Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 

 Table of Contents  
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
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/mmj.mmj_72_19

Rights and Permissions

To investigate the role of endothelial selectin (E-selectin) in atopic dermatitis (AD) through evaluation of the immunohistochemical expressions in lesional skin biopsies.
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.
There were significant elevations in E-selectin cellular localization (P = 0.01) as well as dermal inflammatory infiltrates in AD cases than controls.
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 2021 Mar 7];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.


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

Click here to view

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).

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

Click here to view

  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


Conflicts of interest

There are no conflicts of interest.

  References Top

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
Dharmage SC, Lowe AJ, Matheson MC, Burgess JA, Allen KJ, Abramson MJ, et al. Atopic dermatitis and the atopic march revisited. Allergy 2014; 69:17–27.  Back to cited text no. 2
Han Y, Lee Y, Park H. Nutrient intakes of infants with atopic dermatitis and relationship with feeding type. Nutr Res Pract 2015; 9:57–62.  Back to cited text no. 3
Boguniewicz M, Schmed-Grendelmeier P, Leung DY. Atopic dermatitis. J Allergy Clin Immunol 2006; 118:40–43.  Back to cited text no. 4
Caproni M, Torchia D, Antiga E, Volp W, Fabbri P. Expression of adhesion molecules in atopic dermatitis. Clin Exp Dermatol 2006; 31:813–817.  Back to cited text no. 5
Hanifin JM, Rajka G. Diagnostic features of atopic dermatitis. Acta Derm Venereol Suppl 1980; 92:44–47.  Back to cited text no. 6
Watson P, Kapur N. Atopic dermatitis. Allergy Clin Immunol 2011; 7:1–4.  Back to cited text no. 7
Illi S, von Mutius E, Lau S, Nickel R, Grüber C, Niggemann B, et al. Multicenter Allergy Study Group. The natural course of atopic dermatitis from birth to age 7 years and the association with asthma. J Allergy Clin Immunol 2004; 113:925–931.  Back to cited text no. 8
El-Naggar MM, Saleh AM, Ahmed MA. The Chemokines, RANTES and Eotaxin, in Atopic Dermatitis, Atopic Asthmatics and Allergic Rhinitis Patients: Relation to Disease Severity. Egypt J Med Microbiol 2008; 17:265–278.  Back to cited text no. 9
Zeppa L, Bellini V, Lisi P. Atopic dermatitis in adults. Curr Probl Dermatol 2011; 22:40–46.  Back to cited text no. 10
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
Kim DS, Lee JH, Lee KH, Lee MG. Prevalence and severity of atopic dermatitis. Acta Dermatol Venereol 2012; 92:472–474.  Back to cited text no. 12
Shultz LF, Diepge T, Svensson A. The occurance of atopic dermatitis in north Europe; An International Questionnaire Study. J Am Acad Dermatol 1996; 34:760–764.  Back to cited text no. 13
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
Thomas IN, Myalil JM. Family history in atopic dermatitis. J Egypt Dermatol 2010; 6:4–6.  Back to cited text no. 15
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
Uehara M, Kimura C. Descendant family history of atopic dermatitis. Acta Derm Venereol 1993; 73:62–63.  Back to cited text no. 17
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
Snijders BE, Stelma FF, Reijmerink NE, Thijs C, van der Steege G, Damoiseaux JG, et al. CD14 polymorphisms in mother and infant, soluble CD14 in breast milk and atopy development in the infant (KOALA study). Pediatr Allergy Immunol 2010; 21:541–549.  Back to cited text no. 19
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
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
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
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
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


  [Figure 1], [Figure 2]

  [Table 1]


Similar in PUBMED
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
Patients and Methods
Article Figures
Article Tables

 Article Access Statistics
    PDF Downloaded20    
    Comments [Add]    

Recommend this journal