Rome 2013 Press Release 2013 Poster Terms and Conditions General Information Scientific Programme Overview Main Session 1 - Imaging Main Session 2 - Artificial Vision and Electrical Stimulation of the Eye Main Session 3 - Regeneration / Degeneration Main Session 4 - Inflammation in Retinal Disease

SESSION 4 | Inflammation in Retinal Disease

Saturday 2 February | 11.00 – 13.00 | Room: Salone dei Cavalieri

Chairperson: F. Bandello ITALY, L. Naldini ITALY

This Session opens with the Poster Competition Award


11.00
| G. Richard GERMANY
Announcement of Poster Award

11.05 | M. de Palma SWITZERLAND
Macrophages heterogeneity and function in inflammation and angiogenesis view abstract- click here

Findings in mouse models of cancer indicate that tumor-associated macrophages (TAMs) foster tumor progression and metastasis (1). Gene expression and cell depletion studies however suggest that TAMs comprise molecularly and functionally distinct subsets, which may play different roles in both primary and metastatic tumors. For instance, perivascular TIE2+MRC1+CD11clow TAMs stimulate tumor angiogenesis (2-5), whereas CD11c+MRC1low TAMs express a markedly proinflammatory and angiostatic phenotype (4, 6). Such antagonizing TAM subsets coexist in tumors, occupy distinct niches in the tumor microenvironment, and are present at ratios that vary according to the tumor type and grade (7).

Interestingly, macrophages that resemble the perivascular TIE2+MRC1+CD11clow TAMs are also found in developing and healing organs, suggesting convergent macrophage functions in tumors and nontransformed tissues (4). Recent findings illustrating the multifaceted functions of macrophages in mouse models of cancer and tissue remodeling/regenration will be presented and discussed.

 

1.  Qian BZ, Pollard JW. Macrophage diversity enhances tumor progression and metastasis. Cell 2010; 141: 39-51.
2.  De Palma M, Venneri M A, Galli R, et al. Tie2 identifies a hematopoietic lineage of proangiogenic monocytes required for tumor vessel formation and a mesenchymal population of pericyte progenitors. Cancer Cell 2005; 8: 211-226.
3.  Mazzieri R, Pucci F, Moi D, et al. Targeting the ANG2/TIE2 axis inhibits tumor growth and metastasis by impairing angiogenesis and disabling rebounds of proangiogenic myeloid cells. Cancer Cell 2011; 19: 512-26.
4.  Pucci F, Venneri MA, Biziato D, et al. A distinguishing gene signature shared by tumor-infiltrating Tie2-expressing monocytes, blood "resident" monocytes, and embryonic macrophages suggests common functions and developmental relationships. Blood 2009; 114: 901-914.
5. He H, Xu J, Waren MC, et al. Endothelial cells provide an instructive niche for the differentiation and functional polarization of M2-like macrophages. Blood 2012.
6.  Rolny C, Mazzone M, Tugues S, et al. HRG inhibits tumor growth and metastasis by inducing macrophage polarization and vessel normalization through downregulation of PlGF. Cancer Cell 2011; 19: 31-44.
7.  Squadrito ML, De Palma M. Macrophage regulation of tumor angiogenesis: implications for cancer therapy. Mol Aspects Med 2011; 32: 123-45.

11.27 | C. Ruhrberg UK
Myeloid cells in physiological and pathological retina vascularization view abstract- click here

Myeloid cells have been implicated in retinal and choroidal neovascularization in sight-threatening neovascular eye diseases such as diabetic retinopathy and age-related macular degeneration. The hypoxia-inducible transcription factor 1 alpha (HIF1A) is activated by inflammatory stimuli and hypoxia and is a key driver of vascular endothelial growth factor (VEGFA) gene expression. We have examined retinal neovascularisation after oxygen-induced retinopathy and choroidal neovascularisation after laser injury of Bruch’s membrane in mice with defective HIF1A and VEGF-A expression in myeloid cells.

11.49 | H. Xu UK
Chronic inflammation and retinal angiogenesis view abstract- click here

Neovascular retinal disease is a leading cause of blindness and to a certain extent is orchestrated by or deploys inflammatory responses. Whilst non-infectious uveoretinitis is archetypically driven by CD4+ T cell responses, in the persistent phase of disease, angiogenic responses are observed along with degeneration of the retina and are reliant for full expression on myeloid-derived cell; phenotypically distinct from but potentially sharing common effector responses to age-related macular degeneration. Experimental autoimmune uveoretinitis (EAU) is an animal model for human posterior segment intraocular inflammation.

Following the initial acute phase of severe inflammation (day 21~30 post-immunization), the retina sustains a low-grade inflammatory response with persistent tissue-infiltrating leukocytes for over 4 months. During this persistent phase, angiogenesis is observed in the form of retinal neovascular membranes (RNM) that arise from inflamed venules and post-capillary venules, increase in size as the disease progresses and are associated with infiltrating activated arginase-1+ macrophages. In the absence of thrombospondin-1 (TSP-1), RNM is markedly increased and is associated with arginase-1-CD68+ macrophages, whereas deletion of the chemokine CCL2 or its receptor CCR2 resulted in reduced RNM in association with a predominant neutrophil infiltrate in the acute phase and T cell infiltration in the chronic phase.

The suppressor of cytokine signaling 3 (SOCS3) in macrophages negatively regulates their angiogenic potential, and deletion of SOCS3 in myeloid cells results in massively enhanced retinal angiogenesis under chronic inflammatory conditions. CCR2-mediated macrophage recruitment appears to be important to the angiogenesis response in the inflamed retina, and this response is regulated by constitutive of angiogenic inhibitors like TSP-1 and SOCS3.

12.11 | F. Sennlaub FRANCE
Macrophages  in Age Related Macular Degeneration view abstract- click here

Physiologically the photoreceptor cell layer is devoid of leukocytes or even resident macrophages (microglial cells) that can only be found in the inner retina. In age related macular degeneration (AMD), cells from the monocyte/macrophage linage infiltrate the photoreceptor cell layer. It has so far been unclear if these cells are microglial cells that have migrated from the inner retina or if they are inflammatory monocytes recruited from the blood stream. While microglial cells are known for their neuroprotective properties, inflammatory monocytes recruited from the circulation can lead to a potentially neurotoxic environment. What is the proportion of monocytes and microglial to the infiltrating cells of the photoreceptor cell layer in atrophic macular degeneration? Where do they come from? What are the factors that recruit and maintain them among the photoreceptors? How do they influence photoreceptor degeneration in diseases such as AMD? Understanding the cellular and molecular inflammatroy mediators may hold the key for new therapies of AMD.

12.33 | G. Ferrari ITALY
Angiopoietin 2 and macrophages interplay in the cornea: the angiogenic switch from avascularity to angiogenesis. view abstract- click here

The normal cornea is transparent and totally devoid of blood and lymphatic vessels. Corneal neovascularization affects approximately 4% of the general population and is associated with significant complications and visual loss.  Corneal angiogenesis is commonly associated with infiltration of bone marrow cells. In this study, we have characterized a specific population of  corneal bone marrow cells expressing  markers of Tie2 macrophages. The interaction of these cells with Angiopoetin-2,  a ligand for Tie2, is potentially interesting as a mechanism of  corneal neovascularization.  In this study, we discuss the  potential role in the normal and neovascularized corneas suggesting potential, novel therapeutic approaches.

12.48 | P. Barry IRELAND
Current approach in endophthalmitis prophylaxis following cataract surgery  - Are eye drops finished? view abstract- click here

The ESCRS study on endophthalmitis prophylaxis which was randomised and prospective identified a five fold reduction in post operative endophthalmitis in patients randomly allocated to receive intracameral cefuroxime 1 mg. in 0.1 ml. at the end of the surgery. 

Since these results were published there have been reports of similar outcomes following the adoption of intracameral cefuroxime routinely from different corners of the globe.

The role of pre-operative and post operative topical antibiotic drops can now be questioned. 

Plans for an endophthalmitis registry by the ESCRS in conjunction with EURETINA could record and analyse endophthalmitis cases from around Europe and additionally study endophthalmitis complicating anti-Vegf injections. 

13.00 | End of Session

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