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Abdul N. Hamood, PhD

Abdul N. Hamood, PhD

Professor

Department of Immunology and Molecular Microbiology
Phone: 806.743.4057
Lab: 806.743.1707
Fax: 806.743.2334
Abdul N. Hamood, PhD

Biography

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.

Research

 

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. 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 these genes.
  2. 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.

Laboratory Techniques

  1. Molecular biology techniques including microarray and realt time PCR
  2. In vitro wound biofilm models
  3. Assays for different Pseudomonas aeruginosa virulence factors
  4. Animal models including the murine model of Psudomonas aeruginosa sepsis, the murine model of bacterial biofilms, and the chinchilla model of ear infection

Selected Publications

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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

Publications

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

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