Pamela Hall Laboratory


Principal Investigator:
Pamela Hall, PhD,
Associate Professor,
Pharmaceutical Sciences

Principal Investigator: Pamela Hall, PhD
Associate Professor: Pharmaceutical Sciences


Lab Physical Address
2705 Frontier Ave Suite 208

Lab Mailing Address
Department of Pharmaceutical Sciences
MSC09 5360
1 University of New Mexico 
Albuquerque, NM 87131-0001
Phone: (505) 925-4635
Fax: (505) 925-4549


Research Interests

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 is frequently 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 immune defense mechanisms of otherwise healthy individuals may also contribute. In this regard, our lab is interested in understanding how our immune system defends us against invasive infection by S. aureus, particularly by CA-MRSA, and how we can enhance protection. 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. We are currently pursuing a vaccine designed to produce a neutralizing antibody response to the AIPs, thus blocking virulence. Also, we have found that female mice are much more resistant to infection, and specifically to a S. aureus secreted toxin known as alpha-hemolysin (Hla).  This resistance depends on estrogen, as ovariectomized female mice are no longer protected. We are currently addressing the molecular mechanism by which female mice demonstrate resistance to Hla and infection. This information will provide insight into the role of sex in the innate immune response to S. aureus and Hla and possibly provide clues to the identification of therapeutics to increase host defense.


Recent Research

A Selection of Our Publications

Triplett KD, Pokhrel S, Castleman MJ, Daly SM, Elmore BO, Joyner JA, Sharma G, Herbert G, Campen MJ, Hathaway HJ, Prossnitz ER and PR Hall. GPER activation protects against epithelial barrier disruption by Staphylococcus aureus α-toxin (2019) Scientific Reports. Feb 4;9(1):1343. doi: 10.1038/s41598-018-37951-3.PMCID: 6362070.

Castleman MJ, Pokhrel S, Triplett KD, Kusewitt DF, Elmore BO, Joyner JA, Femling JK, Sharma G, Hathaway HJ, Prossnitz ER and PR Hall. Innate Sex Bias of Staphylococcus aureus Skin Infection Is Driven by α-Hemolysin.(2017) J Immunol. Dec 8. pii: ji1700810. doi: 10.4049/jimmunol.1700810. Epub ahead of print.

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.