Dr. Reid is a Professor in the Departments of Ophthalmology and Vision Science and Biochemistry and Cell Biology at Texas Tech University. He has extensive experience as a biochemist and cell biologist in investigating the modulation of cell growth and wound healing processes. Recently, he has undertaken investigations concerning the structure/function relationships of neuropeptides as they relate to a variety of physiological functions.
The Effect of Topical Substance-P Plus Insulin-like Growth Factor-1 (IGF-1) on Epithelial Healing After Photorefractive Keratectomy in Rabbits.
Transl Vis Sci Technol. 2018 Jan;7(1):12
Authors: Ghiasi Z, Gray T, Tran P, Dubielzig R, Murphy C, McCartney DL, Reid TW
Purpose: To determine whether topical Substance-P (SP) plus insulin-like growth factor-1 (IGF-1) can improve corneal healing after photorefractive surface ablation in a rabbit.
Methods: After a 9.0-mm corneal de-epithelialization using a combination of chemical (18% alcohol) and mechanical debridement, excimer photorefractive surface ablation was performed bilaterally in eight rabbits (16 eyes) with an 8.0-mm ablation zone and 70-μm depth. The right eye was treated with SP (250 μg/mL) and IGF-1 (25 ng/mL) in hyaluronic acid, one drop twice a day, and the other eye treated with only hyaluronic acid. The epithelial healing process was documented photographically twice a day until healing was complete. Six rabbits were sacrificed 6 weeks after photorefractive keratectomy (PRK) and corneas examined histologically.
Results: Seven of eight rabbit eyes treated with SP/IGF-1 healed in a shorter time than the untreated eye. For rabbit #6, both eyes healed at the same time. The average healing time (total time until wound closure) for the treated eyes was 99 hours, while the average healing time for the untreated eyes was 170 hours (P = 0.0490). A persistent epithelial defect was found in two of the nontreated eyes but none in the treated eyes. Corneal pathology showed some degree of epithelial separation in the central corneal wound in three out of six nontreated eyes and in just the treated eye of rabbit #6.
Conclusion: Topical SP plus IGF-1 increases the epithelial healing rate after PRK. There may have been beneficial effects upon cell adhesion as well.
Translational Relevance: Better and faster healing.
PMID: 29372114 [PubMed]
The ability of quaternary ammonium groups attached to a urethane bandage to inhibit bacterial attachment and biofilm formation in a mouse wound model.
Int Wound J. 2015 Dec 28;
Authors: Tran PL, Huynh E, Hamood AN, de Souza A, Schultz G, Liesenfeld B, Mehta D, Webster D, Reid TW
For proper wound healing, control of bacteria or bacterial infections is of major importance. While caring for a wound, dressing material plays a key role as bacteria can live in the bandage and keep re-infecting the wound. They do this by forming biofilms in the bandage, which slough off planktonic bacteria and overwhelm the host defense. It is thus necessary to develop a wound dressing that will inhibit bacterial growth. This study examines the effectiveness of a polyurethane foam wound dressing bound with polydiallyl-dimethylammonium chloride (pDADMAC) to inhibit the growth of bacteria in a wound on the back of a mouse. This technology does not allow pDADMAC to leach away from the dressing into the wound, thereby preventing cytotoxic effects. Staphylococcus aureus, Pseudomonas aeruginosa and Acinetobacter baumannii were chosen for the study to infect the wounds. S. aureus and P. aeruginosa are important pathogens in wound infections, while A. baumannii was selected because of its ability to acquire or upregulate antibiotic drug resistance determinants. In addition, two different isolates of methicillin-resistant S. aureus (MRSA) were tested. All the bacteria were measured in the wound dressing and in the wound tissue under the dressing. Using colony-forming unit (CFU) assays, over six logs of inhibition (100%) were found for all the bacterial strains using pDADMAC-treated wound dressing when compared with control-untreated dressing. The CFU assay results obtained with the tissues were significant as there were 4-5 logs of reduction (100%) of the test organism in the tissue of the pDADMAC-covered wound versus that of the control dressing-covered wound. As the pDADMAC cannot leave the dressing (like other antimicrobials), this would imply that the dressing acts as a reservoir for free bacteria from a biofilm and plays a significant role in the development of a wound infection.
PMID: 26712337 [PubMed - as supplied by publisher]
A study on the ability of quaternary ammonium groups attached to a polyurethane foam wound dressing, to inhibit bacterial attachment and biofilm formation.
Wound Repair Regen. 2014 Dec 3;
Authors: Tran PL, Hamood AN, de Souza A, Schultz G, Liesenfeld B, Mehta D, Reid TW
Bacterial infection of acute and chronic wounds impedes wound healing significantly. Part of this impediment is the ability of bacterial pathogens to grow in wound dressings. In this study, we examined the effectiveness of a polyurethane foam wound dressings coated with poly diallyl-dimethylammonium chloride (pDADMAC-PU) to inhibit the growth and biofilm development by three main wound pathogens: Staphylococcus aureus, Pseudomonas aeruginosa and Acinetobacter baumannii, within the wound dressing. pDADMAC-PU inhibited the growth of all three pathogens. Time-kill curves were conducted both with and without serum to determine the killing kinetic of pDADMAC-PU. pDADMAC-PU killed S. aureus, A. baumannii, and P. aeruginosa. The effect of pDADMAC-PU on biofilm development was analyzed quantitatively and qualitatively. Quantitative analysis, (CFU) assay, revealed that pDADMAC-PU dressing produced more than 8 log reduction in biofilm formation by each pathogen. Visualization of the biofilms by either confocal laser scanning microscopy or scanning electron microscopy confirmed these findings. In addition, it was found that the pDADMAC-PU treated foam totally inhibited migration of bacteria through the foam for all three bacterial strains. These results suggest that pDADMAC-PU is an effective wound dressing that inhibits the growth of wound pathogens both within the wound and in the wound dressing.
PMID: 25469865 [PubMed - as supplied by publisher]
Inhibition of otopathogenic biofilms by organoselenium-coated tympanostomy tubes.
JAMA Otolaryngol Head Neck Surg. 2013 Oct;139(10):1009-16
Authors: Wang JC, Tran PL, Hanes R, Cordero J, Marchbanks J, Reid TW, Colmer-Hamood JA, Hamood AN
IMPORTANCE: Tube occlusion and post-tympanostomy tube otorrhea (PTTO) are 2 major sequelae of tympanostomy tube placement. Plugging negates the function of the tympanostomy tubes and, along with chronic PTTO, can be financially burdensome owing to repeated surgical procedures and additional treatments.
OBJECTIVE: To investigate the effectiveness of an organoselenium (OSe) coating on Donaldson tympanostomy tubes in inhibiting biofilm formation on the tympanostomy tubes.
DESIGN: In vitro microbiologic study; all experiments were performed in a Texas Tech University Health Sciences Center basic sciences laboratory.
INTERVENTIONS: Inhibition of biofilm formation was investigated by incubating OSe-coated vs uncoated (control) tympanostomy tubes in a nutrient broth containing either Staphylococcus aureus (Sa) expressing green fluorescent protein (GFP), nontypeable Haemophilus influenzae (NTHi) expressing GFP, or Moraxella catarrhalis (Mc) for 48 hours at 37 °C. All biofilms were quantified via colony-forming unit (CFU) assays. The Sa and NTHi biofilms were visualized using confocal laser-scanning microscopy (CLSM) and analyzed using the COMSTAT program.
MAIN OUTCOMES AND MEASURES: The CFU assays, CLSM, and COMSTAT analysis revealed that compared with uncoated control tympanostomy tubes, OSe-coated tympanostomy tubes are able to inhibit Sa, NTHi, and Mc biofilm formation.
RESULTS: The Sa and NTHi developed thick mature biofilms containing considerable biomass on uncoated tympanostomy tubes as determined by CLSM and COMSTAT analysis, while the OSe coating on the tympanostomy tubes drastically inhibited biofilm formation by Sa and NTHi. Quantitative CFU analysis revealed that this reduction in biofilm formation was significant, 6 logs for Sa (P < .001) and 4 logs for NTHi (P = .02). OSe coating also inhibited biofilm formation by Mc with a 4.5-log reduction (P < .001).
CONCLUSIONS AND RELEVANCE: The OSe coating is a potential long-lasting agent to prevent biofilm development on tympanostomy tubes by otopathogens.
PMID: 24030785 [PubMed - indexed for MEDLINE]
An organoselenium compound inhibits Staphylococcus aureus biofilms on hemodialysis catheters in vivo.
Antimicrob Agents Chemother. 2012 Feb;56(2):972-8
Authors: Tran PL, Lowry N, Campbell T, Reid TW, Webster DR, Tobin E, Aslani A, Mosley T, Dertien J, Colmer-Hamood JA, Hamood AN
Colonization of central venous catheters (CVCs) by pathogenic bacteria leads to catheter-related bloodstream infections (CRBSIs). These colonizing bacteria form highly antibiotic-resistant biofilms. Staphylococcus aureus is one of the most frequently isolated pathogens in CRBSIs. Impregnating CVC surfaces with antimicrobial agents has various degrees of effectiveness in reducing the incidence of CRBSIs. We recently showed that organoselenium covalently attached to disks as an antibiofilm agent inhibited the development of S. aureus biofilms. In this study, we investigated the ability of an organoselenium coating on hemodialysis catheters (HDCs) to inhibit S. aureus biofilms in vitro and in vivo. S. aureus failed to develop biofilms on HDCs coated with selenocyanatodiacetic acid (SCAA) in either static or flowthrough continuous-culture systems. The SCAA coating also inhibited the development of S. aureus biofilms on HDCs in vivo for 3 days. The SCAA coating was stable and nontoxic to cell culture or animals. This new method for coating the internal and external surfaces of HDCs with SCAA has the potential to prevent catheter-related infections due to S. aureus.
PMID: 22123688 [PubMed - indexed for MEDLINE]
What a study of pterygia teaches us about the cornea? Molecular mechanisms of formation.
Eye Contact Lens. 2010 Sep;36(5):290-5
Authors: Reid TW, Dushku N
Experiments were carried out in the early 1990s to investigate the cell types involved in a pterygium and to determine a possible mechanism of formation. Our first experiments used monoclonal antibodies to keratins and an associated protein (vimentin), to look at the cells that compose a pterygium. These experiments demonstrated that a pterygium is the result of an abnormal limbal basal epithelial stem cell that moves onto Bowman's layer and brings about the dissolution of this layer. More importantly, these data showed that the clear corneal epithelial cells in front of the pterygium also contained these abnormal limbal cells, which we named the pterygium cell. This demonstrated that when a pterygium is removed, a wide area of what appears to be normal epithelium must be removed to inhibit reoccurrence of the growth. Later experiments using expressed sequence tag analysis of an un-normalized unamplified complementary DNA library from surgically removed pterygia were compared with normal cornea and confirmed the role of the epithelial cells in this growth. The gene expression studies also showed that genes involved in cellular migration are stimulated, and this led to studies on polyamine analogs as inhibitors of pterygial migration. Immunohistochemical studies with antibodies to matrix metalloproteinases (MMPs) showed that it is the pterygium cell that produces the MMPs that dissolve Bowman's layer resulting in the growth stimulation of stromal fibroblasts. This led to experiments on the use of MMP inhibitors to inhibit the growth of pterygia.
PMID: 20724855 [PubMed - indexed for MEDLINE]
Doxycycline's effect on ocular angiogenesis: an in vivo analysis.
Ophthalmology. 2010 Sep;117(9):1782-91
Authors: Cox CA, Amaral J, Salloum R, Guedez L, Reid TW, Jaworski C, John-Aryankalayil M, Freedman KA, Campos MM, Martinez A, Becerra SP, Carper DA
PURPOSE: To determine the in vivo effect of doxycycline on choroidal angiogenesis and pterygium growth by using a choroidal neovascular (CNV) murine model, a directed in vivo angiogenesis assay (DIVAA) and a pterygium murine model.
DESIGN: Experimental study.
PARTICIPANTS: Three murine models were investigated with 4 mice minimum per group and 22 maximum per group.
METHODS: Mice received water with or without doxycycline. For the CNV, the neovascular lesion volume was determined in choroid-retinal pigment epithelial flat mounts using confocal microscopy 7 days after laser induction. For DIVAA, silicone capsules containing 10,000 human pterygium epithelial cells were implanted in the flanks of mice subcutaneously. After 11 days, neovascularization (NV) was quantified using spectrofluorometry after murine tail-vein injection of fluorescein isothiocyanate-labeled dextran. A pterygium epithelial cell model was developed by injecting 10,000 human pterygium epithelial cells in the nasal subconjunctival space in athymic nude mice. Doxycycline was started on day 6 at 50 mg/kg per day; corneal lesions that resulted from the injections were compared at days 6 and 15.
MAIN OUTCOME MEASURES: The Student t-test was used to evaluate the data for the CNV and DIVAA models and histologic preparations were used to evaluate pterygia lesions.
RESULTS: There was significantly less NV and lesion volume with doxycycline taken in drinking water versus plain water. With doxycycline treatment, the laser-induced CNV showed a maximal 66% decrease in choroidal blood vessel volume (P< or =0.008) and the DIVAA showed a 30% reduction of blood vessel growth and migration (P<0.004). Histologic preparations demonstrated that pterygium cell lesions regressed when mice were administered doxycycline for 9 days.
CONCLUSIONS: Doxycycline significantly inhibited angiogenesis in 3 murine models. The most dramatic effect was found in the CNV model followed by the pterygia epithelial cell DIVAA model. The anterior segment pterygium model also showed regression histologically. This suggests that doxycycline may be successful as an adjunctive treatment for CNV and pterygia in humans; clinical trials would be necessary to determine if there is a benefit.
PMID: 20605212 [PubMed - indexed for MEDLINE]