Microbiota-produced indole metabolites disrupt mitochondrial function and inhibit Cryptosporidium parvum growth

Authors

Lisa J Funkhouser-Jones, Washington University School of Medicine in St. Louis
Rui Xu, Washington University School of Medicine in St. Louis
Georgia Wilke, Washington University School of Medicine in St. Louis
Yong Fu, Washington University School of Medicine in St. Louis
Lawrence A Schriefer, Washington University School of Medicine in St. Louis
Heyde Makimaa, Washington University School of Medicine in St. Louis
Rachel Rodgers, Washington University School of Medicine in St. Louis
Elizabeth A Kennedy, Washington University School of Medicine in St. Louis
Kelli L VanDussen, Washington University School of Medicine in St. Louis
Thaddeus S Stappenbeck, Washington University School of Medicine in St. Louis
Megan T Baldridge, Washington University School of Medicine in St. Louis
L David Sibley, Washington University School of Medicine in St. Louis

Journal

Cell Reports

Publication Date

7-25-2023

Volume

42

Issue

7

First Page

112680

Document Type

Open Access Publication

DOI

10.1016/j.celrep.2023.112680

Rights and Permissions

Funkhouser-Jones LJ, Xu R, Wilke G, Fu Y, Schriefer LA, Makimaa H, Rodgers R, Kennedy EA, VanDussen KL, Stappenbeck TS, Baldridge MT, Sibley LD. Microbiota-produced indole metabolites disrupt mitochondrial function and inhibit Cryptosporidium parvum growth. Cell Rep. 2023 Jul 25;42(7):112680. doi: 10.1016/j.celrep.2023.112680. Copyright 2023 The Author(s). This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Recommended Citation

Funkhouser-Jones, Lisa J; Xu, Rui; Wilke, Georgia; Fu, Yong; Schriefer, Lawrence A; Makimaa, Heyde; Rodgers, Rachel; Kennedy, Elizabeth A; VanDussen, Kelli L; Stappenbeck, Thaddeus S; Baldridge, Megan T; and Sibley, L David, "Microbiota-produced indole metabolites disrupt mitochondrial function and inhibit Cryptosporidium parvum growth." Cell Reports. 42, 7. 112680 (2023).
https://digitalcommons.wustl.edu/oa_4/2380

Department

ICTS (Institute of Clinical and Translational Sciences)

Additional Links

Supplemental material is available for this article at publisher site.