<--Back to Faculty Listing
Abdul N. Hamood, PhD
Department of Immunology and Molecular Microbiology
Abdul N. Hamood, PhD
Abdul Hamood received his B.S. degree in veterinary medicine and surgery from the
University of Baghdad, Iraq, in 1977. He received his M.S. degree in veterinary medicine
from the University of Missouri, Columbia, USA, in 1984 and his Ph.D. degree in medical
microbiology from the School of Medicine at the same institution in 1985. He was a
Research Fellow at the University of Rochester, Rochester, New York, NY, USA, from
1986 to 1990. In 1991, he was pointed as an Assistant Professor at the Department
of Microbiology and Immunology at Texas Tech University Health Sciences Center, Lubbock,
Tex, USA. Currently, he serves as a Professor at the same department. His research
is focused on the pathogenesis of Pseudomonas aeruginosa infections.
Our research interests involve the regulation of Pseudomonas aeruginosa, virulence genes, and the inhibition of biofilm development by bacterial pathogens.
A. Regulation of P. aeruginosa virulence genes:
- 1. Global regulation of P. aeruginosa genes by ptxR: P. aeruginosa is an opportunistic pathogen that causes serious infections in patients with cystic
fibrosis (CF), severe burns, and immunosuppression, including patients with HIV infections
and neonates. P. aeruginosa produces several cell-associated and extracellular virulence factors. Cell-associated
factors include alginate, pili, and lipopolysaccharide, while extracellular factors
include exotoxin A, exoenzyme S, elastase, phospholipase C, and the siderophores.
Exotoxin A is an ADP-ribosyl tranferase enzyme that interferes with the protein synthesis
process, and causes cell death. We have isolated a P. aeruginosa gene, ptxR, which enhances toxA at the transcription level. Further studies confirmed that PtxR
is a global regulator that regulates the expression of several of P. aeruginosa virulence genes. PtxR regulates the expression of many of these genes through the
density dependent cell-to-cell communication, or quorum sensing (QS) systems. Transcriptional
studies revealed that PtxR regulates the expression of all components of the QS systems.
The effect of ptxR on the QS system is unique in that it enhances the expression of
certain genes but represses the expression of others (See Image 1). We are currently investigating the specific mechanism(s) through which PtxR regulates
- Serum albumin alters the expression of Pseudomonas aeruginosa iron controlled genes: The production of P. aeruginosa virulence factors systemically and certain infection sites is likely to be influenced
by serum. During systemic infections and within infected wounds, P. aeruginosa is exposed to serum or components of serum. We analyzed the effect of serum on the
expression of P. aeruginosa genes using microarray experiments. Serum influenced global gene expression in P. aeruginosa at the early exponential phase of growth. Serum enhanced the expression of 154 genes,
many of which are iron-controlled. The mechanism of enhancement appears to be independent
of iron and the ferric uptake regulator Fur. Serum also influences the expression
of different QS genes. Our goal is to define the complicated network through which
serum regulates the expression of these genes.
B. Inhibiting the development of bacterial biofilms on medical devices:
Within different sites (including burn wounds), infecting microorganisms often exist
in specific structures termed biofilms. Mature biofilms are usually described as mushroom-shaped
multicellular structures with channels that presumably function in delivering nutrients
and removing wastes. Within the biofilm, the microorganisms are surrounded by a glycocalyx
composed of a combination of an extracellular matrix (EPS) that is produced by the
microorganisms and the host surrounding tissues and protect the bacteria from the
effect of different antibiotics. Due to the alarming rate at which antibiotic resistant
strains emerge, we are testing alterative novel approaches to prevent the development
of bacterial biofilms and/or eliminating them. Previous studies have shown that selenium
(Se) bound to a solid matrix retains its ability to catalyze the formation of superoxide
radicals (O2 •¯). These superoxide radicals interfere with bacterial attachment to
solid surfaces. In collaboration with Dr. Ted Reid (department of Ophthalmology, TTUHSC),
Spire Corporation, Bedford, MA, and Selenium Ltd., Austin, TX, we investigated the
effectiveness of selenocyanatodiacetic acid (SCAA) in inhibiting the development of
S. aureus biofilms on hemodialysis catheters. The inner and outer surfaces of hemodialysis
catheters were coated with SCAA and the efficacy of coated catheters in inhibiting
S. aureus biofilms in vitro and in vivo was examined. S. aureus developed biofilms on both sides of uncoated catheters but not on SAA-coated ones.
Similarly, using the modified murine model of chronic biofilm infection, we confirmed
that S. aureus failed to develop a biofilm on either side of the SCAA-coated catheters in vivo (See Image 2). Currently, we are investigating the effectiveness of Selenium coating in inhibiting
the development of bacterial biofilms on other medical devices.
- Molecular biology techniques including microarray and realt time PCR
- In vitro wound biofilm models
- Assays for different Pseudomonas aeruginosa virulence factors
- Animal models including the murine model of Psudomonas aeruginosa sepsis, the murine model of bacterial biofilms, and the chinchilla model of ear infection
- Carty NL, Layland N, Colmer-Hamood JA, Calfee MW, Pesci EC, Hamood AN. 2006. PtxR modulates the expression of QS-controlled virulence factors in the Pseudomonas aeruginosa strain PAO1. Mol. Microbiol. 61(3):782-794.
- Davinic M, Carty NL, Colmer-Hamood JA, San Francisco M, Hamood AN. 2009. The Role of Vfr in Regulating Exotoxin A Production by Pseudomonas aeruginosa. Microbiology 155:2265-2273.
- Hammond AA, Miller KG, Kruczek CJ, Dertien J, Colmer-Hamood JA, Griswold JA, Horswill
AR, Hamood AN. 2011. An in vitor biofilm model to examine the effect of antibiotic ointments on biofilms produced
by burn wound bacterial isolates. Burns 37: 312-321.
- Tran, PL, Reid, TW, Lowry, N., Campbell, T., Webster, DR, Tobin, E, Aslani, A., Mosley,
T., Cortez, J., Dertien, J., Colmer A. Hamood, J., and Hamood, AN.. 2012. An organo-selenium inhibits S. aureus biofilms on hemodialysis catheters in vivo. Antimicrobial.Agent Chemother 56(2):972-978.
- Kruczek C, Wachtel M, Alabady MS, Payton PR, Colmer-Hamood JA, Hamood AN. 2012. Serum albumin alters the expression of Pseudomonas aeruginosa iron-controlled genes. Microbiology Epub ahead of print 2011 Nov 3
For a list of publications by Abdul N. Hamood in PubMed click here
For a more complete list of publications by Abdul N. Hamood in Scopus click here