Neuroinflammation

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Neuroinflammation Background

About Neuroinflammation

Neuroinflammation refers to inflammation that occurs within the central nervous system (CNS), which includes the brain and spinal cord. It is a complex immune response involving various cellular and molecular processes in the brain and is a key component of the body's defense mechanism against injury, infection, and neurodegenerative diseases.

Inflammation is a natural response of the immune system to protect the body from harmful stimuli. However, when it comes to the CNS, neuroinflammation can have both beneficial and detrimental effects. The main cells involved in neuroinflammation are microglia, the resident immune cells of the brain, and astrocytes, the supporting cells that maintain the brain's environment.

Neuroinflammation can be triggered by various factors, including infections, autoimmune responses, traumatic brain injury, stroke, toxins, and the accumulation of abnormal proteins in neurodegenerative diseases like Alzheimer's and Parkinson's diseases. Upon activation, microglia and astrocytes release pro-inflammatory molecules, such as cytokines, chemokines, and reactive oxygen species, which attract immune cells and initiate immune responses.

The acute phase of neuroinflammation is characterized by the activation of microglia and the release of pro-inflammatory factors, which can help remove pathogens, repair damaged tissue, and promote healing. However, if neuroinflammation becomes chronic or dysregulated, it can lead to tissue damage, and neuronal dysfunction, and contribute to the progression of various neurological disorders.

Chronic neuroinflammation is implicated in several neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, and amyotrophic lateral sclerosis (ALS). In these conditions, the sustained release of pro-inflammatory molecules and the accumulation of immune cells can lead to the destruction of neurons, synaptic dysfunction, and cognitive or motor impairments.

Understanding neuroinflammation is crucial for developing therapeutic strategies to modulate or suppress excessive inflammation in neurological diseases. Researchers are investigating various approaches, including anti-inflammatory drugs, immunomodulatory therapies, and targeting specific molecules involved in inflammatory responses.

Positive And Negative Aspects of Neuroinflammatory Processes

The intensity and duration of inflammation account for much of whether immune signals are supportive or destructive to the central nervous system. On the left, we show examples of brief and controlled inflammatory responses that are generally considered beneficial to the host organism. For instance, immune-to-brain signals after infection lead to the subsequent reorganization of host priorities and induction of sickness behaviors. Additionally, there is an important maintenance role of IL-1 and IL-4 in learning and memory. Following traumatic CNS injury, IL-4-driven repolarization of macrophages (M2) has been proven to be highly effective in promoting recovery and axonal regrowth. Immune preconditioning, or euflammation, provides a method for training the innate immune system toward a more neuroprotective phenotype. Conversely, on the right, we demonstrate various maladaptive inflammatory responses. Chronic, uncontrolled inflammation is characterized by increased production of cytokines (IL-1 and TNF), reactive oxygen species (ROS), and other inflammatory mediators (inducible nitric oxide synthase). These markers are highly evident following trauma to the CNS and are accompanied by significant recruitment and trafficking of peripheral macrophages and neutrophils to the site of injury. The transient inflammation after repeated social defeat stress also leads to monocyte and macrophage recruitment and causes anxiety and depression. Additionally, a low-level and chronic inflammatory response driven by IL-1 and IL-6 is caused by aging, follows the acute phase of CNS trauma, and leads to reduced neuronal plasticity and cognitive impairments. A higher degree of chronic inflammation is greatly damaging to the nervous system and is characteristic of neurodegenerative diseases.

Fig.1 Positive and negative aspects of neuroinflammation. (DiSabato DJ, et al., 2016)

Central Players in Neuroinflammation

Microglia are the focal point for any discussion of neuroinflammation. This is because these innate immune cells perform the primary immune surveillance and macrophage-like activities of the CNS, including the production of cytokines and chemokines. Indeed, much of the innate immune capacity of the CNS is mediated by microglia. These cells are resident CNS cells that reside in both the white matter and gray matter of the brain and spinal cord. Overall, microglia comprise 10% of the CNS population.

Neuroinflammatory responses are mediated by several key pro-inflammatory cytokines (IL-1β, IL-6, and TNFα), chemokines (CCL2, CCL5, CXCL1), secondary messengers (NO and prostaglandins) and reactive oxygen species (ROS). Many of these mediators are produced by activated resident CNS cells including microglia and astrocytes. In addition, endothelial cells and perivascular macrophages are also important in interpreting and propagating these inflammatory signals within the CNS.

Available Resources for Neuroinflammation

• Creative BioMart offers a range of neuroinflammation-related products, including recombinant proteins, cell and tissue lysates, and protein pre-coupled magnetic beads.
• Whether you are in academia or the biopharmaceutical industry, we can customize services according to your specific requirements.
• Aside from our products and customized services, we also provide a wealth of resources for your reference, such as information on pathways, protein function, interacting proteins, articles, research areas, and other topics related to neuroinflammation. These resources will assist you in gaining a deeper understanding and application of neuroinflammation-related knowledge.

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Recombinant Human IL6 protein
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Recombinant Human IL18 protein, GST-tagged
Recombinant Mouse Cxcl2 protein, His&SUMO-tagged
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Active Recombinant Human IFNG
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If you have any questions, requirements, or cooperation intentions, please feel free to contact us. We very much look forward to working with you and helping you achieve research and commercial success.

Reference:

1. DiSabato DJ, Quan N, Godbout JP. Neuroinflammation: the devil is in the details. J Neurochem. 2016 Oct;139 Suppl 2(Suppl 2):136-153.