Abstract: 316L stainless steel (SS) is extensively utilized in medical devices, including internal stents, due to its superior mechanical properties. With the increasing prevalence of implanted metal devices, microbiologically influenced corrosion (MIC) has become a serious issue, potentially threatening patient health by increasing the risk of exposure to harmful metal ions in the body. However, the MIC behavior and mechanisms of 316L SS within the intestinal environment are not well understood. This study presents the first evidence that the intestinal electroactive bacterium Lactobacillus plantarum is involved in the MIC of 316L SS. By combining genetic, electrochemical, and materials characterization approaches, we demonstrated that the MIC of 316L SS by L. plantarum was mediated through an extracellular electron transfer (EET) mechanism. The deletion of key EET pathway genes pplA and eetB, significantly attenuated the corrosion by L. plantarum. Materials characterizations further confirmed that L. plantarum disrupts the passive film on the surface of 316L SS via the EET pathway. This study aids the understanding of intestinal MIC mechanisms and the development of novel medical device materials resistant to microbial corrosion.

Key words: Microbiologically influenced corrosion, Stainless steel, Lactobacillus plantarum, Extracellular electron transfer