Vol 3, No 1 (2018)
Original paper
Published online: 2018-07-20

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Reactivity of corneal and conjunctival epithelial cells to lipopolysaccharide (LPS) and/or irradiation with visible light in vitro

Roman Paduch, Anna Matysik-Woźniak, Ryszard Maciejewski, Anselm G. Jünemann, Robert Rejdak
Ophthalmol J 2018;3(1):1-7.

Abstract

INTRODUCTION. Visible light and inflammation caused by bacterial endotoxins strongly influence direct cell interactions and modulate the expression of selected factors, such as nitric oxide (NO) and cyclooxygenase-2 (COX-2). The aim of the study is to establish whether exposition of corneal or conjunctival epithelial cells to visible light and/ or LPS may change their viability, direct cellular interactions and expression of NO and COX-2.

MATERIALS AND METHODS. In vitro cultured human corneal and conjunctival epithelial cells were used in the study. The following assays were performed: Neutral Red (NR) uptake, nitric oxide (NO) quantification by the Griess method, cytoskeletal F-actin organization by fluorescent staining, and COX-2 expression by immunofluorescence.

RESULTS. LPS reduced the viability of the cells, especially conjunctival epithelial cells. All cell stimulation variants tested (visible light and/or LPS treatment) led to decreased nitric oxide (NO) production both by corneal and conjunctival epithelial cells. No changes in cytoskeletal F-actin filaments were observed after the cells had been treated with light or the endotoxin. LPS slightly increased COX-2 expression, but light had no, or a slightly reducing, effect on the level of this enzyme.

CONCLUSIONS. Visible light and/or bacterial endotoxin (LPS) may, depending on the local microenvironmental conditions, cooperate or interfere with each other’s activity in inducing ocular surface inflammation.

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References

  1. Hajrasouliha AR, Kaplan HJ. Light and ocular immunity. Curr Opin Allergy Clin Immunol. 2012; 12(5): 504–509.
  2. Liang H, Brignole-Baudouin F, Labbé A, et al. LPS-stimulated inflammation and apoptosis in corneal injury models. Mol Vis. 2007; 13: 1169–1180.
  3. Ohta S, Matsuda S, Gunji M, et al. The role of nitric oxide in radiation damage. Biol Pharm Bull. 2007; 30(6): 1102–1107.
  4. Weinreb O, Dovrat A, Dunia I, et al. UV-A-related alterations of young and adult lens water-insoluble α-crystallin, plasma membranous and cytoskeletal proteins. European Journal of Biochemistry. 2001; 268(3): 536–543.
  5. Erdinest N, Shohat N, Moallem E, et al. Nitric oxide secretion in human conjunctival fibroblasts is inhibited by alpha linolenic acid. J Inflamm (Lond). 2015; 12: 59.
  6. Seo SJ, Choi HG, Chung HJ, et al. Time course of expression of mRNA of inducible nitric oxide synthase and generation of nitric oxide by ultraviolet B in keratinocyte cell lines. Br J Dermatol. 2002; 147(4): 655–662.
  7. Wang ZY, Håkanson R. Role of nitric oxide (NO) in ocular inflammation. Br J Pharmacol. 1995; 116(5): 2447–2450.
  8. Cruz R, Quintana-Hau JD, González JR, et al. Effects of an ophthalmic formulation of meloxicam on COX-2 expression, PGE2 release, and cytokine expression in a model of acute ocular inflammation. Br J Ophthalmol. 2008; 92(1): 120–125.
  9. Chiang CC, Cheng YW, Lin CL, et al. Cyclooxygenase 2 expression in pterygium. Mol Vis. 2007; 13: 635–638.
  10. Choi H, Lim W, Kim I, et al. Inflammatory cytokines are suppressed by light-emitting diode irradiation of P. gingivalis LPS-treated human gingival fibroblasts: inflammatory cytokine changes by LED irradiation. Lasers Med Sci. 2012; 27(2): 459–467.
  11. Anfuso CD, Olivieri M, Fidilio A, et al. Gabapentin Attenuates Ocular Inflammation: and Studies. Front Pharmacol. 2017; 8: 173.
  12. Ozdal PC, Callejo S, Caissie AL, et al. Cyclooxygenase-2 expression in human irradiated uveal melanomas. Int Ophthalmol. 2008; 28(1): 1–6.