Description of Research: Vincent B. Young
Our group is interested in the role bacteria play
in acute and chronic gastrointestinal (GI) illness.
To this end, we study the role of what would traditionally
be considered “pathogenic bacteria” in
gastrointestinal illness. In addition, we also examine
how the population structure of the indigenous GI
microbiota can influence the host-pathogen interaction
and how changes in the community structure of the
indigenous microbiota itself can lead to pathogenic
states. Specific areas of investigation include:
MURINE MODELS OF INFLAMMATORY BOWEL DISEASE
The bacterium Helicobacter hepaticus have been implicated
as a trigger of inflammatory bowel disease (IBD) in
immune-altered mice. We have been investigating how
H. hepaticus can circumvent normal protective immune
responses and in turn how this leads to the development
of IBD in immune-altered mice.
GASTROINTESTINAL MICROBIAL ECOLOGY
The bacterial community of the gut is part of a
complex ecosystem. A significant proportion of the
members of these bacteria have not been cultured to
date in the laboratory, preventing understanding of
the complete diversity of this ecosystem. The advent
of culture-independent methods to examine the ecology
of this community has provided insight into the role
it plays in various disease processes. We have investigated
the role the gut microbial community plays in the
development of antibiotic-associated diarrhea in humans.
We are also defining the changes in the GI microbiota
related to H. hepaticus-induced IBD and determining
if probiotic organisms exert their beneficial effect
via changes in the gut microbiota.
Theriot CM, Koenigsknecht MJ, Carlson PE Jr, Hatton GE, Nelson AM, Li B, Huffnagle GB, Z Li J, Young VB. Antibiotic-induced shifts in the mouse gut microbiome and metabolome increase susceptibility to Clostridium difficile infection. Nat. Commun. 2014 Jan 20; 5:3114. doi: 10.1038/ncomms4114. PMID: 24445449.
Britton RA, Young VB. Role of the Intestinal Microbiota in Resistance to Colonization by Clostridium difficle. Gastroenterology. 2014 Feb 3. pii: S0016-5085(14)00150-4. doi: 10.1053/j.gastro.2014.01.059. [Epub ahead of print]. PMID: 24503131.
Huse SM, Young VB, Morrison HG, Antonopoulos DA, Kwon J, Dalal S, Arrieta R, Hubert NA, Shen L, Vineis JH, Koval JC, Sogin ML, Chang EB, Raffals LE. Comparison of brush and biopsy sampling methods of the ileal pouch for assessment of mucosa-associated microbiota of human subjects. Microbiome. 2014 Feb 14;2(1):5. [Epub ahead of print]. PMID: 24529162.
Rogers MA, Micic D, Blumberg N, Young VB, Aronoff DM. Storage duration of red blood cell transfusion and Clostridium difficile infection: a within person comparison. PLoS One. 2014;9(2):e89332. doi: 10.1371/journal.pone.0089332. PubMed PMID: 24586694; PubMed Central PMCID: PMC3931729.
Islam J, Taylor AL, Rao K, Huffnagle G, Young VB, Rajkumar C, Cohen J, Papatheodorou P, Aronoff DM, Llewelyn MJ. The role of the humoral immune response to Clostridium difficile toxins A and B in susceptibility to C. difficile infection: A case-control study. Anaerobe. 2014. doi: 10.1016/j.anaerobe.2014.03.011. PubMed PMID: 24708941.
Bassis CM, Theriot CM, Young VB. Alteration of the murine gastrointestinal microbiota by tigecycline leads to increased susceptibility to Clostridium difficile infection. Antimicrob Agents Chemother. 2014;58(5):2767-74. doi: 10.1128/AAC.02262-13. PubMed PMID: 24590475.
Seekatz AM, Aas J, Gessert CE, Rubin TA, Saman DM, Bakken JS, Young VB. Recovery of the gut microbiome following fecal microbiota transplantaion. mBio. 2014;5(3). doi: 10.1128/mBio.00893-14. PubMed PMID: 24939885.
Leslie JL, Huang S, Opp JS, Nagy MS, Kobayashi M, Young VB, Spence JR. Persistence and toxin production by Clostridium difficile within human intestinal organoids results in disruption of epithelial paracellular barrier function. Infect Immun. 2014. doi: 10.1128/IAI.02561-14. PubMed PMID: 25312952.
Sadighi Akha AA, McDermott AJ, Theriot CM, Carlson PE, Jr., Frank CR, McDonald RA, Falkowski NR, Bergin IL, Young VB, Huffnagle GB. IL22 and CD160 play additive roles in the host mucosal response to Clostridium difficile infection in mice. Immunology. 2014. doi: 10.1111/imm.12414. PubMed PMID: 25327211.
Trindade BC, Theriot CM, Leslie JL, Carlson PE, Jr., Bergin IL, Peters-Golden M, Young VB, Aronoff DM. Clostridium difficile-induced colitis in mice is independent of leukotrienes. Anaerobe. 2014;30C:90-8. doi: 10.1016/j.anaerobe.2014.09.006. PubMed PMID: 25230329.