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Evaluation of Interleukin-17 and Interleukin-23 in Pterygium: Immunohistochemistry Study

Tiong KI, Mohd Zahidin AZ, Sumugam SKA, Uchang J, Mohd Isa HD

Asia Pac J Ophthalmol (Phila), 2017;6(5):403-406.
PMID: 28868833 DOI: 10.22608/APO.2017134

PURPOSE: To compare the interleukin-17 (IL-17) and interleukin-23 (IL-23) positive cell counts between pterygium and normal conjunctiva.
DESIGN: A case-control study.
METHODS: This study received ethical approval (NMRR Research ID 23957) and informed consent was obtained from all participants. It involved 20 participants with 20 samples of pterygium and 20 samples of normal conjunctiva that were obtained from the same eye of each participant. All the participants underwent history taking, slit lamp examination, and pterygium excision surgery. Both samples underwent immunohistochemistry procedure. Pretreatment procedure was conducted using heat-induced epitope retrieval with PT link, subsequently followed by EnVision FLEX staining procedure and incubation with anti‒IL-17 antibody and anti‒IL-23 antibody. Slides were examined in high-power fields (400x) for both samples in 3 different fields. Total positive stained cell counts in all 3 fields with IL-17 and IL-23 between pterygium and normal conjunctiva were analyzed by using Wilcoxon signed rank test.
RESULTS: IL-17 positive cell counts for normal conjunctiva showed mean 196.10 ± 80.487 but for pterygium was 331.10 ± 108.416. As for IL-23, the mean for positive cell counts for normal conjunctiva was 62.10 ± 33.462 and IL-23 positive cell counts for pterygium showed mean 102.95 ± 41.378. Both IL-17 and IL-23 were significantly increased in pterygium compared with normal conjunctiva (P < 0.001).
CONCLUSIONS: Both IL-17 and IL-23 were found to be significantly higher in the pterygium group than in the normal conjunctiva group with P < 0.001 by Wilcoxon signed rank test.

Matched MeSH terms: Conjunctiva/metabolism*
Relative quantification of human β‑defensins gene expression in pterygium and normal conjunctiva samples

Abubakar SA, Isa MM, Omar N, Tan SW

Mol Med Rep, 2020 Dec;22(6):4931-4937.
PMID: 33174018 DOI: 10.3892/mmr.2020.11560

The human ocular surface produces highly conserved cationic peptides. Human β‑defensins (HBDs) serve an important role in innate and adaptive immunity. They are primarily expressed in epithelial cells in response to infection and provide the first line of defence against invading microbes. Defensin β1 (DEFB1) is constitutively expressed and regulated by inflammatory mediators including interferon‑γ, lipopolysaccharide and peptidoglycans. DEFB4A is locally induced in response to microbial infection while DEFB109 is induced via Toll‑like receptor 2. The present study examined the expression of the HBD DEFB1, DEFB4A and DEFB109 genes in pterygium. The pterygium tissues and normal conjunctiva samples were obtained from 18 patients undergoing pterygium surgery. The reverse transcription‑quantitative polymerase chain reaction method was employed to determine the expression of DEFB1, DEFB4A and DEFB109 genes. The results revealed that the expression of DEFB1 and DEFB4A was significantly higher and upregulated in pterygium samples when compared with normal conjunctiva samples from each patient (P<0.05), while the expression of DEFB109 was observed to be lower in pterygium samples when compared with normal samples from the same patient. Previous studies have revealed that DEFB1 and DEFB4A genes are present in low concentrations inside the human eye, and they are upregulated during the maturation of keratinocytes, suggesting a possible role in cell differentiation. The DEFB109 gene is present in higher concentrations inside the human eye, though it is newly discovered. It has also been reported that DEFB1 may be involved in carcinogenesis epithelial tumours. Collectively, the current data suggests that HBDs may serve a crucial role in the pathogenesis and development of pterygia, and thus may be considered as novel molecular targets in understanding pterygia development.

Matched MeSH terms: Conjunctiva/metabolism*

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