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ORIGINAL ARTICLE
Year : 2020  |  Volume : 33  |  Issue : 3  |  Page : 1041-1044

Tissue expression of endothelial selectin in patients with atopic dermatitis


1 Department of Dermatology, Andrology and STDs, Faculty of Medicine, Menoufia University, Shebeen El-Kom, Egypt
2 Department of Pathology, Faculty of Medicine, Menoufia University, Shebeen El-Kom, Egypt
3 Dermatology at Ministry of Health, Damanhour, Egypt

Date of Submission28-Feb-2019
Date of Decision12-Mar-2019
Date of Acceptance08-Apr-2019
Date of Web Publication30-Sep-2020

Correspondence Address:
Sawsan S Allam
Dermatology at Ministry of Health, Damanhour, Behera
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mmj.mmj_72_19

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  Abstract 


Objective
To investigate the role of endothelial selectin (E-selectin) in atopic dermatitis (AD) through evaluation of the immunohistochemical expressions in lesional skin biopsies.
Background
AD is a chronic, pruritic inflammatory skin disease that occurs most frequently in children. In AD, the inflammatory cascade is initiated by the release of proinflammatory cytokines from atopic keratinocytes.
Patients and methods
A total of 50 patients with AD and 10 healthy control participants were included in this case–control study. From all participants, skin biopsies were taken, and immunohistochemical staining by E-selectin monoclonal antibodies was done.
Results
There were significant elevations in E-selectin cellular localization (P = 0.01) as well as dermal inflammatory infiltrates in AD cases than controls.
Conclusion
E-selectin participates in AD pathogenesis.

Keywords: atopic dermatitis, endothelial selectin, immunohistochemistry


How to cite this article:
Farag AG, Sharaky DR, El-Shafey EN, Allam SS. Tissue expression of endothelial selectin in patients with atopic dermatitis. Menoufia Med J 2020;33:1041-4

How to cite this URL:
Farag AG, Sharaky DR, El-Shafey EN, Allam SS. Tissue expression of endothelial selectin in patients with atopic dermatitis. Menoufia Med J [serial online] 2020 [cited 2020 Oct 20];33:1041-4. Available from: http://www.mmj.eg.net/text.asp?2020/33/3/1041/296709




  Introduction Top


Atopic dermatitis (AD) is a chronic, pruritic inflammatory skin disease. It follows a relapsing course [1]. Usually, AD starts in early childhood and may represent the initial step of the so-called 'atopic March', which represents the natural history of atopic manifestations [2]. The prevalence of allergic diseases including AD is increasing worldwide. In infants and children, the attack rate is two or three times higher compared with that in adults [3].

The manifestations of AD result from a complex interaction among environmental factors, skin barrier dysfunction, susceptibility genes, and immunological abnormalities [4].

Endothelial selectin (E-selectin) is expressed on the surface of the activated endothelial cell upon stimulation by inflammatory cytokines. In association with intercellular adhesion molecule-1, E-selectin enables adhesion of neutrophils, leukocytes, and monocytes on activated endothelium in the skin [5].

This study aimed to shed light on the role of E-selectin in AD pathogenesis through evaluation of its immunohistochemical expressions in involved skin in patients with AD compared with controls.


  Patients and Methods Top


This case–control study included 50 patients with AD and 10 healthy volunteers (controls). They were selected from Dermatology Outpatient Clinics, Menoufia University Hospital, during the period from May 2016 to February 2017. A written consent form approved by the Committee of Human Rights in Research at Menoufia University was obtained from every participant or his or her parent before the study initiation. We included patients with AD from both sexes and who did not receive any topical (2 weeks) or systemic (1 month) treatment for AD before joining the study.

Any participant having any immunoinflammatory or allergic disorder and/or patients having any skin disease other than AD was excluded from the study.

Methods

The studied individuals were subjected to full history taking and clinical examination. The diagnosis of AD was made according to the criteria of Hanifin and Rajka [6]. Punch biopsies of 4 mm were taken under local anesthesia from involved skin of each patient and matched sites of control participants. The specimens were fixed in 10% formalin solution and sent to Pathology Department, Faculty of Medicine, Menoufia University, where they were subjected to routine tissue processing to be embedded in paraffin blocks.

The method used for immunostaining was the streptavidin–biotin amplified system. In this system, the primary antibody for E-selectin was a polyclonal rabbit antibody raised against E-selectin with cat. YPA1378. It was received as concentrated 0.1 ml (1 mg/ml), with dilution titer 1:200 (Chongqing Biopsies Co., Cat No YPA1390, China) (www. Biospes.com).

Statistical analysis of data

Data were collected, tabulated, and statistically analyzed using a personal computer with statistical package for the social sciences (SPSS) version 15 program (IBM Corp., Armonk, New York, USA) released in 2011. IBM SPSS statistics for Windows, version 20.0. (IBM Corp.) Qualitative data were expressed as number and percentage. Quantitative data were expressed as arithmetic mean, SD, percentage, median, and range. For comparing qualitative variables, we used Fisher's exacts test.


  Results Top


Demographic data of the studied participants and clinical characteristics of patients with AD are demonstrated in [Table 1]. Both the AD patient group and the control group were comparable regarding age (P = 0.44) and sex (P = 0.21) [Table 1].
Table 1: Demographic and clinical data of patients with atopic dermatitis

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Regarding E-selectin immunoreactivity of the studied participants, in the control group, E-selectin immunoreactivity was positive and showed cytoplasmic localization in nine control sections [Figure 1]. In AD patient group, E-selectin immunoreactivity was positive in 45 cases and showed cytoplasmic localization in most of them [Figure 2]. There were significant elevations in cellular localization (P = 0.01) in AD cases than controls. Moreover, in AD cases, E-selectin immunoreactivity in dermal inflammatory infiltrates was significantly expressed than controls (81 vs. 0%).
Figure 1: Cytoplasmic expression of endothelial selectin in the control section (immunoperoxidase ×400 HPF).

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Figure 2: Cytoplasmic expression of endothelial selectin in the atopic dermatitis section (immunoperoxidase, ×200 high power field).

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  Discussion Top


AD is a chronic, highly pruritic, inflammatory and heterogeneous skin disease. It is characterized by periods of remission and relapse. AD usually arises in early childhood, often in infancy, and resolves by early teenage years. Approximately 5–10% of patients with AD have the disease extend into adulthood. The clinical phenotype that characterizes AD is the product of complex interactions among susceptibility genes, the host's environment, defects in skin barrier function, and systemic and local immunologic responses [7]. AD occurs primarily in childhood affecting 15–30% of children, with 45% of cases occurring within the first 6 months of life, whereas 85% of cases diagnosed within the first 5 years [8]. In line with this information, this study showed that the age of patients with AD ranged from 6 to 10 years with a mean ± SD of 6.18 ± 1.68 years, and the age of disease onset ranged from 3 to 7 years, with a mean of 4.3 ± 1.2 years. In agreement with our results, many researchers such as El-Naggar et al. [9] and Zeppa et al. [10] recorded that AD occurs most often in infants and children. Moreover, Edan et al. [11] reported that infantile and childhood stages had a higher prevalence ratio than all adulthood groups. The patients in this study included 14 males and 36 females. Following our finding, Edan et al. [11] reported that AD prevalence in girls was higher than boys. Moreover, Kim et al. [12] found that the prevalence of AD in girls (11.1%) was higher than that in boys (8.1%) (P < 0.005). On the contrary, Shultz et al. [13] and SelÇuk et al. [14] reported male predominance and Thomas and Myalil [15] observed that male to female ratio in AD is 1.5:1. However, Saito [16] reported that both sexes are equally affected by AD.

Regarding family history, of the studied 50 AD cases, 28 (54.5%) cases had a positive family history of atopic diseases. In agreement with this observation, Uehara and Kimura [17] studied the family history of AD in 529 children with AD and reported a positive family history of AD in 316 (59%) children. The role of family history in the development of AD has been reported by Peroni et al.[18], Snijders et al.[19], Lee-Wong et al. [20] and Bohme et al.[21]. They stated that positive family history is a risk factor for AD in children up to 4 years with no difference between the maternal and paternal effect of atopic history. Of the children without parental atopic history, 27.1% developed AD, whereas of those with single or double parental atopic history, 37.9 and 50.0%, respectively, did so. We studied E-selectin immunoreactivity, and it was positive in 90% of control sections; supporting this result, Luo et al. [22] reported that E-selectin is an endothelial-specific adhesion molecule best known for its role in leukocyte adhesion. It is induced by inflammatory stimuli as well as in proliferating endothelial cells under noninflammatory conditions, suggesting that growth signals also regulate E-selectin. Noninflammatory expression of E-selectin is correlated with cellular proliferation in human microvascular endothelial cells. E-selectin was significantly higher in patients with AD than in healthy control participants. The observed upregulation of E-selectin in involved skin of patients with AD could be suggested to be mediated by the release of cytokines such as IL-4 from cells that reside development of Th2 cells, which are predominant in atopic inflammation [23]. This enhanced tissue E-selectin expression in AD cases is important in the interaction with invading T lymphocytes in the epidermis and dermis. Thus, it may be hypothesized that the skin of patients with AD provides a special environment either for homing or for in loco differentiation of Th2 cells [24]. Furthermore, in this study, dermal inflammatory infiltrates demonstrated a significant increase in E-selectin immunoreactivity in AD cases than controls. Supporting this finding, Jung et al. [23] reported that cytokines released by keratinocytes may provide the first signal for the induction of adhesion molecules in AD skin lesions and a concomitant increase in E-selectin expression on dermal cells.


  Conclusion Top


E-selectin participates in AD etiopathogenesis.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Lawrence F, Wynnis L, Sarah L, Chamlin, Lawrence F, Eichenfield M, et al. guideline of care for the management of atopic dermatitis. J Am Acad Dermatol 2014; 70:338–351.  Back to cited text no. 1
    
2.
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6.
Hanifin JM, Rajka G. Diagnostic features of atopic dermatitis. Acta Derm Venereol Suppl 1980; 92:44–47.  Back to cited text no. 6
    
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Edan AI, Al-Hamdi K, Bakr S. The Prevalence of Atopic Eczema/Dermatitis Syndrome (AEDS) In Basrah Providence, IRAQ. Int J Dermatol 2005; 3:49–53.  Back to cited text no. 11
    
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SelÇuk ZT, Caglar T, Enunlu T, Topal T. The prevalence of allergic diseases in primary school children in Edrine, Turkey. Clin Exp Allergy 1997; 27:262–269.  Back to cited text no. 14
    
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Thomas IN, Myalil JM. Family history in atopic dermatitis. J Egypt Dermatol 2010; 6:4–6.  Back to cited text no. 15
    
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Saito H. Much atopy about the skin: genome-wide molecular analysis of atopic eczema. Int Arch Allergy Immunol 2005; 137:318–325.  Back to cited text no. 16
    
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Uehara M, Kimura C. Descendant family history of atopic dermatitis. Acta Derm Venereol 1993; 73:62–63.  Back to cited text no. 17
    
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Peroni DG, Piacentini GL, Bodini A, Rigotti E, Pigozzi R, Boner A. Prevalence and risk factors for atopic dermatitis in preschool children. Br J Dermatol 2008; 158:539–543.  Back to cited text no. 18
    
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Lee-Wong M, Chou V, Karagic M, Moqattash L, Silverberg N, Silverberg J, et al. Prevalence of atopic disorders in Inner-City Asian Americans and the predictive value of family history. J Allergy Ther 2013; 4:127–130.  Back to cited text no. 20
    
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Böhme M, Wickman M, Lennart Nordvall S, Svartengren M, Wahlgren CF. Family history and risk of atopic dermatitis in children up to 4 years. Clin Exp Allergy 2003; 33:1226–1231.  Back to cited text no. 21
    
22.
Luo J, Paranya G, Bischof J. Non inflammatory expression of E-selectin is regulated by cell growth. Blood 1999; 93:3785–3791.  Back to cited text no. 22
    
23.
Jung K, Linse F, Pals ST, Heller R, Moths C, Goebel R, et al. Adhesion molecules in atopic dermatitis: patch tests elicited by house dust mite. Contact Dermatitis 1997; 37:163–172.  Back to cited text no. 23
    
24.
Marinovic Kulisic S, Lipozencic J, Gregorovic G, Lackovic G, Juric-Lekic G. Expression of E selectin in the skin of patients of atopic dermatitis: a morphometric study. Acta Dermatovenerol Croat 2010; 18:141–145.  Back to cited text no. 24
    


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