Toxic strains of E.coli - poisoning from infected food

Pojam 'trovanje hranom' obuhvaća sva oboljenja koja nastaju uzimanjem nezdrave, pokvarene ili otrovne hrane. U većini slučajeva nastaje uslijed zagađenja hrane različitim bakterijama. Jedna od bakterija koja živi u ljudskim crijevima je Esherichia coli (E. coli) i većina sojeva su bezopasni i ne izazivaju reakcije u tijelu uopće. Međutim neki sojevi E. coli mogu uzrokovati štetu, ako ih se unese u ljudsko tijelo, jer proizvode toksine i ti sojevi su patogeni. U ovom radu opisano je trovanje hranom uzrokovano sa E. coli, te svi toksični sojevima ove vrste bakterije. Osvrnut ću se na zadnji slučaj tovanja hranom koji se je dogodio u Njemačkoj 2011.godine i na soj 0104 E. coli. Na kraju ću još nešto reći o pojavi 'superbakterija' i uzroku njihove otpornosti na antibiotike.The term 'food poisoning' includes all diseases caused by taking unhealthy, rotten or poisonous food. In most cases, caused by food contamination with different bacteria. One of the bacteria that live in human intestines is Escherichia coli (E. coli) and most strains are harmless and do not cause reactions in the body in general. However, some strains of E. coli can cause damage if they are entered into the human body, because they produce toxins and these strains are pathogenic. In this work I will write about the food poisoning caused by E. coli, and all toxic strains of this bacterium. I will comment on the latest case of food poisoning that has occurred in Germany 2011 and about E. coli strain 0104. In the end I will still say something about the phenomenon 'superbacteria' and the cause of their resistance to antibiotics

Toxic strains of E.coli - poisoning from infected food

Pojam 'trovanje hranom' obuhvaća sva oboljenja koja nastaju uzimanjem nezdrave, pokvarene ili otrovne hrane. U većini slučajeva nastaje uslijed zagađenja hrane različitim bakterijama. Jedna od bakterija koja živi u ljudskim crijevima je Esherichia coli (E. coli) i većina sojeva su bezopasni i ne izazivaju reakcije u tijelu uopće. Međutim neki sojevi E. coli mogu uzrokovati štetu, ako ih se unese u ljudsko tijelo, jer proizvode toksine i ti sojevi su patogeni. U ovom radu opisano je trovanje hranom uzrokovano sa E. coli, te svi toksični sojevima ove vrste bakterije. Osvrnut ću se na zadnji slučaj tovanja hranom koji se je dogodio u Njemačkoj 2011.godine i na soj 0104 E. coli. Na kraju ću još nešto reći o pojavi 'superbakterija' i uzroku njihove otpornosti na antibiotike.The term 'food poisoning' includes all diseases caused by taking unhealthy, rotten or poisonous food. In most cases, caused by food contamination with different bacteria. One of the bacteria that live in human intestines is Escherichia coli (E. coli) and most strains are harmless and do not cause reactions in the body in general. However, some strains of E. coli can cause damage if they are entered into the human body, because they produce toxins and these strains are pathogenic. In this work I will write about the food poisoning caused by E. coli, and all toxic strains of this bacterium. I will comment on the latest case of food poisoning that has occurred in Germany 2011 and about E. coli strain 0104. In the end I will still say something about the phenomenon 'superbacteria' and the cause of their resistance to antibiotics

Sastav crijevne mikrobiote i čimbenici upale u bolesnika s upalnim bolestima crijeva [Gut microbiota composition and inflammatory markers in IBD patients]

Inflammatory bowel disease (IBD) is a chronic process in the gastrointestinal tract with increasing prevalence that consist of Crohn disease (CD) and ulcerative colitis (UC). The disease is associated with intestinal microbiota composition, immune status and food intake. In this study microbiota composition in intestinal biopsy samples and stool of newly diagnosed IBD patients and non-IBD individuals, as well as inflammatory status from the blood of each participant was investigated. Microbiota composition was determined by the next generation sequencing method while serum biomarkers were detected by specifically tagged antibodies. Results show that the changes in feces and colon microbiota are specific and significant for Crohn's disease (Proteobacteria, Actinobacteria phylum and Dialister genus) and ulcerative colitis (Turibacteraceae, Veillonellaceae, Oxalobacteraceae and Sphingomonadaceae families). These changes in microbiota composition induce activation of certain inflammatory proteins that play a major role in chronic inflammatory response. The most significant differences in a protein level are in CXCL10, IL-6, HGF and IL-17A between CD and control patients and differences observed in CDCP1, FI3L and IL-6 proteins between CD and UC patients. Results of this translational research on newly diagnosed patients could help in better stratification of patients and selection of more suitable therapeutic approaches in the treatment of inflammatory bowel disease

Bioreactor-Based Bone Tissue Engineering

The aim of this chapter is to describe the main issues of bone tissue engineering. Bone transplants are widely used in orthopedic, plastic and reconstructive surgery. Current technologies like autologous and allogenic transplantation have several disadvantages making them relatively unsatisfactory, like donor site morbidity, chronic pain, and immunogenicity and risk hazard from infectious disease. Therefore, regenerative orthopedics seeks to establish a successful protocol for the healing of severe bone damage using engineered bone grafts. The optimization of protocols for bone graft production using autologous mesenchymal stem cells loaded on appropriate scaffolds, exposed to osteogenic inducers and mechanical force in bioreactor, should be able to solve the current limitations in managing bone injuries. We discuss mesenchymal stem cells as the most suitable cell type for bone tissue engineering. They can be isolated from a variety of mesenchymal tissues and can differentiate into osteoblasts when given appropriate mechanical support and osteoinductive signal. Mechanical support can be provided by different cell scaffolds based on natural or synthetic biomaterials, as well as combined composite materials. Three-dimensional support is enabled by bioreactor systems providing several advantages as mechanical loading, homogeneous distribution of cells and adequate nutrients/waste exchange. We also discuss the variety of osteoinductive signals that can be applied in bone tissue engineering. The near future of bone healing and regeneration is closely related to advances in tissue engineering. The optimization of protocols of bone graft production using autologous mesenchymal stem cells loaded on appropriate scaffolds, exposed to osteogenic inducers and mechanical force in bioreactor, should be able to solve the current limitations in managing bone injuries

Stem cells in bone regeneration

Bone defects, including normal fracture healing as well as healing problems represent a global health problem. The need for better treatment of bone defects is one of the central issues of tissue engineering and regenerative medicine. Regenerative orthopedics has several approaches – activation of endogenous stem cells, stem cell therapy and tissue engineering. Development of new treatments is mainly focused on the tissue engineering strategies that include stem cells, bioactive signals and appropriate scaffold support. The aim of this review is to describe a variety of stem cells that have an ability to become bone cells and therefore are of central importance for bone tissue engineering. Several cell types have been proposed as starting material - embryonic stem cells, induced pluripotent stem cells and adult stem cells. Due to ethical and safety issues, embryonic and induced pluripotent stem cells may be more suitable for studying human development and tissue formation under diverse experimental conditions, and represent an excellent base for understanding human diseases and development of innovative therapeutic solutions. Among adult stem cells, mesenchymal stem cells are the most suitable for bone tissue engineering. They can be isolated from variety of mesenchymal tissues and can differentiate into osteoblasts when given appropriate mechanical support and osteoinductive signal. The near future of bone healing and regeneration is closely related to advances in tissue engineering. The optimization of protocols of bone graft production using autologous mesenchymal stem cells loaded on appropriate scaffolds, exposed to osteogenic inducers and mechanical force in bioreactor, should be able to solve the current limitations in managing bone injuries

Differential expression of the fractalkine chemokine receptor (CX3CR1) in human monocytes during differentiation

Circulating monocytes (Mos) may continuously repopulate macrophage (MAC) or dendritic cell (DC) populations to maintain homeostasis. MACs and DCs are specialized cells that play different and complementary immunological functions. Accordingly, they present distinct migratory properties. Specifically, whereas MACs largely remain in tissues, DCs are capable of migrating from peripheral tissues to lymphoid organs. The aim of this work was to analyze the expression of the fractalkine receptor (CX3CR1) during the monocytic differentiation process. Freshly isolated Mos express high levels of both CX3CR1 mRNA and protein. During the Mo differentiation process, CX3CR1 is downregulated in both DCs and MACs. However, MACs showed significantly higher CX3CR1 expression levels than did DC. We also observed an antagonistic CX3CR1 regulation by interferon (IFN)-γ and interleukin (IL)-4 during MAC activation through the classical and alternative MAC pathways, respectively. IFN-γ inhibited the loss of CX3CR1, but IL-4 induced it. Additionally, we demonstrated an association between CX3CR1 expression and apoptosis prevention by soluble fractalkine (sCX3CL1) in Mos, DCs and MACs. This is the first report demonstrating sequential and differential CX3CR1 modulation during Mo differentiation. Most importantly, we demonstrated a functional link between CX3CR1 expression and cell survival in the presence of sCX3CL1.Fil: Panek, Cecilia Analía. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Ramos, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Mejias, María Pilar. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Abrey Recalde, Maria Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Fernández Brando, Romina Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Gori, María Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Salamone, Gabriela Veronica. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Palermo, Marina Sandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentin

Shiga toxin-producing Escherichia coli O157: H7 shows an increased pathogenicity in mice after the passage through the gastrointestinal tract of the same host

Haemolytic uraemic syndrome (HUS) is a rare but life-threatening complication of Shiga toxin (Stx)-producing Escherichia coli (STEC) infections, characterized by acute renal failure, thrombocytopenia and haemolytic anaemia. Although the main infection route is the consumption of contaminated food or water, person-to-person transmission has been suggested in several situations. Moreover, epidemiological data indicate that the horizontal transmission of several pathogens, including STEC, among individuals of the same species requires significantly lower doses than those used in animal models infected with laboratory-cultured bacteria. Thus, the aim of this study was to evaluate whether the passage of a clinically isolated STEC strain through the gastrointestinal tract of mice affects its pathogenicity in mice. To test this, weaned mice were orally inoculated by gavage with either an E. coli O157: H7 isolate from an HUS patient, or the same strain recovered from stools after one or two successive passages through the gastrointestinal tract of the mice. We show that stool-recovered strains are able to induce a more generalized and persistent colonization than the parent strain. Furthermore, a 10 4-fold-reduced inoculum of the stool-recovered strains still causes gut colonization and mouse mortality, which are not observed with the parent strain. These results indicate an increased pathogenicity in stool-recovered strains that may be associated with an increased ability to colonize the mouse intestine.Fil: Fernández Brando, Romina Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Miliwebsky, Elizabeth. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”; Argentina. Dirección Nacional de Institutos de Investigación. Administración Nacional de Laboratorios e Institutos de Salud. Instituto Nacional de Enfermedades Infecciosas; ArgentinaFil: Mejias, María Pilar. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Baschkier, Ariela. Dirección Nacional de Institutos de Investigación. Administración Nacional de Laboratorios e Institutos de Salud. Instituto Nacional de Enfermedades Infecciosas; Argentina. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”; ArgentinaFil: Panek, Cecilia Analía. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Abrey Recalde, Maria Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Cabrera, Gabriel Gustavo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Ramos, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Rivas, Marta. Dirección Nacional de Institutos de Investigación. Administración Nacional de Laboratorios e Institutos de Salud. Instituto Nacional de Enfermedades Infecciosas; Argentina. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”; ArgentinaFil: Palermo, Marina Sandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentin

Functional Capacity of Shiga-Toxin Promoter Sequences in Eukaryotic Cells

Shiga toxins (Stx) are the main virulence factors in enterohemorrhagic Escherichia coli (EHEC) infections, causing diarrhea and hemolytic uremic syndrome (HUS). The genes encoding for Shiga toxin-2 (Stx2) are located in a bacteriophage. The toxin is formed by a single A subunit and five B subunits, each of which has its own promoter sequence. We have previously reported the expression of the B subunit within the eukaryotic environment, probably driven by their own promoter. The aim of this work was to evaluate the ability of the eukaryotic machinery to recognize stx2 sequences as eukaryotic-like promoters. Vero cells were transfected with a plasmid encoding Stx2 under its own promoter. The cytotoxic effect on these cells was similar to that observed upon incubation with purified Stx2. In addition, we showed that Stx2 expression in Stx2-insensitive BHK eukaryotic cells induced drastic morphological and cytoskeletal changes. In order to directly evaluate the capacity of the wild promoter sequences of the A and B subunits to drive protein expression in mammalian cells, GFP was cloned under eukaryotic-like putative promoter sequences. GFP expression was observed in 293T cells transfected with these constructions. These results show a novel and alternative way to synthesize Stx2 that could contribute to the global understanding of EHEC infections with immediate impact on the development of treatments or vaccines against HUSFil: Bentancor, Leticia Verónica. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Bilen, Marcos Fabian. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología. Laboratorio de Ingeniería Genética y Biología Molecular y Celular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Mejias, María Pilar. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Fernández Brando, Romina Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Panek, Cecilia Analía. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Ramos, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Fernández, Gabriela Cristina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Isturiz, Martín Amadeo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Ghiringhelli, Pablo Daniel. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología. Laboratorio de Ingeniería Genética y Biología Molecular y Celular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Palermo, Marina Sandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentin