Rosanna Marsella

University of Florida, Gainesville, Florida, United States

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Publications (81)149.05 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The development of atopic dermatitis (AD) and other cutaneous hypersensitivities involves the activation and differentiation of allergen-specific lymphocytes. Although hypersensitivity is often considered to be a 'T-helper 2-polarized' lymphocyte response, recent evidence suggests that clinical disease is associated with the development of multiple lymphocyte phenotypes. The purpose of this paper is to review recent advances in the understanding of the roles of lymphocytes, cytokines and noncytokine factors in the pathogenesis of canine AD. Citation databases, abstracts and proceedings from international meetings published between 2001 and 2013 were reviewed in this update. Where necessary, older articles were included for background information. The development of canine AD is associated with changes in both cutaneous and circulating lymphocyte populations. These lymphocyte responses are characterized by the production of a complex variety of cytokines, including not only T-helper 2 but also T-helper 1, T-helper 17 and regulatory T-cell responses. In addition, microarray gene expression analysis has enabled the identification of a number of noncytokine factors that appear to be associated with atopic inflammation. These include the calcium-binding protein S100A8, serum amyloid A and a number of protease inhibitors, as well as genes involved in epidermal barrier formation, innate immunity receptors, cell cycle proteins and apoptosis. The development of AD in dogs is characterized by the development of a delicate balance between a variety of T-cell phenotypes and inflammatory mediators, including cytokines, chemokines and noncytokine factors. © 2015 ESVD and ACVD.
    Veterinary Dermatology 04/2015; 26(2):124-e32. DOI:10.1111/vde.12205 · 1.99 Impact Factor
  • Veterinary Dermatology 04/2015; 26(2):77-8. DOI:10.1111/vde.12207 · 1.99 Impact Factor
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    ABSTRACT: Multiple levels of evidence support the role of genetics and the environment in the pathogenesis of canine atopic dermatitis (AD). This review summarizes the current evidence in genetics and the effect of environmental factors on the development and perpetuation of canine AD. Citation databases, abstracts and proceedings from international meetings published between 2001 and 2013 were reviewed in this update. Where necessary, older articles were included for background information. Canine AD is a heritable disease, in which interaction with environmental factors influences disease risk and phenotype. A study of British guide dogs indicated that nearly 50% of the risk of developing AD was determined by an individual's genotype. Genomic studies performed so far in canine AD have uncovered numerous gene candidates likely to be involved in pathogenesis through their role in immunity, skin barrier formation, apoptosis and inflammation. In addition to genetics, there is evidence to suggest that exposure to certain environmental factors influences the prevalence and course of canine AD. For example, living in rural areas or feeding noncommercial diets was negatively associated with the development of AD in dogs, while exposure to high levels of smoke was associated with increased prevalence of allergic skin disease. It is becoming clear that canine AD is genotypically complex and influenced by a variety of environmental factors. Well-designed studies with sufficient statistical power will be critical to identify the complex genetic and environmental factors involved in disease development and progression. Recognition of such factors may help to identify new targets for therapy and enable better disease prevention and management. © 2015 ESVD and ACVD.
    Veterinary Dermatology 02/2015; DOI:10.1111/vde.12198 · 1.99 Impact Factor
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    ABSTRACT: Many studies focusing on clinical and histological signs of canine atopic dermatitis (AD) have been published since its early descriptions decades ago. Findings of these studies contributed to our current knowledge about the disease pathogenesis and allowed establishment of diagnostic criteria used by clinicians and researchers. This review serves as an update on the clinical and histological features of canine AD published by the American College of Veterinary Dermatology Task Force on Canine Atopic Dermatitis in 2001 and summarizes the recent discoveries in these fields. The overall findings of studies focusing on clinical features mirrored those published by the Task Force in 2001. The novelty was the larger number of animals included in these studies, which allowed establishment of a new set of diagnostic criteria that exceeded the sensitivity and specificity of the previous criteria. The same study uncovered some clinical differences between dogs with food-induced and nonfood-induced AD; however, the authors concluded that these two entities cannot be distinguished based on clinical signs only. Another study demonstrated some major breed-specific phenotypes. Several publications addressed the histological features of canine AD skin lesions in experimental models of AD, but none of those addressed naturally occurring lesions. Nevertheless, the histopathological description of the skin reactions was generally similar to that published by the Task Force in 2001. Considerable work has been done in recent years to provide a better definition of the clinical appearance and histopathology of canine AD. New sets of diagnostic criteria have been developed, and additional breed-associated differences in phenotypes have been demonstrated. © 2015 ESVD and ACVD.
    Veterinary Dermatology 02/2015; DOI:10.1111/vde.12196 · 1.99 Impact Factor
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    ABSTRACT: Increased secretion of antimicrobial peptides and cytokines is present in atopic skin. The purpose of this study was to compare the production of β-defensin (cBD)3-like, cathelicidin (cCath) and cytokines in atopic and healthy canine keratinocytes. Seven atopic house dust mites (HDM) sensitive and five healthy age-matched beagles were used. Keratinocytes were stimulated for 24 hours and the supernatant collected. A significantly higher production of cBD3-like was present at baseline in atopic compared with healthy keratinocytes, but cBD3-like did not increase after stimulation. IL-17 and lipopolysaccharide increased cBD3-like in healthy compared with atopic keratinocytes. cCath increased in both groups after stimulation. Atopic keratinocytes exposed to HDM produced more IL-8 and keratinocyte-derived chemokine-like than healthy keratinocytes. Exposure to HDM induced an increased IL-8 in atopic keratinocytes and a decreased IFN-γ in healthy keratinocytes. These results may suggest an over-sensitization of atopic keratinocytes and a possible impairment of the cutaneous defense against micro-organisms. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Experimental Dermatology 02/2015; DOI:10.1111/exd.12660 · 4.12 Impact Factor
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    ABSTRACT: Canine atopic dermatitis (AD) is a common, genetically predisposed, inflammatory and pruritic skin disease. The pathogenesis of canine AD is incompletely understood. The aim of this review is to provide an in-depth update on the involvement of skin barrier and host-microbiome interaction in the pathogenesis of canine AD. Online citation databases and abstracts from international meetings were searched for publications related to skin barrier and host-microbiome interaction (e.g. bacteria, yeast, antimicrobial peptides). A total of 126 publications were identified. This review article focuses on epidermal barrier dysfunction and the interaction between cutaneous microbes (bacteria and yeasts) and the host (antimicrobial peptides). Epidemiological updates on the presence of pathogenic organisms and canine AD are also provided. Major advances have been made in the investigation of skin barrier dysfunction in canine AD, although many questions still remain. Skin barrier dysfunction and host-microbiome interactions are emerging as primary alterations in canine AD. Based on this review, it is clear that future studies focused on the development of drugs able to restore the skin barrier and increase the natural defences against pathogenic organisms are needed. © 2015 ESVD and ACVD.
    Veterinary Dermatology 02/2015; DOI:10.1111/vde.12197 · 1.99 Impact Factor
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    ABSTRACT: Canine atopic dermatitis (AD) is considered to be an immunoglobulin E (IgE)-mediated hypersensitivity response to environmental allergens. The role of other antibody isotypes and nonenvironmental allergens in disease pathogenesis remains unclear. The objective of this review is to provide an update on advances in the understanding of the relevance of specific antibody isotypes, autoallergens and nonenvironmental allergens in the pathogenesis of canine AD. Citation databases, abstracts and proceedings from international meetings published between 2001 and 2013 were reviewed. Where necessary, older articles were included for background information. Neither total nor allergen-specific IgE necessarily correlates with clinical disease in canine AD. Some dogs exhibit clinical signs that are indistinguishable from AD but have no demonstrable allergen-specific IgE (atopic-like dermatitis). Allergen-specific immunoglobulin G may be demonstrated in canine AD, but there is no evidence that this isotype plays a role in disease development. Although humans with AD may develop serum IgE against autoallergens, this finding has not been substantiated in the dog. In contrast, adverse food reactions are frequently co-associated with AD in the dog. Ingestion of food and environmental allergens may trigger exacerbations of AD. Determination of the role of IgE in the pathogenesis of canine AD still requires clarification. Clinical trials and research studies must distinguish atopic dogs with allergen-specific IgE or skin test reactivity from those without. There is no convincing evidence demonstrating a pathogenic role for either allergen-specific immunoglobulin G or autoallergens in canine AD, but food items may be triggers for disease flares in certain individuals. © 2015 ESVD and ACVD.
    Veterinary Dermatology 02/2015; DOI:10.1111/vde.12201 · 1.99 Impact Factor
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    ABSTRACT: The pathogenesis of canine atopic dermatitis (AD) involves dysfunction of the adaptive immune system. Recent evidence suggests that nonantigen-specific inflammatory elements may play a role in the development and perpetuation of canine AD. The objective of this review is to provide an update on recent advances in the understanding of the role of innate immune cells, keratinocytes, lipid metabolism and nutrition in the pathogenesis of AD in dogs. Citation databases, abstracts and proceedings from international meetings published between 2001 and 2013 are reviewed in this update. Where necessary, older articles are included for background information. Members of the innate immune system (including dendritic cells, Langerhans cells and mast cells) and keratinocytes interact with each other and with environmental antigens during both induction and effector phases of atopic inflammation. The responses of these cells and associated noncellular factors (such as complement and protease-activated receptors) to environmental stimuli influence the entire future course of the immune response to a given agent. Abnormalities in lipid metabolism may also influence the pathogenesis of canine AD via the production of inflammatory mediators and by alteration of epidermal barrier function and antigen presentation. However, a lack of fully controlled studies precludes definitive interpretation of these data. Evidence indicates that the cells and noncellular components of the innate immune system and the epidermis may play critical roles during both the sensitization and the effector phases of canine AD. Derangements in lipid metabolism may be involved in the pathogenesis of AD in dogs, but additional controlled studies are required in this area. © 2015 ESVD and ACVD.
    Veterinary Dermatology 02/2015; DOI:10.1111/vde.12199 · 1.99 Impact Factor
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    Ibrahim Ozmen, Rosanna Marsella
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    ABSTRACT: Atopic Dermatitis (AD) is a prevalent disease that affects both humans and animals. Dogs share similar environments with the owners and spontaneously develop a disease that is clinically and immunologically identical to AD in humans. In past decades AD has become more and more common in both dogs and humans, possibly due to the increased exposure to indoor allergens and decreased exposure to parasites and beneficial bacteria. The allergic component plays an important role in both species. Allergen specific immunotherapy (ASIT) has been used with great success in veterinary medicine for decades for the treatment of AD and traditionally has been accomplished with subcutaneous injections. In human medicine, ASIT has been traditionally used for respiratory manifestations of atopic disease and only recently considered for the therapy of AD. Interestingly, dogs primarily express cutaneous manifestations of atopic disease and only rarely progress from cutaneous into respiratory disease, a process referred in human medicine as “atopic march”. Recently, sublingual immunotherapy has been replacing subcutaneous immunotherapy both in human and veterinary medicine due to its ease and safety, leading to increased compliance. The purpose of this mini review is to focus on the use of sublingual immunotherapy for AD highlighting similarities and differences between humans and dogs.
    10/2014; 1(3):136-149. DOI:10.3390/vetsci1030136
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    Marsella R, Johnson C, Ahrens K
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    ABSTRACT: Atopic dermatitis (AD) is a common skin disease that affects humans and animals. Skin impairment has been described in human and canine AD. Equine AD is recognized in practice but little is known about its pathogenesis. As remarkable similarities exist across species in terms of cutaneous manifestations of AD, it was speculated that skin abnormalities may also exist in atopic horses. This case report describes the ultrastructure of the stratum corneum of two normal and two atopic horses. Biopsies were taken from sites predisposed to AD and examined using electron microscopy. Stratum corneum in normal samples was compacted with organized lipid lamellae while in atopic samples disorganized lipid lamellae, retained lamellar bodies and amorphous lipids were found. These changes are very similar to what reported in AD in other species. It is currently unknown whether these abnormalities in atopic horses are primary or secondary and their importance in allergen penetration.
    Research in Veterinary Science 10/2014; DOI:10.1016/j.rvsc.2014.06.012 · 1.51 Impact Factor
  • Rosanna Marsella
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    ABSTRACT: Allergies are common in horses. It is important to identify and correct as many factors as possible to control pruritus and make the patient comfortable. Culicoides hypersensitivity is a common component in allergic horses. The main treatment continues to be rigorous fly control and avoidance of insect bites. Environmental allergies are best addressed by early identification of the offending allergens and formulation of allergen-specific immunotherapy to decrease the need for rescue medications. Food allergy is best managed with food avoidance. Urticaria is one of the manifestations of allergic disease wherein detection of the triggering cause is essential for management.
    The Veterinary clinics of North America. Equine practice 12/2013; 29(3):551-557. DOI:10.1016/j.cveq.2013.08.006 · 1.05 Impact Factor
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    ABSTRACT: Filaggrin is a structural protein that has attracted increasing interest over the past decade for its role in the pathogenesis of human atopic dermatitis (AD). Null mutations in its sequence are considered risk factors in the development of AD. To investigate canine filaggrin mRNA and protein expression in the skin of atopic beagles with experimentally induced AD compared with breed-matched healthy control dogs. All dogs were environmentally challenged for 3 days consecutively with allergens to which the atopic dogs had been sensitized. Skin biopsy specimens were taken from six healthy and seven atopic beagles before and after allergen challenge. Canine filaggrin mRNA was measured using quantitative real-time PCR. Indirect immunofluorescence was used to localize the filaggrin protein in canine skin. Analysis of variance with Tukey's multiple comparison test (over-time effect) and unpaired Student's t-test (treatment effect) were used. Values of P ≤ 0.05 were considered significant. Analysis of variance showed a significantly higher expression of filaggrin mRNA in atopic dogs compared with healthy control dogs (P = 0.004 on day 3 and P = 0.01 on day 10) and a decreased mRNA expression on day 3 in healthy control dogs (effect of time, P = 0.006). On blinded evaluation, filaggrin immunofluorescence was distributed homogeneously in the stratum granulosum and the stratum corneum in healthy dogs. Atopic dogs showed a patchy immunofluorescence pattern, which was exacerbated after environmental challenge. Altered epidermal filaggrin mRNA expression and protein distribution was detected in this experimental model.
    Veterinary Dermatology 06/2013; 24(3):329-e73. DOI:10.1111/vde.12031 · 1.99 Impact Factor
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    C Pellicoro, R Marsella, K Ahrens
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    ABSTRACT: This study investigated the effects of a skin protectant solution (dimethicone 2%) on clinical signs and skin barrier function in canine atopic dermatitis (AD). Eighteen dogs with AD were randomly divided into two groups, one received dimethicone and the other received the vehicle (cyclomethicone) on selected areas (pinnae, groin, and axillae) daily for 4 weeks. Owners and investigators were blinded regarding group allocation. Clinical efficacy was evaluated using a scoring system and skin barrier by measuring the transepidermal water loss. Twelve dogs completed the study (50% drop rate in the vehicle and 20% in the dimethicone). For clinical signs, analysis of variance showed an effect of time (P < 0.005; day 0 > day 28) and region (axillae < groin < pinnae) but no effect of group or group × time interaction. For transepidermal water loss, analysis of variance showed only a main effect of region (axillae > pinnae > groin). Pearson found no correlation between transepidermal water loss and clinical scores. In this pilot study dimethicone had no significant effect on clinical signs and transepidermal water loss in canine atopic dermatitis.
    04/2013; 2013:239186. DOI:10.1155/2013/239186
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    ABSTRACT: Atopic dermatitis (AD) results from complex interactions between an impaired skin barrier and immunological stimulation. Filaggrin is a key protein for the skin barrier, and its expression is decreased in subsets of atopic dogs and can be modified by inflammation; thus, immunomodulatory approaches may alter its expression. Probiotics have been explored for the prevention and treatment of allergies, owing to their immunomodulatory properties; however, it is currently unknown whether they can modulate filaggrin expression. The purpose of this study was to evaluate whether probiotics can modulate filaggrin expression in an experimental model of canine AD. Eighteen atopic (11 probiotic exposed and seven control) and five normal beagles were challenged for three consecutive days with Dermatophagoides farinae. Skin biopsies were taken before (day 0), at the peak (day 3) and after the end of the allergen challenge (day 10). Immunohistochemistry for filaggrin was done using a polyclonal antibody specific for canine filaggrin, and staining was scored both subjectively (for intensity, granularity and continuity) and objectively, by tracing the stratum granulosum and calculating the percentage of filaggrin per unit traced area. Analysis of variance of the percentage of filaggrin in the stratum granulosum showed a significant effect of group (P = 0.0414, AD < normal), time (P = 0.0066, days 3 and 10 > day 0) and marginal group × time interaction (P = 0.0606). Within the atopic group, exposure to probiotics did not change filaggrin expression. No significant differences were found in the subjective scores among groups. It is concluded that probiotic exposure early in life does not alter filaggrin expression in this AD model.
    Veterinary Dermatology 04/2013; 24(2):260-e57. DOI:10.1111/vde.12006 · 1.99 Impact Factor
  • Rosanna Marsella
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    ABSTRACT: BACKGROUND: Filaggrin expression is decreased in subsets of humans and dogs with atopic dermatitis (AD). Filaggrin expression is modulated by inflammation, but it is unknown whether expression is inversely correlated with clinical signs. HYPOTHESIS/OBJECTIVES: To investigate the correlation between filaggrin expression and the severity of clinical signs in an experimental model of canine AD. ANIMALS: Eighteen atopic research beagle dogs sensitized to house dust mite allergens. METHODS: Dogs were challenged with house dust mites for 3 days consecutively (days 1-3) and skin biopsies collected on days 1 (before allergen challenge), 3 (peak of challenge) and 10 (at resolution of lesions). Clinical signs were scored using a modified version of CADESI-03, the Canine Atopic Dermatitis Extent and Severity Index. Immunohistochemical staining was measured subjectively by three investigators who graded filaggrin staining for continuity, granularity and intensity. For objective evaluation of staining, the stratum granulosum and epidermis were traced, and the percentage of filaggrin per unit stratum granulosum and epidermal area were calculated. Correlations were investigated using Pearson's product-moment correlation (for linear correlations) and Spearman's rank correlation (for nonlinear correlations), pooling all days together and then separately on each day, using total clinical scores and either subjective or objective filaggrin scores. RESULTS: The only significant correlation was found between the subjective filaggrin scores and total clinical scores on day 1. CONCLUSIONS AND CLINICAL IMPORTANCE: No inverse correlation exists between the severity of clinical signs and filaggrin expression; the clinical relevance of filaggrin in canine AD is unknown.
    Veterinary Dermatology 02/2013; 24(2). DOI:10.1111/vde.12007 · 1.99 Impact Factor
  • Rosanna Marsella
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    ABSTRACT: Skin barrier dysfunction exists in both human and canine atopic dermatitis, leading to increased water loss and potentially facilitating allergen penetration and sensitization. Both lipid (e.g. ceramides) and protein (e.g. filaggrin) abnormalities have been described. Some are genetically inherited (e.g. filaggrin mutations are one of the major risk factors in humans) and some are secondary and linked to inflammation. In humans, numerous studies have shown efficacy of emollients and moisturizers in barrier restoration, and this approach has been for years the mainstay of therapy. Recently, this strategy has shown promise as a preventative function. In veterinary medicine, evidence regarding skin barrier impairment is rapidly building. Decreased ceramides and filaggrin (in some subsets of dogs) have been described. Altered metabolism of ceramides has also been proposed. Despite these preliminary data and the availability of products marketed to improve the skin barrier, evidence regarding the clinical benefit of skin repair intervention is still limited. Preliminary studies have demonstrated that topical application of fatty acids and ceramides and systemic administration of fatty acids improve lipid deficiencies in the skin of dogs with atopic dermatitis, but limited clinical evidence exists. Disease remission in humans is paralleled by an improved skin barrier, both with calcineurin inhibitors and glucocorticoids. In veterinary medicine, a preliminary study on ciclosporin and prednisone failed to detect significant improvement of water loss, while successful immunotherapy correlated with an improved skin barrier. Controlled, large studies are needed to address the question of which skin repair approach is clinically most effective and whether this can be used as a preventative strategy.
    Veterinary Dermatology 02/2013; 24(1):73-e18. DOI:10.1111/j.1365-3164.2012.01073.x · 1.99 Impact Factor
  • Journal of the American Veterinary Medical Association 07/2012; 241(2):194-207. DOI:10.2460/javma.241.2.194 · 1.67 Impact Factor
  • Rosanna Marsella
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    ABSTRACT: Cutaneous impairment plays a crucial role in atopic dermatitis (AD). Transepidermal water loss (TEWL) measurement is an indirect assessment of skin barrier function and correlates with disease severity in humans. Skin impairment also exists in canine AD; however, concerns exist regarding variability and reliability of TEWL measurements in dogs. The purposes of this retrospective study were twofold: first, to investigate the correlation between severity of dermatitis [measured by Canine Atopic Dermatitis Extent and Severity Index (CADESI)] and TEWL; and second, to evaluate whether increased TEWL at a young age correlates with disease severity later in life. Data from atopic beagles and dogs with natural AD were analysed. Transepidermal water loss was measured in atopic beagles (n=24) with an open chamber and in dogs with naturally occurring AD with a closed chamber device (two studies, with n=14 and n=18). Pearson product-moment correlation was used for analyses. Transepidermal water loss of the inguinal region, axilla, antebrachial flexure and pinna was analysed. Correlations were investigated for each study, separately first and then jointly. They included CADESI and TEWL of individual regions, total CADESI and total TEWL of all measured regions, and total CADESI and TEWL of key regions. In atopic beagles, TEWL measured at 1 year of age pre- and post-allergen challenge was correlated with CADESI at 1, 3 and 6 years of age. Overall, low correlation coefficients were found; therefore, a biologically relevant connection could not be demonstrated. The main significant positive correlation was found between TEWL in the pinna and total CADESI. It is concluded that TEWL does not correlate with disease severity.
    Veterinary Dermatology 06/2012; 23(3):238-e49. DOI:10.1111/j.1365-3164.2012.01055.x · 1.99 Impact Factor
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    Rosanna Marsella, Domenico Santoro, Kim Ahrens
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    ABSTRACT: Probiotics modulate the immune response and may have protective effects against atopic dermatitis (AD). Clinical trials using dogs with spontaneous disease are limited by confounding factors such as different diets, environments and sensitizations while a more controlled evaluation is possible using experimental models. A validated model of canine AD showed that early exposure to Lactobacillus rhamnosus GG (LGG) significantly decreases allergen-specific IgE and partially prevents AD in the first 6 months of life. This study is a follow-up three years after discontinuation of LGG. Clinical signs were evaluated after allergen challenge with ragweed, timothy, Dermatophagoides farinae. Allergen-specific IgE, IL-10 and TGF-β were measured on the 1st day of challenge, before allergen exposure. Normal dogs were included as controls. Analyses included seven dogs in the non-probiotic and nine in the probiotic litter. For clinical scores, a 2-Group × 9-Time Analysis of Variance showed significant effects of group (p=0.0003, probiotic<controls), time (p<0.0001) and group × time interaction (p<0.0001). IL-10 for all allergens was significantly higher in the control group than probiotics-exposed dogs. Allergen-specific IgE and TGF-β did not differ between litters. Early exposure to probiotics has long-term clinical and immunological effects in this model and larger studies using dogs with spontaneous disease are needed.
    Veterinary Immunology and Immunopathology 03/2012; 146(2):185-9. DOI:10.1016/j.vetimm.2012.02.013 · 1.75 Impact Factor
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    ABSTRACT: Antimicrobial peptides (AMPs) are small immuno-modulatory proteins important in defense against pathogenic organisms. Defensins and cathelicidin are the most frequently studied human AMPs. An increase in AMPs in atopic humans has been reported recently. Our goals were to determine the distribution of AMPs and evaluate their mRNA and protein expression in non-lesional (Day 0), acute lesional skin (Day 3) and post-challenged skin after resolution of skin lesions (Day 10) using a canine model of atopic dermatitis (AD). All dogs were environmentally challenged for three consecutive days with house dust mite. Clinical evaluation of atopic beagles was performed using a CADESI score at each time point before and after environmental challenge. Skin biopsies were taken from six healthy and seven atopic beagles before and after allergen challenge (Day 0, Day 3 and Day 10). The transcription of canine cathelicidin (cCath) and beta-defensins (cBD)-1, -2 and -3 mRNA was quantified using quantitative-RT-PCR while the protein distribution of cBD2, cBD3 and cCath was detected by indirect immunofluorescence. A significant effect, over-time, was seen in CADESI score in AD beagles with an increase score after challenge (Day 3). Quantitative analysis showed a significant difference in mRNA transcript levels between groups (with atopic dogs having more than controls) for all AMPs but cBD2. No effect over time was evident for either group. No significant differences were seen for the AMP protein patterns of distribution (homogenous distribution). Although, these results showed no differences in AMP's localization after allergen exposure in each group; atopic dogs had a higher mRNA expression of AMPs when compared with healthy dogs, a similar finding to humans.
    Veterinary Immunology and Immunopathology 08/2011; 144(3-4):382-8. DOI:10.1016/j.vetimm.2011.08.004 · 1.75 Impact Factor

Publication Stats

1k Citations
149.05 Total Impact Points

Institutions

  • 1997–2015
    • University of Florida
      • • Department of Small Animal Clinical Sciences
      • • College of Veterinary Medicine
      Gainesville, Florida, United States
  • 2014
    • Çorlu Military Hospital
      Tzirallum, Tekirdağ, Turkey
  • 2010
    • Cornell University
      • Department of Clinical Sciences
      Итак, New York, United States