Supplementary Materials

Supplementary Material for:

Endotoxemia-mediated inflammation potentiates aminoglycoside-induced ototoxicity

Ja-Won Koo, Lourdes Quintanilla-Dieck, Meiyan Jiang, Jianping Liu, Zachary D. Urdang, Jordan J. Allensworth, Campbell P. Cross, Hongzhe Li, Peter S. Steyger*

*Corresponding author. E-mail: steygerp{at}ohsu.edu

Published 29 July 2015, Sci. Transl. Med. 7, 298ra118 (2015)
DOI: 10.1126/scitranslmed.aac5546

This PDF file includes:

  • Materials and Methods
  • Fig. S1. LPS treatment enhances cochlear lateral wall uptake of GTTR.
  • Fig. S2. OHC uptake of GTTR is accelerated by LPS exposure.
  • Fig. S3. Renal uptake of GTTR is reduced only at high doses of LPS.
  • Fig. S4. LPS induces acute anorexia.
  • Fig. S5. LPS does not alter BLB permeability yet vasodilates apical strial capillaries.
  • Fig. S6. Serum serotonin, but not histamine, concentrations were decreased with increasing doses of LPS.
  • Fig. S7. TLR4-mediated inflammatory markers are modulated by LPS.
  • Fig. S8. LPS-induced GTTR uptake by cochlear lateral wall cells in control C3H/HeOuJ and TLR4-hyporesponsive C3H/HeJ mice.
  • Fig. S9. Absolute ABR thresholds are elevated by chronic kanamycin, or kanamycin plus LPS, dosing.
  • Fig. S10. Threshold shifts induced by chronic kanamycin, or kanamycin plus LPS, dosing.
  • Fig. S11. Effect of chronic kanamycin treatment, with or without LPS, on ABRs, OHC survival and BLB permeability.
  • Fig. S12. Absolute ABRs, threshold shifts and weight changes induced by chronic LPS, kanamycin, or LPS+kanamycin in C57BL/6 mice.
  • Fig. S13. Acute LPS-induced endotoxemia does not alter ABR thresholds.
  • Fig. S14. Schematic displaying potential mechanisms for aminoglycoside trafficking across the BLB.
  • Fig. S15. Acute LPS and aminoglycoside dosing paradigm.
  • Fig. S16. ELISA and qRT-PCR experimental designs for 6- and 24-hour LPS exposures.
  • Fig. S17. Chronic LPS–induced endotoxemia and kanamycin ototoxicity protocol.
  • Table S1. Number of mice in each condition for Figs. 1 and 2A and fig. S1.
  • Table S2. Probability of significant difference in GTTR serum concentrations for Fig. 2A.
  • Table S3. Probability of a significant difference in threshold shifts 1 day after chronic LPS–induced endotoxemia with or without kanamycin treatment.
  • Table S4. Probability of a significant difference in threshold shifts 1.5 weeks after chronic LPS–induced endotoxemia with or without kanamycin treatment.
  • Table S5. Probability of significant difference in threshold shifts 3 weeks after chronic LPS–induced endotoxemia with or without kanamycin treatment.
  • Table S6. Probability of a significant difference in threshold shifts immediately after chronic LPS–induced endotoxemia with or without kanamycin treatment.
  • Table S7. Probability of a significant difference in OHC survival 3 weeks after chronic LPS–induced endotoxemia with or without kanamycin treatment.
  • Table S8. Probability of a significant difference in OHC survival immediately after chronic LPS–induced endotoxemia with or without kanamycin treatment.
  • Table S9. Probability of decreasing OHC survival 3 weeks after chronic LPS–induced endotoxemia with or without kanamycin treatment compared to immediately after treatment.

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