VP32.03: The impact of bacterial infection on the fetoplacental complex state

Active development of the territories of Siberia and the Far East requires the use of materials that are able to work under the combined influence of low temperatures and a complex state. When operating equipment parts at low temperatures, it is necessary to take into account the impact of static and dynamic loads, as well as the influence of an external aggressive environment. The paper studies corrosion-resistant cold-resistant metastable austenitic steels, which are widely used for manufacturing parts of low-temperature equipment. Tests were performed to assess the strength and ductility characteristics of smooth samples and samples with annular notches for static stretching in the temperature range from 293 to 77 K.

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The impact of RAGE inhibition in animal models of bacterial sepsis: a systematic review and meta-analysis

Journal of International Medical Research ◽

10.1177/0300060517713856 ◽

2017 ◽

Vol 46 (1) ◽

pp. 11-21 ◽

Cited By ~ 4

Author(s):

Xin Zhao ◽

Yan-nian Liao ◽

Qian Huang

Keyword(s):

Animal Models ◽

Bacterial Infection ◽

Meta Analysis ◽

Survival Rates ◽

Bacterial Sepsis ◽

Glycation End Products ◽

Cytokine Levels ◽

Beneficial Impact ◽

The Impact ◽

Bacterial Outgrowth

Objective To evaluate the impact of inhibition of the receptor for advanced glycation end products (RAGE) on the outcome of bacterial sepsis in animal models. Methods Relevant publications were identified by systematic searches of PubMed, ISI Web of Science and Elsevier-Scopus databases. Results A total of Eleven studies with moderate quality were selected for analysis. A meta-analysis of survival rates revealed a significant advantage of RAGE inhibition in comparison with controls (HR 0.67, 95% CI 0.52–0.86). This effect was most pronounced in polymicrobial infection (HR 0.28, 95% CI 0.14–0.55), followed by Gram positive (G+) bacterial infection (HR 0.70, 95% CI 0.50–0.97) and Gram negative (G−) bacterial infection (HR 0.89, 95% CI 0.58–1.38). For G+ bacterial infection, RAGE inhibition decreased bacterial outgrowth and dissemination, inflammatory cell influx, plasma cytokine levels, and pulmonary injury. Conclusions RAGE inhibition appears to have a beneficial impact on the outcome of sepsis in animal models, although there are discrepancies between different types of infection.

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Lipopolysaccharide administration alters extracellular vesicles in human lung-cancer cells and mice

10.1101/2020.04.17.046367 ◽

2020 ◽

Author(s):

Leandra B. Jones ◽

Sanjay Kumar ◽

Courtnee’ R. Bell ◽

Brennetta J. Crenshaw ◽

Mamie T. Coats ◽

...

Keyword(s):

Membrane Protein ◽

Bacterial Infection ◽

Cell Line ◽

Extracellular Vesicles ◽

A549 Cells ◽

Human Lung Cancer ◽

Diagnostic Tools ◽

The Impact

AbstractExtracellular vesicles (EVs) play a fundamental role in cell and infection biology and have the potential to act as biomarkers for novel diagnostic tools. In this study, we explored the in vitro impact of bacterial lipopolysaccharide administration on a cell line that represents a target for bacterial infection in the host. Administration of lipopolysaccharide at varying concentrations to this A549 cell line caused only modest changes in cell death, but EV numbers were significantly changed. After treatment with the highest concentration of lipopolysaccharide, EVs derived from A549 cells packaged significantly less interleukin-6 and lysosomal-associated membrane protein 1. We also examined the impact of lipopolysaccharide administration on exosome biogenesis and cargo composition in BALB/c mice. Serum-isolated EVs from lipopolysaccharide-treated mice showed significantly increased lysosomal-associated membrane protein 1 and toll-like receptor 4 levels compared with EVs from control mice. In summary, this study demonstrated that EV numbers and cargo were altered using these in vitro and in vivo models of bacterial infection.

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Approach to Neonates and Young Infants with Fever without a Source Who Are at Risk for Severe Bacterial Infection

Mediators of Inflammation ◽

10.1155/2018/4869329 ◽

2018 ◽

Vol 2018 ◽

pp. 1-11 ◽

Cited By ~ 5

Author(s):

Susanna Esposito ◽

Victoria Elisa Rinaldi ◽

Alberto Argentiero ◽

Edoardo Farinelli ◽

Marta Cofini ◽

...

Keyword(s):

At Risk ◽

Bacterial Infection ◽

Bacterial Infections ◽

Laboratory Data ◽

Unknown Origin ◽

Clinical Findings ◽

Reactive Protein ◽

Young Infants ◽

High Risk Infants ◽

The Impact

Introduction. Among neonates and infants <3 months of age with fever without a source (FWS), 5% to 15% of cases are patients with fever caused by a serious bacterial infection (SBI). To favour the differentiation between low- and high-risk infants, several algorithms based on analytical and clinical parameters have been developed. The aim of this review is to describe the management of young infants with FWS and to discuss the impact of recent knowledge regarding FWS management on clinical practice. Materials and Methods. PubMed was used to search for all of the studies published over the last 35 years using the keywords: “fever without source” or “fever of unknown origin” or “meningitis” or “sepsis” or “urinary tract infection” and “neonate” or “newborn” or “infant <90 days of life” or “infant <3 months”. Results and Discussion. The selection of neonates and young infants who are <3 months old with FWS who are at risk for SBI remains a problem without a definitive solution. The old Rochester criteria remain effective for identifying young infants between 29 and 60 days old who do not have severe bacterial infections (SBIs). However, the addition of laboratory tests such as C-reactive protein (CRP) and procalcitonin (PCT) can significantly improve the identification of children with SBI. The approach in evaluating neonates is significantly more complicated, as their risk of SBIs, including bacteremia and meningitis, remains relevant and none of the suggested approaches can reduce the risk of dramatic mistakes. In both groups, the best antibiotic must be carefully selected considering the clinical findings, the laboratory data, the changing epidemiology, and increasing antibiotic resistance of the most common infectious bacteria.

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The impact of bacterial infection on mast cell degranulation

Immunologic Research ◽

10.1007/s12026-011-8250-x ◽

2011 ◽

Vol 51 (2-3) ◽

pp. 215-226 ◽

Cited By ~ 20

Author(s):

Jordan Wesolowski ◽

Fabienne Paumet

Keyword(s):

Mast Cell ◽

Bacterial Infection ◽

Mast Cell Degranulation ◽

The Impact

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The Innate Immune System Favors Emergency Monopoiesis at the Expense of DC Differentiation to Control Bacterial Infections

Blood ◽

10.1182/blood.v124.21.2722.2722 ◽

2014 ◽

Vol 124 (21) ◽

pp. 2722-2722

Author(s):

Kristin Bieber ◽

Karina A. Pasquevich ◽

Manina Günter ◽

Matthias Grauer ◽

Oliver Pötz ◽

...

Keyword(s):

Immune System ◽

Bacterial Infection ◽

Bacterial Infections ◽

Conflicts Of Interest ◽

Bacterial Load ◽

Innate Immune ◽

General Response ◽

The Impact ◽

Myeloid Progenitors

Abstract Dendritic cells (DCs) are critical in host defense against infection, bridging the innate and adaptive immune system. Patients with sepsis display reduced circulating and splenic DCs and impaired DC function that may contribute to prolonged immune suppression and exacerbation of infection. However, the mechanisms of pathogen-induced DC depletion remain poorly understood. Here, a mouse model of systemic bacterial infection was employed to analyze the impact of different bacterial pathogens on DC development in vivo. We found that the numbers of bone marrow (BM) hematopoietic progenitors committed to the DC lineages were reduced following systemic infection with different Gram-positive and Gram-negative bacteria. In parallel, a TLR4-dependent increase of committed monocyte progenitors in the BM as well as mature monocytes in the spleen was observed. In line, adoptively transferred FLT3+ myeloid progenitors (MPs) developed preferentially to monocytes at the expense of DCs in infected animals. Analyses performed on mixed BM chimeras suggested that both the reduction of DC progenitors and the induction of monopoiesis following infection were dependent on extrinsic TLR4 signaling driving the secretion of IFN-g regulated chemokines. Consistently, these effects were completely abrogated by suppression of IFN-g signaling. Elevated monocyte numbers in the spleen triggered by infection were due to a CCR2-dependent egress from the BM. In CCR2-deficient mice, in which monocytosis reportedly is abrogated, we observed a significantly increased bacterial load in the spleen and a reduced survival rate, highlighting the importance of monocytes for bacterial clearance. Together, our data provide evidence for a general response of myeloid progenitors upon bacterial infection to enhance monocyte production, thereby increasing the availability of innate immune cells as a first line of defense against invading pathogens. Concomitantly the development of DCs is impaired, which may be responsible for transient immunosuppression in e.g. bacterial sepsis. Disclosures No relevant conflicts of interest to declare.

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The impact of antibiotics on the metabolic status of obese adults without bacterial infection: a systematic review and meta-analysis

Annals of Translational Medicine ◽

10.21037/atm-20-1007a ◽

2020 ◽

Vol 8 (17) ◽

pp. 1059-1059

Author(s):

Naofumi Yoshida ◽

Yoshihiro Saito ◽

Yasushi Tsujimoto ◽

Shunsuke Taito ◽

Masahiro Banno ◽

...

Keyword(s):

Systematic Review ◽

Bacterial Infection ◽

Meta Analysis ◽

Metabolic Status ◽

Obese Adults ◽

The Impact

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The Intestinal Microbiota Interferes with the microRNA Response upon Oral Listeria Infection

mBio ◽

10.1128/mbio.00707-13 ◽

2013 ◽

Vol 4 (6) ◽

Cited By ~ 51

Author(s):

Cristel Archambaud ◽

Odile Sismeiro ◽

Joern Toedling ◽

Guillaume Soubigou ◽

Christophe Bécavin ◽

...

Keyword(s):

Bacterial Infection ◽

Intestinal Microbiota ◽

Mirna Expression ◽

Target Genes ◽

Host Protein ◽

Protein Coding ◽

Content Type ◽

Protein Coding Genes ◽

The Impact

ABSTRACT The intestinal tract is the largest reservoir of microbes in the human body. The intestinal microbiota is thought to be able to modulate alterations of the gut induced by enteropathogens, thereby maintaining homeostasis. Listeria monocytogenes is the agent of listeriosis, an infection transmitted to humans upon ingestion of contaminated food. Crossing of the intestinal barrier is a critical step of the infection before dissemination into deeper organs. Here, we investigated the role of the intestinal microbiota in the regulation of host protein-coding genes and microRNA (miRNA or miR) expression during Listeria infection. We first established the intestinal miRNA signatures corresponding to the 10 most highly expressed miRNAs in the murine ileum of conventional and germfree mice, noninfected and infected with Listeria. Next, we identified 6 miRNAs whose expression decreased upon Listeria infection in conventional mice. Strikingly, five of these miRNA expression variations (in miR-143, miR-148a, miR-200b, miR-200c, and miR-378) were dependent on the presence of the microbiota. In addition, as is already known, protein-coding genes were highly affected by infection in both conventional and germfree mice. By crossing bioinformatically the predicted targets of the miRNAs to our whole-genome transcriptomic data, we revealed an miRNA-mRNA network that suggested miRNA-mediated global regulation during intestinal infection. Other recent studies have revealed an miRNA response to either bacterial pathogens or commensal bacteria. In contrast, our work provides an unprecedented insight into the impact of the intestinal microbiota on host transcriptional reprogramming during infection by a human pathogen. IMPORTANCE While the crucial role of miRNAs in regulating the host response to bacterial infection is increasingly recognized, the involvement of the intestinal microbiota in the regulation of miRNA expression has not been explored in detail. Here, we investigated the impact of the intestinal microbiota on the regulation of protein-coding genes and miRNA expression in a host infected by L. monocytogenes, a food-borne pathogen. We show that the microbiota interferes with the microRNA response upon oral Listeria infection and identify several protein-coding target genes whose expression correlates inversely with that of the miRNA. Further investigations of the regulatory networks involving miR-143, miR-148a, miR-200b, miR-200c, and miR-378 will provide new insights into the impact of the intestinal microbiota on the host upon bacterial infection.

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Prevention of the fetoplacental complex disorders in women at risk and the risk of preterm birth (Literature review)

Reproductive health of woman ◽

10.30841/2708-8731.2.2021.232522 ◽

2021 ◽

Vol 2 ◽

pp. 32-36

Author(s):

O.V. Laba

Keyword(s):

Preterm Birth ◽

Pregnant Women ◽

Placental Abruption ◽

Reproductive Potential ◽

Fetal Distress ◽

Smoking During Pregnancy ◽

Complex Disorders ◽

Placental Dysfunction ◽

Fetoplacental Complex ◽

The Impact

The obstetrician-gynaecologist practitioners consider a woman’s health from her reproductive potential support standpoint, and the problem of miscarriage is considered as one of the most important health problems in the world. The difficulty in solving the premature birth problem is the presence of many factors and preconditions that determine the risks of miscarriage. The article provides an overview of current international guidelines for assessing the root causes and preconditions for preterm birth. The problem of preterm birth risks is discussed, taking into account both the socio-economic living conditions of pregnant women and the factors that accompany the formation of the pathogenesis of preterm birth (placental dysfunction). There were examination and evaluation of the clinical significance of the factors that can lead to dysfunction of the fetoplacental complex (partial placental abruption, low placentation, placental dysfunction, premature placental maturation, placental malnutrition/hypertrophy, polyhydramnios/dehydration, placental abruption syndrome and growth retardation syndrome, fetal-placental blood flow, acute/chronic fetal distress). It was noted that hemodynamic disorders in the placenta depend on both the nature and duration of adverse factors. Those factors are pregnancy in unfavourable terms for the birth of children (up to 18 and after 40 years), high frequency of extragenital pathology, complicated reproductive history, genital infectious diseases (chlamydial infections, trichomoniasis, urogenital mycoplasmosis), smoking during pregnancy, the impact of environmental and economical character.Attention is paid to the hemodynamic disorders assessment (vascularization of the lower uterus) in pregnant women and determination of their role in the fetoplacental dysfunction development. The role of the hemodynamic disorders in the placenta is considered as the morphological and biochemical adaptive reactions abnormality.

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Peptidoglycan sensing by octopaminergic neurons modulates Drosophila oviposition

eLife ◽

10.7554/elife.21937 ◽

2017 ◽

Vol 6 ◽

Cited By ~ 26

Author(s):

C Leopold Kurz ◽

Bernard Charroux ◽

Delphine Chaduli ◽

Annelise Viallat-Lieutaud ◽

Julien Royet

Keyword(s):

Immune Response ◽

Bacterial Infection ◽

Immune Cells ◽

Behavioral Change ◽

Behavioral Response ◽

Molecular Mechanisms ◽

Egg Laying ◽

Signaling Cascade ◽

Host Behavior ◽

The Impact

As infectious diseases pose a threat to host integrity, eukaryotes have evolved mechanisms to eliminate pathogens. In addition to develop strategies reducing infection, animals can engage in behaviors that lower the impact of the infection. The molecular mechanisms by which microbes impact host behavior are not well understood. We demonstrate that bacterial infection of Drosophila females reduces oviposition and that peptidoglycan, the component that activates Drosophila antibacterial response, is also the elicitor of this behavioral change. We show that peptidoglycan regulates egg-laying rate by activating NF-κB signaling pathway in octopaminergic neurons and that, a dedicated peptidoglycan degrading enzyme acts in these neurons to buffer this behavioral response. This study shows that a unique ligand and signaling cascade are used in immune cells to mount an immune response and in neurons to control fly behavior following infection. This may represent a case of behavioral immunity.

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