Pamela Hall Laboratory
Associate Professor: Pharmaceutical Sciences
Contact the Laboratory
Lab Physical Address
2705 Frontier Ave Suite 208
Lab Mailing Address
Department of Pharmaceutical Sciences
1 University of New Mexico
Albuquerque, NM 87131-0001
Phone: (505) 925-4635
Fax: (505) 925-4549
Staphylococcus aureus bacteria commonly colonize a large percentage of the population. Historically known as an agent of nosocomial infection (hospital-acquired) in patients with predisposing health conditions, recent years have witnessed a dramatic rise in S. aureus infections in apparently healthy individuals in the community setting (community-acquired). Further complicating this problem, S. aureus has acquired resistance genes which protect the bacterium from frequently utilized methicillin-type antibiotics. These strains, known as methicillin-resistant Staphylococcus aureus (MRSA), are seen in both hospital-acquired (HA-MRSA) and community-acquired (CA-MRSA) infections. MRSA has recently been highlighted in the press due to its impact on both public health and on the added financial burden to patient care.
The rise in CA-MRSA infections is due to changes in virulence of strains causing the infections, but previously unidentified defects in innate defense mechanisms of otherwise healthy individuals may also contribute. In this regard, our lab is interested in understanding how our innate immune system defends us against invasive infection by S. aureus, particularly by CA-MRSA. S. aureus utilizes a peptide-pheromone based communication system, called quorum-sensing, to switch from an adherent colonizing phenotype to a virulent phenotype capable of causing invasive infection. The peptide pheromones responsible for signaling this change in virulence are referred to as autoinducing peptides or AIPs. It was recently demonstrated that apolipoprotein B (apoB), a component of both very-low density lipoprotein (VLDL) and low density lipoprotein (LDL) particles, can bind to AIPs and prevent the switch to an invasive bacterial phenotype. We are currently addressing the molecular mechanism by which apoB antagonizes quorum sensing. This information will provide insight into the role of this molecule as an innate defense protein and possibly provide clues to identification of therapeutic inhibitors of MRSA quorum sensing.
A Selection of Our Publications
Daly SM, Joyner JA, Triplett KD, Elmore BO, Pokhrel S., Frietze K, Peabody D, Chackerian B and PR Hall. (2017) VLP-based vaccine induces immune control of Staphylococcus aureus virulence regulation. Scientific Reports, 2017 Apr 4;7(1):637. doi: 10.1038/s41598-017-00753-0.
Manifold-Wheeler BC, Elmore BO, Triplett KD, Otto M and PR Hall. (2016) Serum lipoproteins are critical for pulmonary innate defense against Staphylococcus aureus quorum sensing. J Immunol. 2016 Jan 1;196(1):328-35.
Castleman MJ, Febbraio M and PR Hall. (2015) CD36 is essential for regulation of the host response to Staphylococcus aureus alpha-toxin-mediated dermonecrosis. J Immunol. 2015 Sep 1;195(5):2294-302.
Elmore BO, Triplett KD and PR Hall. (2015) Apolipoprotein B48, the structural component of chylomicrons, is sufficient to antagonize Staphylococcus aureus quorum-sensing. PLoS One. May 5;10(5):e0125027. doi: 10.1371/journal.pone.0125027.
Daly, S.M., Elmore, B.O., Kavanaugh, J.S., Triplett, K.D., Figueroa, M., Raja, H.A., El-Elimat, T., Crosby, H.A., Femling, J.K., Cech, N.B., Horswill, A.R.,Oberlies, N.H. and P.R. Hall. (2015) ω-Hydroxyemodin Limits Staphylococcus aureus Quorum Sensing-Mediated Pathogenesis and Inflammation. Antimicrobial Agents and Chemotherapy. April 2015 ; 59:4 2223-2235.
O’Rourke J.P., Daly S.M., Triplett K.D., Peabody D., Chackerian B. and P.R. Hallmar. (2014) Development of a mimotope vaccine targeting the Staphylococcus aureus quorum sensing pathway. PLoS One. Nov 7;9(11):e111198. doi: 10.1371/journal.pone.0111198.