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

open access

Page views 604
Article views/downloads 811
Get Citation

Connect on Social Media

Connect on Social Media

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.

Article available in PDF format

View PDF Download PDF file

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.