglobin and the downregulation of the macrophage receptor with collagenous structure (MARCO). Immunohistochemistry confirmed the downregulation of MARCO at sites of pathogen-induced tissue destruction. Neither host factor has ever been described in the context ofL. pneumophilainfections. This work demonstrates that the tissue explant model reproduces realistic features of Legionnaires' disease and reveals new functions for bacterial OMVs during infection. Our model allows us to characterize early steps of human infection which otherwise are not feasible for investigations.

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Quantitative assessment of bacterial invasion of chronic ulcers

The American Journal of Surgery ◽

10.1016/0002-9610(83)90075-2 ◽

1983 ◽

Vol 145 (2) ◽

pp. 260-262 ◽

Cited By ~ 16

Author(s):

Monroe Schneider ◽

Carlos W. Vildozola ◽

Steven Brooks

Keyword(s):

Quantitative Assessment ◽

Bacterial Invasion ◽

Chronic Ulcers

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The role of gut-associated lymphoid tissues and mucosal defence

British Journal Of Nutrition ◽

10.1079/bjn20041356 ◽

2005 ◽

Vol 93 (S1) ◽

pp. S41-S48 ◽

Cited By ~ 169

Author(s):

Maria Luisa Forchielli ◽

W. Allan Walker

Keyword(s):

Immune System ◽

Breast Milk ◽

Gastrointestinal Disease ◽

Bacterial Colonization ◽

Adaptive Immune Response ◽

Atopic Disease ◽

Mucosal Immune System ◽

Bacterial Invasion ◽

Lymphoid Tissues ◽

Protective Function

The newborn infant leaves a germ-free intrauterine environment to enter a contaminated extrauterine world and must have adequate intestinal defences to prevent the expression of clinical gastrointestinal disease states. Although the intestinal mucosal immune system is fully developed after a full-term birth, the actual protective function of the gut requires the microbial stimulation of initial bacterial colonization. Breast milk contains prebiotic oligosaccharides, like inulin-type fructans, which are not digested in the small intestine but enter the colon as intact large carbohydrates that are then fermented by the resident bacteria to produce SCFA. The nature of this fermentation and the consequent pH of the intestinal contents dictate proliferation of specific resident bacteria. For example, breast milk-fed infants with prebiotics present in breast milk produce an increased proliferation of bifidobacteria and lactobacilli (probiotics), whereas formula-fed infants produce more enterococci and enterobacteria. Probiotics, stimulated by prebiotic fermentation, are important to the development and sustainment of intestinal defences. For example, probiotics can stimulate the synthesis and secretion of polymeric IgA, the antibody that coats and protects mucosal surfaces against harmful bacterial invasion. In addition, appropriate colonization with probiotics helps to produce a balanced T helper cell response (Th1 = Th2 = Th3/Tr1) and prevent an imbalance (Th1 > Th2 or Th2 > Th1) contributing in part to clinical disease (Th2 imbalance contributes to atopic disease and Th1 imbalance contributes to Crohn's disease andHelicobacter pylori-induced gastritis). Furthermore, a series of pattern recognition receptors, toll-like receptors on gut lymphoid and epithelial cells that interact with bacterial molecular patterns (e.g. endotoxin (lipopolysaccharide), flagellin, etc.), help modulate intestinal innate immunity and an appropriate adaptive immune response. Animal and clinical studies have shown that inulin-type fructans will stimulate an increase in probiotics (commensal bacteria) and these bacteria have been shown to modulate the development and persistence of appropriate mucosal immune responses. However, additional studies are needed to show that prebiotics can directly or indirectly stimulate intestinal host defences. If this can be demonstrated, then prebiotics can be used as a dietary supplement to stimulate a balanced and an appropriately effective mucosal immune system in newborns and infants.

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