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Related Concept Videos

Inflammatory Response01:28

Inflammatory Response

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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
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Inflammatory Response II: Inflammatory Exudate and Tissue Repair01:24

Inflammatory Response II: Inflammatory Exudate and Tissue Repair

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The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the...
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Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

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The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Cholinergic Receptors: Nicotinic01:15

Cholinergic Receptors: Nicotinic

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Nicotinic receptors are ligand-gated ion channels that are activated by acetylcholine and nicotine. Upon activation, they cause a rapid increase in the permeability of cells to K+, Na+, and Ca2+, followed by depolarization and excitation. They are in the autonomic ganglia, skeletal neuromuscular junction, CNS, and adrenal medulla.
There are two types of nicotinic receptors: neuromuscular (NM/NM/N1) and neuronal (NN/NN/N2). The two families differ based on their location and selectivity to...
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CNS Depressants: Alcohol and Nicotine01:27

CNS Depressants: Alcohol and Nicotine

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Ethanol, a clear colorless alcohol, has been consumed by humans for millennia, but its effects on the body are far from benign. At lower doses, it induces decreased inhibitions and loquaciousness, leading to its social appeal. However, it can cause severe consequences at higher doses, such as coma and respiratory depression, due to its zero-order elimination kinetics. Chronic ethanol abuse wreaks havoc on multiple organ systems, particularly the CNS and the liver. Abrupt cessation of ethanol...
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Increased Recovery Time and Decreased LPS Administration to Study the Vagus Nerve Stimulation Mechanisms in Limited Inflammatory Responses
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Nicotine Regulates LPS-Induced Inflammatory Responses in HMC3 Microglia and Exerts Neuronal Protection.

Yuhan Qin1,2, Xiaohui Yan1,2, Yanbo Luo2

  • 1Beijing Life Science Academy, Beijing, 102209, China.

Mediators of Inflammation
|January 26, 2026
PubMed
Summary

Low-concentration nicotine inhibits microglia inflammation via α7 nicotinic acetylcholine receptor (α7 nAChR) activation, promoting neuronal survival. This suggests potential therapeutic applications for neuroinflammatory conditions.

Keywords:
HMC3PI3Kcell coculturelipopolysaccharidemicroglianeurodegenerative diseaseneuroinflammationneuronnicotineα7 nAChR

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Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Microglia play a crucial role in neuroimmune responses in the central nervous system.
  • The α7 nicotinic acetylcholine receptor (α7 nAChR) on microglia mediates cholinergic anti-inflammatory pathways.
  • Nicotine's effect on microglia-mediated inflammation requires further investigation.

Purpose of the Study:

  • To investigate the modulatory effects of nicotine on neuroinflammation in an in vitro microglial model.
  • To explore the potential indirect neuroprotective effects of nicotine on neurons.
  • To elucidate the molecular mechanisms underlying nicotine's actions on microglia.

Main Methods:

  • Utilized an in vitro microglial cell inflammation model (HMC3 cells).
  • Analyzed inflammatory phenotype indicators and molecular mechanisms.
  • Established an HMC3 microglia-SH-SY5Y neuronal co-culture system to assess indirect neuroprotection.

Main Results:

  • Nicotine inhibited lipopolysaccharide-induced inflammation in HMC3 microglia.
  • Nicotine promoted the release of neurotrophic factors and enhanced neuronal survival.
  • These effects were mediated by α7 nAChR activation and increased PI3K phosphorylation.

Conclusions:

  • Low-concentration nicotine exerts immunomodulatory effects on microglia, reducing neuroinflammation.
  • Nicotine demonstrates potential indirect neuroprotective effects by altering the microglial immune environment.
  • Findings offer insights into the therapeutic potential of nicotine in neurological disorders.