IDO1 and depressive symptom measurement: This TLR4-KP axis was validated <i>in vitro</i>: LPS-stimulated BV2 microglia showed increased IDO1/KMO/QUIN expression, which was abolished by TAK-242 pretreatment.<h4>Conclusion</h4>Our findings establish a novel TLR4-KP-QUIN pathway as a critical mediator of post-TBI depression, providing a mechanistic basis for TLR4-targeted therapies.