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Inflammatory Response

Inflammatory Response

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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D-Amino acids differentially trigger an inflammatory environment in vitro.

Siew Hwei Yap^1,2, Cheng Siang Lee¹, Nur Diyana Zulkifli³

¹Centre of Excellence for Research in AIDS (CERiA), Universiti Malaya, Kuala Lumpur, Malaysia.

|February 3, 2024

Summary

D-serine and D-alanine trigger distinct inflammatory pathways in liver cancer cells. D-serine induces apoptosis via mitochondrial dysfunction, while D-alanine promotes inflammation without significant cell death.

Keywords:

D-Alanine D-Amino acid oxidase D-Serine Inflammation TNF-α

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Area of Science:

Biochemistry
Molecular Biology
Immunology

Background:

Accumulation of D-amino acids (D-AAs) is linked to age-related diseases and immune activation.
D-AA metabolism by D-amino oxidase (DAO) generates hydrogen peroxide (H2O2), a reactive oxygen species implicated in cellular processes.
Excessive H2O2 contributes to oxidative stress and cell death, characteristic of aging pathologies.

Purpose of the Study:

To investigate the molecular mechanisms of D-serine (D-Ser) and D-alanine (D-Ala) in human liver cancer cells (HepG2).
To examine H2O2 production, pro-inflammatory cytokine/chemokine secretion, and cell death induced by D-Ser and D-Ala.
To elucidate the distinct pathways activated by D-Ser and D-Ala in HepG2 cells.

Main Methods:

Treatment of HepG2 cells with D-Ser and D-Ala.
Measurement of H2O2 production and mitochondrial membrane potential (MMP).
Analysis of activated NF-κB, TNF-α, and IL-8 secretion, and assessment of apoptosis.

Main Results:

D-Ser decreased H2O2 production, induced MMP depolarization, and upregulated activated NF-κB, TNF-α, and IL-8, leading to apoptosis.
D-Ala increased H2O2 production, upregulated activated NF-κB, TNF-α, and IL-8, but did not induce significant apoptosis.
Both D-Ser and D-Ala induce inflammatory responses via unique pathways, with D-Ser uniquely associated with apoptotic cell death.

Conclusions:

D-Ser and D-Ala differentially regulate inflammatory responses and cell death in liver cancer cells.
D-Ser-induced apoptosis is linked to mitochondrial dysfunction and inflammatory signaling.
Further research is needed to understand D-AA-induced inflammation, particularly in aging contexts.