Publications by authors named "Lisa B Mamo"

Article Synopsis
  • Pemphigus foliaceus (PF) is an autoimmune skin disease in dogs, marked by pustules and caused by IgG autoantibodies targeting desmocollin-1 (DSC1), which is crucial for skin cell adhesion.
  • Previous research indicated that passive transfer of these autoantibodies can induce skin disease, but the recruitment of neutrophils remained unexplained.
  • Our study aimed to clarify the role of IgA autoantibodies in PF, but after removing significant amounts of IgG from dog sera, we found no increase in IgA levels, suggesting that IgA does not play a pathogenic role in this condition.
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Background: Atopic dogs often are managed with allergen-specific immunotherapy (AIT) and concurrent dosages of ciclosporin (CSA) or oclacitinib to alleviate their clinical signs. Both drugs might affect proper tolerance induction by inhibiting regulatory T-cell (Treg) induction.

Hypothesis/objectives: We evaluated Treg cell numbers and serum interleukin (IL)-10 and transforming growth factor-beta (TGF-β)1 levels in dogs diagnosed with atopic dermatitis (AD) and successfully treated with either CSA or oclacitinib for nine or more months.

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Background: Canine trunk-dominant pemphigus foliaceus (PF) is mentioned rarely in the literature.

Hypothesis/objectives: The goal of this study was to provide clinical description of trunk-dominant PF and to demonstrate the prevalence of serum antikeratinocyte, anti-desmocollin-1 (DSC1) and anti-desmoglein-1 (DSG1) antibodies, and determine their diagnostic value in this particular PF phenotype.

Materials And Methods: Clinically relevant information was collected from 31, 25 and 34 dogs with trunk-dominant and facial PF and superficial pyoderma (SP), respectively.

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Background: Circulating anti-keratinocyte immunoglobulin (Ig)G targeting desmosomal proteins have been identified in people and dogs with pemphigus foliaceus (PF). By contrast, detection attempts in PF-affected cats have been largely unsuccessful.

Hypothesis/objectives: To detect circulating anti-keratinocyte autoantibodies in PF-affected cats and determine their titres and tissue-staining patterns.

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Background: Polyautoimmunity, the concurrent expression of two or more distinct autoimmune diseases (ADs) in a single individual, is a known phenomenon in humans and has been rarely reported in dogs. To the best of the authors' knowledge, comorbid pemphigus foliaceus (PF) and generalized discoid lupus erythematosus (GDLE) has not been reported in dogs.

Hypothesis/objectives: To describe the clinical, histological and immunological features and treatment outcome of two unrelated dogs with comorbid PF and GDLE.

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Background: Hyperkeratotic erythema multiforme (HKEM) is a clinically distinct dermatosis and poorly characterized syndrome, comprised of hyperkeratotic plaques with variable symmetry and apoptosis similar to "classic" erosive canine EM. Hyperkeratotic EM has a protracted clinical course and, although treatments with glucocorticoids, azathioprine and/or ciclosporin have been tried, rates of remission are low.

Objectives: To describe successful treatment of HKEM in two dogs using oclacitinib.

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Background: Epidermolysis bullosa acquisita (EBA) is a rare autoimmune subepidermal blistering disease of dogs and humans.

Objectives: Our objectives were to describe clinical phenotypes, histopathology and treatment outcomes of canine EBA.

Animals: Twenty dogs diagnosed with EBA based on a subepidermal blister formation and collagen VII autoreactivity.

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Background: Pemphigus foliaceus (PF) is the most common IgG-mediated autoimmune skin disease in dogs. Studies of human PF have revealed the presence of other antigen-specific autoantibody isotypes, thereby uncovering new avenues of investigation of the disease pathomechanism.

Hypothesis/objectives: The aim was to obtain information about the autoantibody isotype response in canine PF.

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Objectives: This pilot study assesses the degree of hemolysis induced by cardiopulmonary bypass and determines its association with acute kidney injury in pediatric patients. Further, it evaluates the degree to which the use of urinary biomarkers neutrophil gelatinase-associated lipocalin and cystatin C correlate with the presence of acute kidney injury and hemolysis following cardiopulmonary bypass.

Design: Prospective observational study.

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Background: Red blood cell (RBC) transfusion is common in intensive care unit (ICU) patients and is associated with complications that appear related to the duration of blood storage. We hypothesize that hemolysis of stored RBCs results in increases in the availability of non-heme-bound iron, which inhibits macrophage activation.

Study Design And Methods: RBCs were sampled at multiple time points to evaluate hemolysis and iron release.

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Background: Hepcidin serves as a major regulator of systemic iron metabolism and immune function. Airway epithelial cells have an extensive interface with the environment, and so must be able to respond locally to the presence of particulates, infection, and inflammation. Therefore, we hypothesized that hepcidin is expressed in airway epithelial cells and is regulated by early phase cytokines.

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Catalytically active iron in the lung causes oxidative stress and promotes microbial growth that can be limited by intracellular sequestration of iron within ferritin. Because cellular iron uptake requires membrane ferrireductase activity that in the gut can be provided by duodenal cytochrome b (Dcytb), we sought Dcytb in the lung to test the hypothesis that it contributes to epithelial iron regulation by reducing Fe(3+) for cellular iron transport. Dcytb expression was found in respiratory epithelium in vitro and in vivo and was responsive to iron concentration.

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Antioxidant defenses in the neonatal lung are required to adapt to the oxygen (O(2))-rich postnatal environment, and oxidant/antioxidant imbalance is a predisposition to lung injury when high concentrations of inspired O(2) are used in neonatal lung diseases. The lung's main extracellular enzymatic defense against superoxide, extracellular superoxide dismutase (EC-SOD), is closely regulated during development. In testing the hypothesis that developmental change in EC-SOD expression and activity in the immature lung would be disrupted by hyperoxia, we found a doubling of lung EC-SOD protein in newborn rats exposed to 95% O(2) for 1 week.

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Extracellular superoxide dismutase (EC-SOD), which scavenges extracellular superoxide (O.), is highly regulated in the developing lung. In the prenatal rabbit, EC-SOD is predominantly intracellular and inactive, and postnatally, active EC-SOD is secreted.

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