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International immunopharmacology

ISSN 1878-1705

3 papers in the library · 28 citations · publishing 2024-2026

Papers

Psilocybin and psilocin regulate microglial immunomodulation and support neuroplasticity via serotonergic and AhR signaling.

International immunopharmacology June 26, 2025 Salma Laabi, Claire LeMmon, Callie Vogel et al. 15 citations

Psilocybin and its active metabolite psilocin suppress the pro-inflammatory cytokine TNF-α and increase levels of the neuroplasticity marker BDNF in activated microglia. These effects are mediated through 5-HT2A, 5-HT2B, 5-HT7, and TrkB signaling. AhR activation is required for psilocin-induced BDNF upregulation but not for TNF-α suppression. IL-10 levels remain unchanged under normal conditions but rise when serotonergic, TrkB, or AhR signaling is blocked, indicating a compensatory anti-inflammatory shift. The compounds promote a microglial phenotype that reduces inflammation and supports neuroplasticity via distinct receptor-specific pathways.

DOI: 10.1016/j.intimp.2025.114940 Full text Psilocin 5-ht2a 5-ht2b 5-ht7 +12

Esketamine mitigates mechanical ventilation-induced lung injury in chronic obstructive pulmonary disease rats via inhibition of the MAPK/NF-κB signaling pathway and reduction of oxidative stress.

International immunopharmacology September 30, 2024 San-Ying Cai, Ang Liu, Wen-Xi Xie et al. 13 citations

In a rat model of chronic obstructive pulmonary disease (COPD) receiving mechanical ventilation, esketamine reduced lung injury by dampening inflammation and oxidative stress. Rats given esketamine showed lower lung water content, reduced permeability, and decreased levels of pro-inflammatory cytokines (TNF-α, IL-6, IL-8) while increasing the anti-inflammatory cytokine IL-10. The drug also lowered markers of oxidative stress (malondialdehyde and myeloperoxidase) and raised the antioxidant enzyme superoxide dismutase. These effects were linked to reduced activation of the MAPK and NF-κB signaling pathways. Esketamine appears to protect lung tissue in ventilated COPD rats through these mechanisms.

DOI: 10.1016/j.intimp.2024.112725 Full text Esketamine Inflammation Mechanical ventilation Oxidative stress +5

(2R,6R)-HNK improved LPS-induced depression-like behavior by inhibiting Vcam1/Caspase-1/IL-1β pathway.

International immunopharmacology August 1, 2026 Jinghua Zhao, Ruxin Zhang, Jiarui Pan et al.

The ketamine metabolite (2R,6R)-hydroxynorketamine (HNK) reduces depression-like behavior in mice by suppressing neuroinflammation and neuronal pyroptosis. In experiments with male C57BL/6J mice and PC12 cells, HNK lowered expression of NLRP3, caspase-1, GSDMD, and interleukin-1β at both protein and mRNA levels, lessened neuronal injury, and reduced lactate dehydrogenase release. Transcriptomic analysis identified Vcam1 as a key differentially expressed gene. Overexpressing Vcam1 increased pyroptosis markers, while HNK reduced Vcam1 expression; knocking down Vcam1 had opposite effects. HNK thus attenuates LPS-induced pyroptosis and neuroinflammation partly by downregulating the Vcam1/caspase-1/IL-1β pathway, offering insights for depression treatment.

DOI: 10.1016/j.intimp.2026.116833 Full text Depression 2r,6r-hnk Neuroinflammation Pyroptosis +1