Publications by authors named "Christoph Rummel"

Alzheimer's disease (AD) was first described over a century ago. However, the mechanisms underlying the disease are not well understood to this day. This has negatively impacted our ability to create animal models to design and test targeted reliable treatments for the disease.

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Introduction: During acute inflammation, immune-to-brain signaling plays a pivotal role in the generation of sickness responses such as fever or hypothermia. Neutrophil granulocytes (NG) are a crucial component of the immune system and modulate inflammation. Moreover, neutropenic fever is a severe condition for immunocompromised patients that can be life threatening.

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Alzheimer's disease (AD) is the most common form of dementia globally and is characterised by reduced mitochondrial respiration and cortical deposition of amyloid-β plaques and neurofibrillary tangles comprised of hyper-phosphorylated tau. Despite its characterisation more than 110 years ago, the mechanisms by which AD develops are still unclear. Dysregulation of microglial phagocytosis of amyloid-β may play a key role.

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Objective: Adverse childhood experiences (ACEs) are associated with a greater risk of obesity and cardiometabolic disease. Adipokines, including leptin and adiponectin, play vital roles in biological processes linked to obesity and cardiometabolic risk. The adiponectin/leptin ratio may represent a marker of impaired hormonal regulation of adipose tissue.

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Oxylipins and specialized pro-resolving lipid mediators (SPMs) derived from polyunsaturated fatty acids (PUFAs) are mediators that coordinate an active process of inflammation resolution. While these mediators have potential as circulating biomarkers for several disease states with inflammatory components, the source of plasma oxylipins/SPMs remains a matter of debate but may involve white adipose tissue (WAT). Here, we aimed to investigate to what extent high or low omega (n)-3 PUFA enrichment affects the production of cytokines and adipokines (RT-PCR), as well as oxylipins/SPMs (liquid chromatography-tandem mass spectrometry) in the WAT of mice during lipopolysaccharide (LPS)-induced systemic inflammation (intraperitoneal injection, 2.

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The Great Pacific Garbage Patch, a significant collection of plastic introduced by human activities, provides an ideal environment to study bacterial lifestyles on plastic substrates. We proposed that bacteria colonizing the floating plastic debris would develop strategies to deal with the ultraviolet-exposed substrate, such as the production of antioxidant pigments. We observed a variety of pigmentation in 67 strains that were directly cultivated from plastic pieces sampled from the Garbage Patch.

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Alzheimer's disease (AD) is prevalent around the world, yet our understanding of the disease is still very limited. Recent work suggests that the cornerstone of AD may include the inflammation that accompanies it. Failure of a normal pro-inflammatory immune response to resolve may lead to persistent central inflammation that contributes to unsuccessful clearance of amyloid-beta plaques as they form, neuronal death, and ultimately cognitive decline.

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The pollution of the marine environment with plastic debris is expected to increase, where ocean currents and winds cause their accumulation in convergence zones like the North Pacific Subtropical Gyre (NPSG). Surface-floating plastic (>330 μm) was collected in the North Pacific Ocean between Vancouver (Canada) and Singapore using a neuston catamaran and identified by Fourier-transform infrared spectroscopy (FT-IR). Baseline concentrations of 41,600-102,700 items km were found, dominated by polyethylene and polypropylene.

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Inflammation involves the activation of innate immune cells and is believed to play an important role in the development and progression of both infectious and non-infectious diseases such as neurodegeneration, autoimmune diseases, pulmonary and cancer. Inflammation in the brain is marked by the upregulation of translocator protein (TSPO) in microglia. High TSPO levels are also found, for example, in macrophages in cases of rheumatoid arthritis and in malignant tumor cells compared to their relatively low physiological expression.

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Plastics are produced with a staggering array of chemical compounds, with many being known to possess hazardous properties, and others lacking comprehensive hazard data. Furthermore, non-intentionally added substances can contaminate plastics at various stages of their lifecycle, resulting in recycled materials containing an unknown number of chemical compounds at unknown concentrations. While some national and regional regulations exist for permissible concentrations of hazardous chemicals in specific plastic products, less than 1 % of plastics chemicals are subject to international regulation [1].

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Microcephaly is often caused by an impairment of the generation of neurons in the brain, a process referred to as neurogenesis. While most neurogenesis in mammals occurs during brain development, it thought to continue to take place through adulthood in selected regions of the mammalian brain, notably the hippocampus. However, the generality of neurogenesis in the adult brain has been controversial.

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Specialized pro-resolving mediators (SPMs) and especially Resolvin E1 (RvE1) can actively terminate inflammation and promote healing during lung diseases such as acute respiratory distress syndrome (ARDS). Although ARDS primarily affects the lung, many ARDS patients also develop neurocognitive impairments. To investigate the connection between the lung and brain during ARDS and the therapeutic potential of SPMs and its derivatives, mice were crossbred with RvE1 receptor knockout mice.

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Chronic hypoxia-induced pulmonary hypertension (CHPH) is a severe disease that is characterized by increased proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs) leading to pulmonary vascular remodeling. The resulting increase in pulmonary vascular resistance (PVR) causes right ventricular hypertrophy and ultimately right heart failure. In addition, increased PVR can also be a consequence of hypoxic pulmonary vasoconstriction (HPV) under generalized hypoxia.

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Inflammatory processes within the peripheral nervous system (PNS) are associated with symptoms of hyperalgesia and allodynia. Pro-inflammatory mediators, such as cytokines or prostaglandins, modulate the excitability of nociceptive neurons, called peripheral sensitization. Here, we aimed to examine if previously reported effects of in vitro stimulation with lipopolysaccharide (LPS) on primary cell cultures of dorsal root ganglia (DRG) reflect changes in a model of LPS-induced systemic inflammation in vivo.

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Sensory circumventricular organs (sCVOs) are pivotal brain structures involved in immune-to-brain communication with a leaky blood-brain barrier that detect circulating mediators such as lipopolysaccharide (LPS). Here, we aimed to investigate the potential of sCVOs to produce n-3 and n-6 oxylipins after LPS-stimulation. Moreover, we investigated if norepinephrine (NE) co-treatment can alter cytokine- and oxylipin-release.

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Introduction: Gabapentin and pregabalin are drugs to treat neuropathic pain. Several studies highlighted effects on presynaptic terminals of nociceptors. Via binding to α2δ subunits of voltage-gated calcium channels, gabapentinoids modulate the synaptic transmission of nociceptive information.

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Background: Compression of epidural adipose tissue (EAT) within the scope of cauda equina syndrome (CES) could lead to an enhanced expression of inflammatory mediators, possibly contributing to pain amplification in dogs.

Objectives: To analyze expression of inflammatory adipo(-cyto)kines within the EAT of dogs with CES.

Animals: Client-owned dogs: 15 dogs with CES and 9 dogs euthanized for unrelated medical reasons (controls).

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The theme of this BBI-Health special issue is to promote the research, creativity and forward-thinking of future key opinion leaders in the field of psychoneuroimmunology (PNI). We asked contributing researchers to identify new ideas and spaces for innovation to map out the future trajectory of our discipline. This special issue provides global and diverse views from early career investigators focused on science, society, and/or policy, with an emphasis on diversity in all its aspects.

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Purpose: Previously, we have shown that CyPPA (cyclohexyl-[2-(3,5-dimethyl-pyrazol-1-yl)-6-methyl-pyrimidin-4-yl]-amine), a pharmacological small-conductance calcium-activated potassium (SK)-channel positive modulator, antagonizes lipopolysaccharide (LPS)-induced cytokine expression in microglial cells. Here, we aimed to test its therapeutic potential for brain-controlled sickness symptoms, brain inflammatory response during LPS-induced systemic inflammation, and peripheral metabolic pathways in mice.

Methods: Mice were pretreated with CyPPA (15 mg/kg IP) 24 hours before and simultaneously with LPS stimulation (2.

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Objective: We investigated whether it is possible to induce a state of "LPS-sensitization" in neurons of primary cultures from rat dorsal root ganglia by pre-treatment with ultra-low doses of LPS.

Methods: DRG primary cultures were pre-treated with low to ultra-low doses of LPS (0.001-0.

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Plastics undergo successive fragmentation and chemical leaching steps in the environment due to weathering processes such as photo-oxidation. Here, we report the effects of leachates from UV-irradiated microplastics towards the chlorophyte Scenedesmus vacuolatus. The microplastics tested were derived from an additive-containing electronic waste (EW) and a computer keyboard (KB) as well as commercial virgin polymers with low additive content, including polyethylene (PE), polyethylene terephthalate (PET), polypropylene (PP), and polystyrene (PS).

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Neuroinflammation within the superficial dorsal horn (SDH) of the spinal cord induces inflammatory pain with symptoms of hyperalgesia and allodynia. Glial activation and production of inflammatory mediators (e.g.

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