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Background <p>Biodegradable plastics are increasingly being used as a sustainable alternative, but their degradation in biological environments may produce transformation products with unexpected toxicological characteristics. These products generate a distribution pattern in the kidneys that differs from other organs, with the accumulation of low-molecular-weight polylactic acid microplastics (PLA MPs) being far higher than that of high-molecular-weight tissues.</p> Methods <p>PLA is used as a representative bioplastic. We used polymeric and oligomeric MPs to simulate their original and partially degraded states. Mice were exposed to these MPs through repeated oral administration under controlled experimental exposure conditions for 28 consecutive days to study the accumulation and inflammatory damage caused by PLA oligomer and polymer MPs in the kidneys. In combination with <i>in vitro</i> transcriptomic analysis, we explored the potential mechanisms by which oligomers drive nephrotoxicity.</p> Results <p>Exposure to PLA oligomer MPs results in significantly higher accumulation in the kidneys compared to PLA polymer MPs, and triggers more severe inflammatory damage. The mechanism is that renal macrophages preferentially phagocytose PLA oligomer MPs and decode them through macrophage scavenger receptor 1 (MSR1), activating phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling and inducing chemokine ligand 2 (CCL2)-dependent macrophage recruitment, thereby establishing a self-amplifying inflammatory loop. Inhibiting MSR1 or PI3K/AKT effectively reduces oligomer-driven cytokine production, macrophage infiltration, and renal injury, narrowing the toxicity gap between oligomeric and polymeric PLA MPs in the kidneys.</p> Conclusions <p>These findings reveal that biodegradation can heighten the inflammatory potential of MPs, and that distinct polymerization states of the same material elicit different immune interpretations. Our work provides mechanistic clarity on how degradability reshapes microplastic toxicity, underscoring the need to incorporate degradation-state profiling into the safety assessment of biodegradable MPs.</p>

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Degradation reshapes the toxic identity of polylactic acid microplastics through MSR1-dependent immune decoding in mouse kidney

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月14日

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  • Xiaoqing Chen,
  • Yanhong Deng,
  • Xiyun Huang,
  • Xiaohong Yang,
  • Zhiming Li,
  • Yuji Huang,
  • Yizhou Zhong,
  • Hao Li,
  • Lichun Ma,
  • Shiyue Tang,
  • Hongyi Xian,
  • Boxuan Liang,
  • Zhenlie Huang

摘要

Background

Biodegradable plastics are increasingly being used as a sustainable alternative, but their degradation in biological environments may produce transformation products with unexpected toxicological characteristics. These products generate a distribution pattern in the kidneys that differs from other organs, with the accumulation of low-molecular-weight polylactic acid microplastics (PLA MPs) being far higher than that of high-molecular-weight tissues.

Methods

PLA is used as a representative bioplastic. We used polymeric and oligomeric MPs to simulate their original and partially degraded states. Mice were exposed to these MPs through repeated oral administration under controlled experimental exposure conditions for 28 consecutive days to study the accumulation and inflammatory damage caused by PLA oligomer and polymer MPs in the kidneys. In combination with in vitro transcriptomic analysis, we explored the potential mechanisms by which oligomers drive nephrotoxicity.

Results

Exposure to PLA oligomer MPs results in significantly higher accumulation in the kidneys compared to PLA polymer MPs, and triggers more severe inflammatory damage. The mechanism is that renal macrophages preferentially phagocytose PLA oligomer MPs and decode them through macrophage scavenger receptor 1 (MSR1), activating phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling and inducing chemokine ligand 2 (CCL2)-dependent macrophage recruitment, thereby establishing a self-amplifying inflammatory loop. Inhibiting MSR1 or PI3K/AKT effectively reduces oligomer-driven cytokine production, macrophage infiltration, and renal injury, narrowing the toxicity gap between oligomeric and polymeric PLA MPs in the kidneys.

Conclusions

These findings reveal that biodegradation can heighten the inflammatory potential of MPs, and that distinct polymerization states of the same material elicit different immune interpretations. Our work provides mechanistic clarity on how degradability reshapes microplastic toxicity, underscoring the need to incorporate degradation-state profiling into the safety assessment of biodegradable MPs.