Tamara K. Redman

University of Alabama at Birmingham, Birmingham, Alabama, United States

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Publications (5)49.15 Total impact

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    ABSTRACT: To elucidate the role of mucosal macrophages in intestinal human cytomegalovirus (HCMV) disease, primary lamina propria macrophages (LPM) were isolated from normal human jejunum, infected with HCMV, and studied for their cytokine responses. HCMV infection of LPM was confirmed by the presence of HCMV IE72 (UL123), pp65 (UL83), and glycoprotein B (UL55) proteins, which were detected by immunofluorescence, beginning at postinfection (pi) day 3, and were sustained through pi day 12 in 0.1%-0.5% of LPM. The late protein pp28 (UL99) was also detected up to pi day 12, consistent with productive infection. HCMV infection in LPM was characterized by quantitative competitive polymerase chain reaction, with maximum levels of HCMV DNA detected at pi day 7. HCMV infection of the LPM augmented lipopolysaccharide-inducible chemokine (interleukin [IL]-8 and macrophage inflammatory protein-1alpha) and cytokine (IL-6) production. These findings suggest that mucosal macrophages, via enhanced mediator production, play an important role in intestinal inflammation associated with HCMV infection.
    The Journal of Infectious Diseases 04/2002; 185(5):584-90. DOI:10.1086/339007 · 5.78 Impact Factor
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    ABSTRACT: To create an allergy model in the dog, allergic Beagles with high levels of serum immunoglobulin E (IgE) and eosinophilia were bred; resulting puppies were sensitized to ragweed by intraperitoneal (IP) injection within 24 hours of birth through 22 weeks of age. At least 50% of the puppies developed high levels of serum IgE and eosinophilia. As young adults, 6 of these dogs, and 6 control age-matched, nonallergic, nonimmunized dogs were exposed by inhalation to ragweed twice at 13-day intervals, and a third time 45 days later. Total and ragweed-specific serum IgE and ragweed-specific serum IgG were increased significantly in allergic dogs relative to baseline. Allergic dogs had significantly greater levels of antibody specific for ragweed, as well as higher eosinophil counts in the bronchoalveolar lavage fluid, compared to nonallergic dogs. Airway reactivity to histamine in allergic, but not nonallergic dogs, increased significantly after aerosol exposure to ragweed. After a third exposure to ragweed, airway responses to histamine were elevated in the allergic dogs and remained high for at least 5 months. These results demonstrate the potential of the allergic dog model for investigating the underlying pulmonary immune mechanisms and therapeutic treatment of allergic asthma.
    Experimental Lung Research 01/2001; 27(5):433-51. DOI:10.1080/019021401300317143 · 1.75 Impact Factor
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    ABSTRACT: A hallmark of asthma is mucin overproduction, a condition that contributes to airway obstruction. The events responsible for mucin overproduction are not known but are thought to be associated with mediators of chronic inflammation. Others have shown that T-helper 2 (Th2) lymphocytes are required for mucous cell metaplasia, which then leads to mucin overproduction in animal models of allergy. We hypothesized that Th2 cell mediators are present in asthmatic airway fluid and directly stimulate mucin synthesis in airway epithelial cells. Results in cultured airway epithelial cells showed that samples of asthmatic fluid stimulated mucin (MUC5AC) synthesis severalfold more potently than non-asthmatic fluid. Consistent with this, lavage fluid from the airways of allergen-challenged dogs stimulated mucin synthesis severalfold more potently than that from non-allergen-challenged dogs. Fractionation of dog samples revealed 2 active fractions at <10 kDa and 30-100 kDa. Th2 cytokines in these molecular weight ranges are IL-9 (36 kDa), IL-5 (56 kDa), and IL-13 (10 kDa). Antibody blockade of ligand-receptor interaction for IL-9 (but not IL-5 or IL-13) inhibited mucin stimulation by dog airway fluid. Furthermore, recombinant IL-9, but not IL-5 or IL-13, stimulated mucin synthesis. These results indicate that IL-9 may account for as much as 50-60% of the mucin-stimulating activity of lung fluids in allergic airway disease.
    Journal of Clinical Investigation 11/1999; 104(10):1375-82. DOI:10.1172/JCI6097 · 13.77 Impact Factor
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    ABSTRACT: To evaluate the role of tumor necrosis factor alpha (TNF-alpha), a key inflammatory cytokine, in cytomegalovirus-associated gastrointestinal disease, we quantitated the level of TNF-alpha messenger RNA (mRNA) in esophageal mucosa from patients with cytomegalovirus-associated esophagitis and acquired immunodeficiency syndrome. Four patients underwent endoscopic biopsy of their cytomegalovirus-associated esophageal ulcers before and after ganciclovir therapy. The level of TNF-alpha mRNA in coded esophageal specimens was assessed by in situ hybridization, reverse-transcription polymerase chain reaction, and quantitative polymerase chain reaction. Esophageal mucosa from 3 patients whose ulcers healed or markedly improved contained before therapy numerous macrophages expressing TNF-alpha mRNA and high tissue levels of TNF-alpha mRNA that decreased substantially or were not detectable after therapy. In contrast, esophageal specimens from the single patient whose ulcer worsened after therapy contained many mucosal macrophages expressing TNF-alpha mRNA before as well as after therapy, and the high number of molecules of TNF-alpha mRNA present in the tissue before therapy increased further after treatment. Increased macrophage production and high tissue levels of TNF-alpha mRNA are associated with cytomegalovirus-associated esophageal ulcers and probably contribute to the inflammatory response associated with cytomegalovirus-induced gastrointestinal disease.
    Gastroenterology 01/1998; 114(1):77-82. · 13.93 Impact Factor
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    ABSTRACT: Background & Aims: To evaluate the role of tumor necrosis factor α (TNF-α), a key inflammatory cytokine, in cytomegalovirus-associated gastrointestinal disease, we quantitated the level of TNF-α messenger RNA (mRNA) in esophageal mucosa from patients with cytomegalovirus-associated esophagitis and acquired immunodeficiency syndrome. Methods: Four patients underwent endoscopic biopsy of their cytomegalovirus-associated esophageal ulcers before and after ganciclovir therapy. The level of TNF-α mRNA in coded esophageal specimens was assessed by in situ hybridization, reverse-transcription polymerase chain reaction, and quantitative polymerase chain reaction. Results: Esophageal mucosa from 3 patients whose ulcers healed or markedly improved contained before therapy numerous macrophages expressing TNF-α mRNA and high tissue levels of TNF-α mRNA that decreased substantially or were not detectable after therapy. In contrast, esophageal specimens from the single patient whose ulcer worsened after therapy contained many mucosal macrophages expressing TNF-α mRNA before as well as after therapy, and the high number of molecules of TNF-α mRNA present in the tissue before therapy increased further after treatment. Conclusions: Increased macrophage production and high tissue levels of TNF-α mRNA are associated with cytomegalovirus-associated esophageal ulcers and probably contribute to the inflammatory response associated with cytomegalovirus-induced gastrointestinal disease.GASTROENTEROLOGY 1998;114:77-82
    Gastroenterology 01/1998; 114(1):77-82. DOI:10.1016/S0016-5085(98)70635-3 · 13.93 Impact Factor