Amniotic membrane modulates innate immune response inhibiting PRRs expression and NF-kappa B nuclear translocation on limbal myofibroblasts

作者：Dominguez Lopez Alfredo; Bautista de Lucio Victor Manuel; Serafin Lopez Janet; Robles Sanchez Edson; Garfias Yonathan^*

来源：Experimental Eye Research, 2014, 127: 215-223.

DOI：10.1016/j.exer.2014.08.002

• TLR-3
• MDA-5
• RIG-1
• inflammatory cytokines
• amniotic membrane
• limbal myofibroblasts

Corneal damage observed in a viral infection such as herpetic stromal keratitis is mainly caused by proinflammatory molecules released by resident cells in the response to viral antigens. There are pattern recognition receptors like MDA5, RIG-1, and TLR3, that recognize viral dsRNA and after activation, the innate immune response is exacerbated inducing the synthesis and secretion of inflammatory cytokines through NF-kappa B activation. Amniotic membrane (AM) has demonstrated to reduce inflammation by several mechanisms, however the effect of AM on innate immune receptors such as MDA5, RIG-1, and TLR3 has not been reported. In this study, we have determined that the presence of AM significantly inhibited the synthesis and secretion of proinflammatory cytokines on human limbal myofibroblasts (HLM) stimulated with poly I:C. Similarly, the presence of AM reduced the protein expression of MDA5, RIG-1, and TLR3 on poly I:C stimulated HLM. Additionally, the presence of the AM significantly inhibited the NF-kappa B nuclear translocation when the HLM were poly I:C stimulated, and concomitantly, the AM was able to relocate cadherins affecting the myofibroblastic cellular morphology. These results suggest that AM generates an anti-inflammatory microenvironment, and specific inhibition of NF kappa B nuclear translocation on infected corneal tissue would reduce the inflammation undesirable effects, explaining in part the beneficial usefulness of transplanting AM on herpetic stromal keratitis.

• 出版日期2014-10