Abstract

To investigate human beta-defensins (HBDs) and cathelicidin LL-37 (LL-37) expressions in patients with pterygium. In this retrospective consecutive case series, 26 pterygium specimens and 15 normal conjunctival specimens of 15 control subjects were in vestigated. Expressions of HBD-1, HBD-2, HBD-3, and LL-37 were assessed using immuno histochemical staining. A brown color in the cytoplasm and/or nuclei of epithelial cells indicated positive staining for HBDs and LL-37. For each antibody, the intensity of the reaction (negative [-], weak [1+], moderate [2+], or strong [3+]) was determined to describe the immunoreactions. The median age was 52 years in both groups. There were no significant differences in age and sex between the groups (p=0.583, p=0.355, respectively). Of the 26 pterygium specimens, 15 (57.7%) (14 weak, 1 moderate staining) showed HBD-2 expression, which was not observed in any of the control specimens. One (3.8%) pterygium and one (6.7%) control specimen demonstrated weak staining for HBD-3. HBD-2 expression was significantly higher in the pterygium specimens than in the controls (p=0.002). None of the tissue specimens had positive staining for HBD-1 or LL-37 in either group (both; p=1.00). HBD-2 expression was higher in pterygium specimens than in the controls. HBD-2 expression that might be stimulated by inflammatory cytokines may be related to inflammation and fibrovascular proliferation and may play a role in pterygium pathogenesis.

Highlights

  • Pterygia develop from the growth of fibrovascular tissue of bulbar conjunctiva into the interpalpebral area of the cornea

  • Uma cor castanha no citoplasma ou nos núcleos de células epiteliais foi definida como coloração positiva para human beta-defensins (HBDs) e LL-37

  • HBD-1, HBD-2, HBD-3, and LL-37 levels in both groups are shown in table 1

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Summary

Introduction

Pterygia develop from the growth of fibrovascular tissue of bulbar conjunctiva into the interpalpebral area of the cornea. Epidemiological studies have shown that chronic ultraviolet exposure has a major role in pterygium pathogenesis[1]. Chronic inflammation due to some or all of the above factors probably causes fibrovascular proliferation. Growth factors, stem cell factors, and pro-angiogenic factors may all have a role in inflammation and fibrovascular proliferation of pathogenesis of pterygium[1]. It has been shown that the expression of human alpha-defensin, which is an antimicrobial peptide (AMP), is increased in the tears of patients with pterygia because of fibrovascular proliferation or associated inflammation[2]. It has been reported that some AMPs may be stimulated by proinflammatory cytokines, such as interleukin (IL)-1 alpha, IL-1 beta, and tumor necrosis factor-alpha[3,4]

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