Interleukin-1 Receptor Type I Gene-Deficient Mice Are Less Susceptible to<i>Staphylococcus epidermidis</i>Biomaterial-Associated Infection than Are Wild-Type Mice

Boelens, Jaap Jan; Poll, Tom van der; Zaat, Sebastian A. J.; Murk, Jean Luc; Weening, Jan J.; Dankert, J.

doi:10.1128/iai.68.12.6924-6931.2000

Cited by 25 publications

(21 citation statements)

References 55 publications

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“…Similarly, administering an IL‐1R antagonist or IL‐1β blocking antibodies reduces neuronal death subsequent to ischemia (Relton and Rothwell, 1992; Yamasaki et al, 1995; Loddick and Rothwell, 1996). Disruption of IL‐1 signaling also confers protection to a host in other inflammatory disorders such as bacterial infection and endotoxin administration (Labow et al, 1997; Boelens et al, 2000; Sewnath et al, 2002). As decreasing IL‐1 signaling is neuroprotective and there is no evidence that IL‐1 directly kills neurons or glial cells, it has been suggested that IL‐1 stimulates, directly or indirectly, the production of toxic intermediates that kill brain cells.…”

Section: Disrupting Il‐1 Signaling Delays Neuroinflammation and Neuromentioning

confidence: 99%

Interleukin‐1: A master regulator of neuroinflammation

Basu

Krady

Levison

2004

J of Neuroscience Research

316

255

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Interleukins 1alpha and 1beta (IL-1) are very potent signaling molecules that are expressed normally at low levels, but are induced rapidly in response to local or peripheral insults. IL-1 coordinates systemic host defense responses to pathogens and to injury and not surprisingly it has similar effects within the central nervous system (CNS). Numerous reports have correlated the presence of IL-1 in the injured or diseased brain, and its effects on neurons and nonneuronal cells in the CNS, but it is only recently that the importance of IL-1 signaling has been recognized. This article reviews studies that demonstrate that IL-1 is at or near the top of the hierarchical cytokine signaling cascade in the CNS that results in the activation of endogenous microglia and vascular endothelial cells to recruit peripheral leukocytes (i.e., neuroinflammation). The IL-1 system thus provides an attractive target for therapeutic intervention to ameliorate the destructive consequences of neuroinflammation.

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Section: Disrupting Il‐1 Signaling Delays Neuroinflammation and Neuromentioning

confidence: 99%

Interleukin‐1: A master regulator of neuroinflammation

Basu

Krady

Levison

2004

J of Neuroscience Research

316

255

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“…Mice lacking the IL-1rα gene sustain 50% less damage after cerebral hypoxia/ischaemia [63]. Furthermore disruption of IL-1 signaling also confers protection to a host in other inflammatory disorders such as bacterial infections and endotoxin administration [113,114]. More recent studies have employed transgenic animals with specific modifications of selected genes to investigate the contribution of inflammation to acute neurodegeneration.…”

Section: Experimental Studies and Therapeutic Prospectsmentioning

confidence: 98%

Proinflammatory Cytokines and Chemokines in Neonatal Brain Damage

Xanthou¹

2006

CPR

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During perinatal asphyxia the inflammatory response to tissue injury and the production of cytokines occur after the excitotoxic cascade, at the reperfusion state, as hypoxia upregulates numerous proinflammatory genes of cytokines and chemokines. During perinatal infections CD14 and TLRs expressed on various cells bind to pathogen derived molecules and induce the synthesis of proinflammatory cytokines and chemokines. When the infection is located in uterus these inflammatory mediators enter the fetal circulation by crossing the placenta. Subsequently they cross the blood-brain barrier and cause local inflammation in the fetal brain. In experimental studies as well as in clinical, epidemiologic and neuropathologic studies concerning the newborn infant, an association between perinatal asphyxia and/or infection, cytokines, chemokines and brain damage has been found. In this review we analyse the mechanisms through which proinflammatory cytokines and chemokines may lead to neurodegeneration and brain damage. Particular emphasis is given to the white matter damage of the brain of preterm infants. Preterm infants are more vulnerable to brain damage because of their immature vascular ependymal factors, immature oligodendrocytes and deficient endogenous protective mechanisms. The methods used to modify or block the activity of proinflammatory cytokines and chemokines in order to prevent brain damage are being discussed.

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“…It was suggested the importance of the host response to various biomaterials in the pathogenesis of biomaterial associated infection (BAI), rather than for the extent of adherence of bacteria to biomaterial. Therefore Local inhibition of IL-1β activity may be of benefit to the host as an adjunctive therapy for infections associated with biomaterials [69].…”

Section: Discussionmentioning

confidence: 99%

Efficacy of Some Antibiotics in Curing Resistant <i>Escherichia coli</i> Infection

El-Banna¹,

El-Aziz²,

El-Mahdy³

et al. 2015

JBM

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There is growing interest in re-evaluation of older antibiotics with the wide spread of pathogen resistance, especially gram negative bacteria, which impair treatment of some infections. In contrast various studies have reported that some antibiotics have efficacy in clearing resistant bacterial infections. On account of that it was interesting to evaluate the efficacy of erythromycin, chloramphenicol and/or tenoxicam in curing and/or relieving wound infection of highly resistant Escherichia coli and investigate the possible mechanisms beyond their antibacterial activity. This was achieved through evaluating highly resistant E. coli strains in vitro using agar dilution and in vivo rat models of E. coli infected wound and acute inflammation by carrageenin, where possible mechanisms were evaluated through measuring immunological mediators and histopathological examination. This study revealed that in vivo, erythromycin alone or in combination with tenoxicam significantly improved the healing of infected skin wounds with E. coli irresspective of resistancy in vitro. In addition to the improvement of immunological mediators involved in inflammatory reaction, oxidative stress and in cytokines expression as response to the bacterial infection in vivo. On the other hand chloramphenicol neither alone nor in combination with tenoxicam, achieved any significant effect. Tenoxicam didn't show antimicrobial activity alone nor in combination with tested antibiotics in vitro, but it has shown synergestic activity in combination with tested antibiotics in vivo. Thus we concluded that immunomodulatory activity of erythromycin through anti-inflammatory and antioxidant effects was the possible mechanisms by which this antibiotic had healed infection with resistant E. coli in vivo, despite its resistancy to this antibiotic in vitro.

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Interleukin-1 Receptor Type I Gene-Deficient Mice Are Less Susceptible toStaphylococcus epidermidisBiomaterial-Associated Infection than Are Wild-Type Mice

Cited by 25 publications

References 55 publications

Interleukin‐1: A master regulator of neuroinflammation

Interleukin‐1: A master regulator of neuroinflammation

Proinflammatory Cytokines and Chemokines in Neonatal Brain Damage

Efficacy of Some Antibiotics in Curing Resistant <i>Escherichia coli</i> Infection

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Interleukin-1 Receptor Type I Gene-Deficient Mice Are Less Susceptible toStaphylococcus epidermidisBiomaterial-Associated Infection than Are Wild-Type Mice

Cited by 25 publications

References 55 publications

Interleukin‐1: A master regulator of neuroinflammation

Interleukin‐1: A master regulator of neuroinflammation

Proinflammatory Cytokines and Chemokines in Neonatal Brain Damage

Efficacy of Some Antibiotics in Curing Resistant &lt;i&gt;Escherichia coli&lt;/i&gt; Infection

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Efficacy of Some Antibiotics in Curing Resistant <i>Escherichia coli</i> Infection