Rationale: COPD is characterized by a progressive and irreversible loss of lung function, to which emphysema is a contributor. Emphysema is characterized by destruction of alveolar walls, that are composed of the alveolar epithelium, the endothelium and mesenchymal cells. It is increasingly realized that microvascular endothelial cell (dys)function contributes toemphysema development. Therefore, the aim is to study the role of that pulmonary microvascular endothelial cells in alveolar repair and regeneration. 
Methods: EpCAM+ (i.e. epithelial) cells isolated from mouse lungs (BALB/c) were seeded in matrigel and deposited on a monolayer of the pulmonary microvascular endothelial cell line (HPMEC.ST1.R), resulting in both airway and alveolar epithelial organoids. Human resected lung tissue was used to isolate HTII-280+ alveolar cells and CD31+ endothelial cells. Endothelial cells (P2) were allowed to form a monolayer in the bottom of a culture plate and freshly isolated HTII-280+ alveolar cells were seeded in basement membrane matrix (BME2) inside the insert. 
Results and Conclusion: The presence of HPMEC.ST1.R cells increased alveolar organoid number but not airway organoids isolated from murine lungs. Similarly, human primary lung endothelial cells cultured and expanded in vitro (P2), induced an increase (1.7X) in human alveolar organoid number, at day 10 after isolation from human lung tissue. Collectively these results show that pulmonary endothelial cells support alveolar progenitor cell function as shown by an increased number of alveolar organoids. We hypothesize that this function is disturbed in emphysema, and therefore we are currently analyzing the impact of COPD-relevant triggers such as cigarette smoke and inflammatory mediators on endothelial cell-driven alveolar repair using this co-culture model. Furthermore, we are expanding our model to include human induced pluripotent stem cell (hiPSC)-derived lung cells.


The role of pulmonary endothelial cells in alveolar repair and regeneration

Background: Dysfunctional of alveolar microvascular endothelial cells drives microangiopathies in chronic obstructive pulmonary disease (COPD). Tobacco smoking and air pollution are two major causes of COPD. We hypothesized that cigarette smoke (CS) and diesel exhaust particles (DEP) might impact on pulmonary microvascular endothelial repair in vitro.
Methods: Immortalized human pulmonary microvascular endothelial cells (HPMECs) were starved for 24 h followed by treatments with either vehicle control, CS extract (CSE) (1%, 2.5%, 5%), DEP (50, 100, 200 µg/ml), or IL-1ß (0.1, 1ng/ml) for 24h. Post-analyses comprised PCR analysis and scratch wound healing assays. 
Results: In the wound healing assay, 83% closure was observed within the vehicle group at 12h, which was reduced to 76%, 59% and 57% by 1%, 2.5%, and 5% CSE respectively; 87%, 89% and 82% by 50-, 100-, and 200 µg/ml DEP respectively; and increased to 93% and 97% by IL-1ß (0.1-, 1ng/ml). After 24h treatments, the wound closed 96-100% in vehicle, IL-1ß (0.1-, 1ng/ml) and DEP (50-, 100 µg/ml) groups; however, the wound closed 95%, 85%, 73% and 91% by 1%, 2.5%, 5%CSE and DEP (200 µg/ml) respectively. The wound closed slower when cells were first pretreated for 24 h with DEP. The gene expression levels of the pro-inflammatory IL-6 and CXCL8/IL-8 were increased in HPMECs treated with DEP (100 µg/ml) or IL-1ß (0.1-, 1ng/ml) but not by CSE; the gene expression of the aging associated marker P16 decreased by CSE (2.5%, 5%) or DEP (50-, 200 µg/ml) whereas the expression of P21 increased by IL-1ß (0.1-, 1ng/ml). The expression level of the oxidative stress responsive gene MGST1 increased by CSE, DEP or IL-1ß in a concentration-dependent manner.
Conclusions: Both CSE and DEP exposure impair the wound repair function of pulmonary microvascular endothelial cells and this dysfunction was associated with changes in markers of oxidative stress, and to a lesser extent senescence and inflammation. 


Cigarette smoke and air pollution induce dysfunctional pulmonary microvascular endothelial repair

poster

[![](https://assets.underline.io/uploads/markdown_image/1/image/261902fdf187a88bfa74da226ff77186.png)](https://drive.google.com/file/d/1gUViQJJHCSgM38OhwpDoTdN89evCsZ-7/view?usp=sharing)
[![](https://assets.underline.io/uploads/markdown_image/1/image/1605292c232e6f185c7f87ee38e8502a.png)](https://drive.google.com/file/d/1kPkznVX_6cx-n846z_pUtyVDZql9KImc/view?usp=sharing)


### **Welcome Message**

Welcome to the inaugural **Dutch Lung Congress.**  We have all missed our opportunities to network and interact with our colleagues in the last twelve months or more.  While our desire was to meet face to face once again, when it became evident that this would not be possible until much later in 2021 (or even into 2022) the hard working committee organizing the Dutch Lung Congress found, what we hope will be, an excellent alternative to facilitate our annual meeting.

The Dutch Lung Congress aims to bring together everyone interested in research related to pulmonary diseases in the Netherlands.  We hope this event will provide opportunities for multidisciplinary interactions to enhance our approaches for addressing these challenging diseases.  Each session will include input from patients, clinical and basic and/or translational scientists discussing the latest information around the central themes chosen by the organizing committee.  One advantage of holding our congress as a virtual event this year is that we will have the opportunity to hear from world leading experts from all over the globe.  We hope you enjoy the programme the organizing committee have put together and will engage in dynamic discussions with all the speakers.

One highlight of our congress will be the Young Investigator Session.  Remember to join us for this exciting session when we will hear from the presenters who submitted the top scoring abstracts.  This promises to be a session full of exciting science that will display the strengths that constitute the future talent in our field.

When we are not listening to these great presentations we can all meet in Gathertown.  Within this interactive platform you will be able to meet colleagues and friends for networking. Enjoy a private chat over a virtual coffee, visit the booths of our sponsors and other parties, chat with the Young Investigator Board members or take some timeout in the relaxation spaces.  While in Gathertown take the opportunity to visit all the diverse posters on display. Chat live with the presenters or leave them a question on the discussion board for them to engage with you.  Make sure you check for any messages each time you enter Gathertown to make the most of your networking opportunities.

We look forward to seeing you during the DLC and the great scientific (and other) discussions we are anticipating during our 2021 meeting.

On behalf of the DLC organizing Committee
<br>**Janette Burgess
<br>Chair, DLC Organizing Committee**
![](https://assets.underline.io/uploads/markdown_image/1/image/f461fb275d9667fb2a76a30813388e90.png)



### Special Session: Publieksmiddag
![](https://assets.underline.io/uploads/markdown_image/1/image/77e768dd500e6205175e5cafba59abdc.png)






![](https://assets.underline.io/uploads/markdown_image/1/image/f461fb275d9667fb2a76a30813388e90.png)
**More about the committee team:**:
[Barbro N. Melgert, PhD] (https://drive.google.com/file/d/1q_IIH3JvTivumCUzzsZGX7BgD41HxQmk/view?usp=sharing)
// [Bas Holverda, PhD] (https://drive.google.com/file/d/1QKXHmTTQjgs4OZVuM8doXU055S-fu_uU/view?usp=sharing)
// [Frits Franssen, PhD] (https://drive.google.com/file/d/1d7HRUJaqGuRFzkPN3SVgkbBfqFkDkWq2/view?usp=sharing)
// [Janette Burgess, PhD] (https://drive.google.com/file/d/1VHFlrEN6uCQGeeW3Lj4I8aTw7HsB0GFr/view?usp=sharing)
// [Michel van den Heuvel, PhD] (https://drive.google.com/file/d/1JeOEP8MHxiK_4lONr8UM2HaxdxpkAmA2/view?usp=sharing)
// [Patrick Bhairosing] (https://drive.google.com/file/d/1xI8ORq-g1bbVcrlRDviZ9NhAwanc4dFl/view?usp=sharing)
// [Gimano Amatngalim, PhD] (https://drive.google.com/file/d/1fyVDDKARLNjRk_JZk8_GyhGMjmp6DWHp/view?usp=sharing)
// [Peter Kunst, PhD] (https://drive.google.com/file/d/1QhtB4nQezpAjbfUAcBnINc-Bm3Shy2Lf/view?usp=sharing)
// [Dr. Michel van den Heuvel, Prof., MD, PhD] (https://drive.google.com/file/d/1JBdNEBXZCEikEZhJ6MoD5DhQfXMz3bP6/view?usp=sharing)
![](https://assets.underline.io/uploads/markdown_image/1/image/f461fb275d9667fb2a76a30813388e90.png)

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Andries van der Meer

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The role of pulmonary endothelial cells in alveolar repair and regeneration

Cigarette smoke and air pollution induce dysfunctional pulmonary microvascular endothelial repair

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