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Bibliografías temáticas / Bacterial diseases Interlukins. Bacterial Infections Neutrophil Activation

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Literatura académica sobre el tema "Bacterial diseases Interlukins. Bacterial Infections Neutrophil Activation"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 7 de febrero de 2022

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Artículos de revistas sobre el tema "Bacterial diseases Interlukins. Bacterial Infections Neutrophil Activation"

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Cuypers, Fabian, Björn Klabunde, Manuela Gesell Salazar, et al. "Adenosine Triphosphate Neutralizes Pneumolysin-Induced Neutrophil Activation." Journal of Infectious Diseases 222, no. 10 (2020): 1702–12. http://dx.doi.org/10.1093/infdis/jiaa277.

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Abstract Background In tissue infections, adenosine triphosphate (ATP) is released into extracellular space and contributes to purinergic chemotaxis. Neutrophils are important players in bacterial clearance and are recruited to the site of tissue infections. Pneumococcal infections can lead to uncontrolled hyperinflammation of the tissue along with substantial tissue damage through excessive neutrophil activation and uncontrolled granule release. We aimed to investigate the role of ATP in neutrophil response to pneumococcal infections. Methods Primary human neutrophils were exposed to the pneu

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2

Fontoura, Marina Alves, Rebeca Fróes Rocha, and Rafael Elias Marques. "Neutrophil Recruitment and Participation in Severe Diseases Caused by Flavivirus Infection." Life 11, no. 7 (2021): 717. http://dx.doi.org/10.3390/life11070717.

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Neutrophils are first-line responders to infections and are recruited to target tissues through the action of chemoattractant molecules, such as chemokines. Neutrophils are crucial for the control of bacterial and fungal infections, but their role in the context of viral infections has been understudied. Flaviviruses are important human viral pathogens transmitted by arthropods. Infection with a flavivirus may result in a variety of complex disease manifestations, including hemorrhagic fever, encephalitis or congenital malformations. Our understanding of flaviviral diseases is incomplete, and

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Al Moussawi, Khatoun, та Barbara I. Kazmierczak. "Distinct Contributions of Interleukin-1α (IL-1α) and IL-1β to Innate Immune Recognition of Pseudomonas aeruginosa in the Lung". Infection and Immunity 82, № 10 (2014): 4204–11. http://dx.doi.org/10.1128/iai.02218-14.

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ABSTRACTThe bacterial pathogenPseudomonas aeruginosacauses acute infections associated with significant morbidity and mortality.P. aeruginosaelicits strong innate immune responses in immunocompetent hosts, and the resulting recruitment of neutrophils to the site of infection is necessary for bacterial clearance.P. aeruginosalipopolysaccharide and flagellin are recognized by extracellular Toll-like receptors, but the most rapid responses to infection occur when cytosolic receptors sense flagellin or type 3 secretion system (T3SS) structural proteins. The subsequent activation of the NLRC4 infla

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Leid, Jeff G., Mathias Kerr, Candice Selgado, et al. "Flagellum-Mediated Biofilm Defense Mechanisms of Pseudomonas aeruginosa against Host-Derived Lactoferrin." Infection and Immunity 77, no. 10 (2009): 4559–66. http://dx.doi.org/10.1128/iai.00075-09.

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ABSTRACT Chronic infection with the gram-negative organism Pseudomonas aeruginosa is a leading cause of morbidity and mortality in human patients, despite high doses of antibiotics used to treat the various diseases this organism causes. These infections are chronic because P. aeruginosa readily forms biofilms, which are inherently resistant to antibiotics as well as the host's immune system. Our laboratory has been investigating specific mutations in P. aeruginosa that regulate biofilm bacterial susceptibility to the host. To continue our investigation of the role of genetics in bacterial bio

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5

Marin-Esteban, Viviana, Isabelle Turbica, Guillaume Dufour, et al. "Afa/Dr Diffusely Adhering Escherichia coli Strain C1845 Induces Neutrophil Extracellular Traps That Kill Bacteria and Damage Human Enterocyte-Like Cells." Infection and Immunity 80, no. 5 (2012): 1891–99. http://dx.doi.org/10.1128/iai.00050-12.

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ABSTRACTWe recently documented the neutrophil response to enterovirulent diffusely adherentEscherichia coliexpressing Afa/Dr fimbriae (Afa/Dr DAEC), using the human myeloid cell line PLB-985 differentiated into fully mature neutrophils. Upon activation, particularly during infections, neutrophils release neutrophil extracellular traps (NETs), composed of a nuclear DNA backbone associated with antimicrobial peptides, histones, and proteases, which entrap and kill pathogens. Here, using fluorescence microscopy and field emission scanning electron microscopy, we observed NET production by PLB-985

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Didierlaurent, Arnaud, John Goulding, Seema Patel, et al. "Sustained desensitization to bacterial Toll-like receptor ligands after resolutionof respiratory influenza infection." Journal of Experimental Medicine 205, no. 2 (2008): 323–29. http://dx.doi.org/10.1084/jem.20070891.

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The World Health Organization estimates that lower respiratory tract infections (excluding tuberculosis) account for ∼35% of all deaths caused by infectious diseases. In many cases, the cause of death may be caused by multiple pathogens, e.g., the life-threatening bacterial pneumonia observed in patients infected with influenza virus. The ability to evolve more efficient immunity on each successive encounter with antigen is the hallmark of the adaptive immune response. However, in the absence of cross-reactive T and B cell epitopes, one lung infection can modify immunity and pathology to the n

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7

Singel, Kelly L., and Brahm H. Segal. "NOX2-dependent regulation of inflammation." Clinical Science 130, no. 7 (2016): 479–90. http://dx.doi.org/10.1042/cs20150660.

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NADPH oxidase (NOX) isoforms together have multiple functions that are important for normal physiology and have been implicated in the pathogenesis of a broad range of diseases, including atherosclerosis, cancer and neurodegenerative diseases. The phagocyte NADPH oxidase (NOX2) is critical for antimicrobial host defence. Chronic granulomatous disease (CGD) is an inherited disorder of NOX2 characterized by severe life-threatening bacterial and fungal infections and by excessive inflammation, including Crohn's-like inflammatory bowel disease (IBD). NOX2 defends against microbes through the direc

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Lee, Sang-C., Seong-A. Ju, Ha-N. Pack, et al. "4-1BB (CD137) Is Required for Rapid Clearance of Listeria monocytogenes Infection." Infection and Immunity 73, no. 8 (2005): 5144–51. http://dx.doi.org/10.1128/iai.73.8.5144-5151.2005.

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ABSTRACT 4-1BB (CD137), a member of the tumor necrosis factor receptor superfamily, is a T-cell-costimulatory receptor that is expressed on activated T cells, dendritic cells, and NK cells. Little has been reported about its role in early host defense against bacterial infection. In this study, we report that 4-1BB-deficient (4-1BB−/−) mice are much more susceptible to Listeria monocytogenes (intracellular bacteria) infections than wild-type mice. Upon L. monocytogenes infection, 4-1BB−/− mice showed a lower survival rate, a higher bacterial burden in organs, and larger hepatic microabscesses

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Zurita, E., G. Moreno, A. Errea, M. Ormazabal, M. Rumbo, and D. Hozbor. "The Stimulated Innate Resistance Event in Bordetella pertussis Infection Is Dependent on Reactive Oxygen Species Production." Infection and Immunity 81, no. 7 (2013): 2371–78. http://dx.doi.org/10.1128/iai.00336-13.

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ABSTRACTThe exacerbated induction of innate immune responses in airways can abrogate diverse lung infections by a phenomenon known as stimulated innate resistance (StIR). We recently demonstrated that the enhancement of innate response activation can efficiently impairBordetella pertussiscolonization in a Toll-like receptor 4 (TLR4)-dependent manner. The aim of this work was to further characterize the effect of lipopolysaccharide (LPS) on StIR and to identify the mechanisms that mediate this process. Our results showed that bacterial infection was completely abrogated in treated mice when the

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Teske, Sabine, Andrea A. Bohn, Jean F. Regal, Joshua J. Neumiller, and B. Paige Lawrence. "Activation of the aryl hydrocarbon receptor increases pulmonary neutrophilia and diminishes host resistance to influenza A virus." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 1 (2005): L111—L124. http://dx.doi.org/10.1152/ajplung.00318.2004.

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Unlike their role in bacterial infection, less is known about the role of neutrophils during pulmonary viral infection. Exposure to pollutant 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD, dioxin) results in excess neutrophils in the lungs of mice infected with influenza A virus. TCDD is the most potent agonist for the aryl hydrocarbon receptor (AhR), and exposure to AhR ligands has been correlated with exacerbated inflammatory lung diseases. However, knowledge of the effects of AhR agonists on neutrophils is limited. Likewise, the factors regulating neutrophil responses during respiratory viral

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Tesis sobre el tema "Bacterial diseases Interlukins. Bacterial Infections Neutrophil Activation"

1

Caver, Tony E. "Role of IgG-bound TGF[beta]1 and IAP in modulating neutrophil-mediated host defense against bacterial infection." free to MU campus, to others for purchase, 1996. http://wwwlib.umi.com/cr/mo/fullcit?p9809663.

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