Jay V. Solnick, MD, PhD


SOM: Medical Microbiology & Immunology
Center for Comparative Medicine
University of California, Davis
Davis, CA 95616
(530) 752-1333 (phone)
(530) 752-7914 (fax)

Research InterestHelicobacter pylori

Helicobacter pylori is a gram-negative spiral bacterium that was discovered in 1981 by Barry Marshall and Robin Warren, who in 2005 were awarded the Nobel Prize in Physiology or Medicine for their discovery.  H. pylori infects the gastric mucosa of approximately half the world’s population, and it is particularly common in developing countries.  Although infection is asymptomatic in most cases, about 10% of those infected will develop peptic ulcer and 1-3% will develop gastric cancer, which is the second most common cause of cancer death in the world.  The overall goal of the Solnick laboratory is to understand the pathogenic mechanisms by which H. pylori causes gastroduodenal diseases.

Functional Plasticity in the H. pylori Type IV Secretion System (T4SS)

Most strains of H. pylori that cause disease express a bacterial secretion system, a sort of molecular syringe that injects a bacterial protein inside the gastric cells and causes inflammation that can lead to peptic ulcer disease or gastric cancer. One of the essential components of the H. pylori secretion system is a protein called CagY, which is unusual because it contains a series of repetitive amino acid motifs that are encoded by a very large number of direct DNA repeats. We recently discovered that DNA recombination in cagY changes the protein motif structure and alters the function of the secretion system. Using mouse and non-human primate models, we have demonstrated that CagY is a sort of molecular rheostat that “tunes” the host inflammatory response, and likely contributes to persistent infection.  The current focus of the lab is to address three questions regarding plasticity in the H. pylori T4SS. First, what is the mechanism by which recombination in CagY alters T4SS function? Second, how does the host immune response select cagY variants that alter T4SS function? Finally, what is the role of plasticity in the H. pylori T4SS during human infection? Determining the mechanism by which CagY functions will enhance our understanding of the effects of H. pylori on human health, and could lead to novel applications for the modulation of host cell function.

Moonens, K, Gideonsson, P, Subedi, S, Bugaytsova, J, Romaõ, E, Mendez, M, Nordén, J., Fallah, M, Rakhimova, L., Shevtsova, A, Lahmann, M., Castaldo, G, Brännström, K, Coppens, F, Lo, AW, Ny, T, Solnick, JV, Vandenbussche, G, Oscarson, S, Hammarström, L, Arnqvist, A, Berg, D, Muyldermans, S, Borén, T, Remut, H. Structural Insight in Adaptive and Redox-sensitive ABO Glycan Binding by Helicobacter pylori. Cell Host Microbe, 2016, 19:55-66.

Ozcan S, Barkauskas DA, Renee Ruhaak L, Torres J, Cooke CL, An HJ, Hua S, Williams CC, Dimapasoc LM, Han Kim J, Camorlinga-Ponce M, Rocke D, Lebrilla CB, Solnick JV. Serum glycan signatures of gastric cancer. Cancer Prev Res, 2014, 7:226-35.

Moore ME, Lam A, Bhatnagar S, Solnick JV. Environmental determinants of transformation efficiency in Helicobacter pylori. J Bacteriol. 2014,196:337-44.

Linz, B, Windsor, HM, McGraw, JJ ,Hansen, LM , Gajewski, JP,Tomsho,LP, Hake,CM, Solnick, JV,  Schuster, SC, and Marshall, BJ.  A mutation burst during the acute phase of Helicobacter pylori infection in humans and rhesus macaques.  Nat Commun. 2014, 5:4165

Barrozo, RM, Cooke, CL, Hansen, LM, Lam, AM, Gaddy, JA, Johnson, EM, Cariaga, TA, Suarez, G, Peek, RM Jr, Cover, TL, and Solnick, JV. Functional plasticity in the type IV secretion system of Helicobacter pylori. PLoS Pathogens, 2013, Feb;9(2):e1003189

Martin ME, Bhatnagar S, George MD, Paster BJ, Canfield DR, Eisen JA, Solnick, JV. The impact of Helicobacter pylori infection on the gastric microbiota of the rhesus macaque. PLoS One. 2013 Oct 8;8(10):e76375.

Cai, Lucy

Junior Specialist

Hansen, Lori

SRA III / Lab Manager

    Skoog, Emma

    Post-doctoral Researcher