Human-Practices

Text about Gensch.

Text about Salavei

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Purpose
In our project, we are utilizing the membrane-permeabilizing ability of antimicrobial peptides (AMPs) to target P. aeruginosa in the lungs of patients suffering from pneumonia. Dr. Wimley, from the Tulane University School of Medicine in New Orleans, USA, is at the forefront of developing synthetically engineered AMPs as alternatives to conventional antibiotics, particularly against ESKAPE pathogens. In his recent work published in ACS Infectious Diseases (Ghimire et al., 2023), Dr. Wimley has demonstrated how AMPs, which often face challenges such as low solubility, can be synthetically evolved into more potent versions. Following his talk at our institute on his newest and most effective AMP, D-CONGA-Q7, we seized the opportunity to obtain his expertise in the field of AMPs.

Contribution
During his presentation, Dr. Wimley strongly emphasized the urgency of finding new ways to combat the growing global threat of antimicrobial resistance. Although AMPs are a promising addition to conventional antibiotic treatments, their use is often limited by high production costs, susceptibility to proteases, and low solubility. While Dr. Wimley is focused on improving parent AMPs through synthetic modifications, he was also very intrigued by our idea to produce the AMP directly within the pathogen we aim to target.

The main topic during our meeting was the stability of the AMP once produced in the pathogen. Due to their relatively short half-life, the peptide is degraded quickly after bacterial cell death. Although this should decrease the risk of a strong immune response in the lung, Dr. Wimley raised the concern that the bacterial cell might only produce enough AMP to harm itself. Therefore, only one bacterium per plasmid delivery would be killed. If we could implement some kind of delay mechanism, we could theoretically reduce the number of transport vesicles and plasmids during the treatment and also target bacteria that are able to develop resistance against the targeting systems on our carriers. He suggested that instead of encoding only one AMP on the delivered plasmid, we could include a string of AMPs interrupted by pathogen-specific protease cleavage sites. This approach would activate AMP functionality only after proteolytic cleavage, producing a larger volume of AMPs for each successful plasmid delivery.
In Wimley’s most recent work, the peptide D-CONGA-Q7 demonstrated a very high killing rate, especially against the ESKAPE pathogen P. aeruginosa. However, this version of the peptide consists of D-amino acids, decreasing susceptibility to proteolytic degradation. Since CAPTURE is characterized by the delivery of a plasmid that forces the pathogen itself to produce the AMP, using D-amino acids is not feasible. According to Dr. Wimley, peptides retain their functionality if for all amino acids the other enantiomer is used. Although he has not tested the L-configuration of the D-CONGA-Q7 peptide, he believes there is a high likelihood that the bacterially produced peptide would maintain its function.

Implementation
In the initial planning phase of our project, we decided to use a different AMP called Sushi S1, with the intention of comparing the effectiveness of various AMPs in our experimental setup. Dr. Wimley kindly offered us a small sample of his synthesized peptide, D-CONGA-Q7, to compare its function to Sushi S1. Since our first tests indicated that D-CONGA-Q7 was more effective than Sushi S1, we considered switching the peptide sequence in our plasmid.

Outlook
Due to time constraints, we have decided to stick to our initial approach of encoding only one AMP on our delivered plasmid and postpone the implementation of Dr. Wimley’s suggested delay mechanism. However, we have already started researching Pseudomonas-specific proteases and their cleavage sites, in case we have enough time to compare the efficiency of the different strategies.
Depending on the results of further experiments, we are considering replacing the Sushi S1 peptide encoded on our plasmid with the sequence of D-CONGA-Q7. This change will allow us to test whether the expressed L-enantiomer of the AMP is as potent as the synthesized D-version.

Text about Römer

Text about Rios-Munos

Text about Makshakova

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Purpose
Anna Ruppl is a PhD student in the group of Dr. Allmendinger. She deals with the stabilization and manufacturing of mRNA-lipid nanoparticles by lyophilization. We met her together with Valentin Bender, as both are part of the Department of Pharmaceutical Technology and Biopharmacy at the University of Freiburg. We are particularly interested in whether our liposomes remain stable after synthesizing and bonding with the plasmid. We also want to know whether direct transport through the airways is effective and feasible. In addition, both Ruppl and Bender are familiar with liposomes. We would like to seek their advice on which lipids are best suited for liposomes and how best to produce them and reduce their size if necessary.

Contribution
Ruppl told us that there are additional problems with the transport of mRNA in liposomes. We should therefore focus on achieving the highest possible fusion efficiency, as transport through liposomes should not usually cause lasting damage to the plasmid. They also advised us to use positively charged lipids, such as DOTAP, as these are more efficient for encapsulation and targeting than uncharged lipids. However, they emphasized that cationic lipids are more toxic to mammalian cells than uncharged lipids. The formation of liposomes should also be more difficult with cationic lipids. The surface modifications already presented by Römer, such as Gb3, can help us here. They also recommend that we read other papers that specialize in exact and specific formation. They recommend adding the plasmid during rehydration and PVA swelling. In general, they encourage us to test different options to create a comparison and draw our own conclusions. With plasmid encapsulation, they leave all options open, although they favor the former. To reduce the size of our GUVs, they recommend hand extrusion with Hamilton syringes and sterile filters. The lipid solution is pressed 21 times between the 2 syringes.
When we proposed our idea to administer the drug as an aerosol using a nebulizer (which we had already received positive feedback for from Dr. Römer, Dr. Tümmler, and Dr. Rieg), Ruppl and Bender suggested looking into the start-up RNHale, which is developing inhalable, RNA-containing lipid nanoparticles. However, they cautioned that this application is quite complicated. There are many parameters to consider, which would massively prolong our project. As an alternative, they suggested administering CAPTURE intravenously. From the meeting with Rieg, we learned that CAPTURE will passively attach to the lungs. So it remains a realistic alternative.
Mathematical modeling can be combined well with dual centrifugation, but they warned us that such modeling requires high computing power.

Implementation
For our next experiments, we plan to use the cationic lipid DOTAP, but we will probably use this lipid in combination with a neutral lipid, DOPE, to ensure encapsulation as efficiently as possible while trying not to damage mammalian cells. We are planning experiments to test this approach. We will also integrate our plasmids during rehydration and try to encapsulate our plasmids in liposomes for the first time. We will also try extrusion, as it seems to be the most effective method after Bender, Ruppl, and Römer have explained it to us. We are getting support from the Signalhaus in Freiburg, where our laboratory is based.

Outlook
We are considering the possibility of using Gb3 to modify our liposome surface. We want to read more literature for future applications. As we are not planning to manufacture hardware, we just want to find out about a suitable application. Based on the information from Bender and Ruppl that ingestion with a nebulizer is rather difficult to implement, we definitely have to continue looking at intravenous and inhalation applications.

Purpose
Valentin Bender is a PhD student in the group of Prof. Dr. Suess. He specializes in RNA formulations for cardiovascular diseases. We met him together with Anna Ruppl, as both are part of the Department of Pharmaceutical Technology and Biopharmacy at the University of Freiburg. We are particularly interested in whether our liposomes remain stable after synthesizing and bonding with the plasmid. We also want to know whether direct transport through the airways is effective and feasible. In addition, both Ruppl and Bender are familiar with liposomes. We would like to seek their advice on which lipids are best suited for liposomes and how best to produce them and reduce their size if necessary.

Contribution
Ruppl told us that there are additional problems with the transport of mRNA in liposomes. We should therefore focus on achieving the highest possible fusion efficiency, as transport through liposomes should not usually cause lasting damage to the plasmid. They also advised us to use positively charged lipids, such as DOTAP, as these are more efficient for encapsulation and targeting than uncharged lipids. However, they emphasized that cationic lipids are more toxic to mammalian cells than uncharged lipids. The formation of liposomes should also be more difficult with cationic lipids. The surface modifications already presented by Römer, such as Gb3, can help us here. They also recommend that we read other papers that specialize in exact and specific formation. They recommend adding the plasmid during rehydration and PVA swelling. In general, they encourage us to test different options to create a comparison and draw our own conclusions. With plasmid encapsulation, they leave all options open, although they favor the former. To reduce the size of our GUVs, they recommend hand extrusion with Hamilton syringes and sterile filters. The lipid solution is pressed 21 times between the 2 syringes.
When we proposed our idea to administer the drug as an aerosol using a nebulizer (which we had already received positive feedback for from Dr. Römer, Dr. Tümmler, and Dr. Rieg), Ruppl and Bender suggested looking into the start-up RNHale, which is developing inhalable, RNA-containing lipid nanoparticles. However, they cautioned that this application is quite complicated. There are many parameters to consider, which would massively prolong our project. As an alternative, they suggested administering CAPTURE intravenously. From the meeting with Rieg, we learned that CAPTURE will passively attach to the lungs. So it remains a realistic alternative.
Mathematical modeling can be combined well with dual centrifugation, but they warned us that such modeling requires high computing power.

Implementation
For our next experiments, we plan to use the cationic lipid DOTAP, but we will probably use this lipid in combination with a neutral lipid, DOPE, to ensure encapsulation as efficiently as possible while trying not to damage mammalian cells. We are planning experiments to test this approach. We will also integrate our plasmids during rehydration and try to encapsulate our plasmids in liposomes for the first time. We will also try extrusion, as it seems to be the most effective method after Bender, Ruppl, and Römer have explained it to us. We are getting support from the Signalhaus in Freiburg, where our laboratory is based.

Outlook
We are considering the possibility of using Gb3 to modify our liposome surface. We want to read more literature for future applications. As we are not planning to manufacture hardware, we just want to find out about a suitable application. Based on the information from Bender and Ruppl that ingestion with a nebulizer is rather difficult to implement, we definitely have to continue looking at intravenous and inhalation applications.

Text about Hess

Text about Ramasamy

Text about Kirchmair

Text about Germer

Text about Putnam

Text about Müller

Text about DeLisa

Text about Huang

Text about Rabe

Text about Kırpat

Purpose
Prof. Dr. Peter Walentek and his workgroup focus on the molecular mechanisms of cilia and mucociliary epithelium. They are well-versed in lung organoids and the implementation and execution of experiments with and on lung cells. With his help, we want to find out how we can best carry out experiments without animal testing and how we can best imitate the mucosa to prove CAPTURE. We also want to ask for his general expertise on our project. His expertise in future implementations of CAPTURE in hospitals is also valuable due to his proximity to Freiburg University Hospital.

Contribution
At the beginning, we asked him how we could best cultivate and process mammalian cells. He is convinced that healthy cultured cells survive longer in PBS and that there should be no lysis. He also recommended that we clean the cells with FBS if we no longer wanted to continue working with PBS. He also suggested that we use lung cells instead of HEK cells to get a better proof of concept. Calu-3 cells are easy-to-cultivate lung cells that almost every laboratory working with cell cultures can use.
Also interesting for our experiments are Air Liquid Interface Cultures, which, as Walentek explains, are cells from donated lungs. We should read up on this further. He suggests selected literature for this. We should also use a suitable reporter gene that individually marks all CAPTURE, encapsulation, and fusion processes. This allows us to intervene more effectively and find reasons and solutions to problems more quickly. If our sushi might not work well enough, he suggests aquaporins. We can use them to produce similar membrane pores.
Walentek believes that the introduction of liposomes into the lungs through a nebulizer will definitely work. However, he cautions that it is very difficult to bring to the market. The path to a finished, prescription drug is an obstacle for many researchers, even those with experience. According to him, animal experiments cannot be avoided. Experiments for lung drugs are often carried out on ferrets, as they are the closest to human lungs. He also suggests that we should illustrate the nebulizer on our graphical abstract so that viewers have an idea of how CAPTURE can be introduced. For a good proof of concept, he offers us the opportunity to test mucus-like texture in his laboratory, which is produced from frog embryos. We can drip our cargo with the carrier onto the mucus and see how it behaves. In the building where the meeting took place, the IMITATE (Institute for Disease Modelling and Targeted Medicine) Freiburg, we also found a guide for start-ups in the southwest of Germany. It is called Impact Start-ups, a brief guide through a startup ecosystem by the urban management marketing of Freiburg and Startinsland, a startup alliance in the Freiburg area.

Implementation
We will now investigate the cause of our prematurely dying HEK cells in PBS in the laboratory. We have also received new and more suitable plates. We will use them to repeat the previous expression series and determine whether the problem was related to our vessels. We will definitely take his experience in applying for animal testing and implementing medical products on the market into account in CAPTURE. In particular, the idea of administering CAPTURE with a nebulizer is a good one, but difficult to implement. We are aware that this step would not take place within the framework of iGEM, but we already want to explore how we can best prepare CAPTURE for the market.

Outlook
We are now also planning experiments with lung cells, as we believe that experiments with lung cells will have a more lasting impact on our proof of concept. We are certainly interested in accepting his offer to apply CAPTURE to the mucosa of frog embryos in his laboratory, provided there is sufficient time available. Additionally, in preparation for clinical implementation, we would like to explore potential funding opportunities and collaborative partnerships.The meeting with Walentek turned out to be a double stroke of luck, enabling us to improve both our laboratory work and our commercialization efforts for the future.

Text about Helmstädter

Text about Boldt

Purpose
In our ongoing efforts to explore alternatives to animal testing, we had the opportunity to engage with Prof. Dr. Jens Kurreck, a leading researcher known for his work in developing organ models that aim to reduce reliance on animal experiments. Our contact with him was facilitated through the organization Doctors Against Animal Experiments. Prof. Kurreck's research focuses not only on providing better alternatives but also on advancing the search for innovative solutions. Given his expertise, we sought his guidance on how we might avoid animal testing in clinical trials and gain insights into viable animal-free research methods.

Contribution
Prof. Kurreck emphasized that using animals, particularly mice, in experiments is fundamentally flawed due to the significant differences in pathogenesis between animals and humans. He highlighted that experimental results obtained from mice are often not translatable to human biology, making such experiments scientifically unsound. Despite decades of animal-based research, he noted that mortality rates have remained constant over the past 40 to 50 years, with 90% of all drugs failing during clinical trials. This alarming statistic underscores the urgent need for models that are more appropriate and comparable to human physiology.
Kurreck's research group has successfully developed three different lung models designed to outperform traditional animal models in predicting human responses. They are also in the process of developing a model for cystic fibrosis (CF). However, Kurreck advised against using our CAPTURE platform on CF models due to their high genetic variability, which would make the results too nonspecific.
He strongly recommended the use of human-derived cell lines, such as HEK293 or Calu-3 cells, which can be cultured in the laboratory and provide more reliable and human-relevant data. Furthermore, Kurreck suggested that we reach out to Prof. Dr. Donald Ingber from Harvard University, who is pioneering the use of organ-on-a-chip technologies for modeling human organs and disease processes.

Implementation
Our meeting with Prof. Kurreck reaffirmed our commitment to avoiding animal testing. We were particularly struck by the revelation that many animal experiments fail to produce reliable or translatable data regarding the efficacy of treatments in humans. For our future experiments, we will shift our focus toward the use of human mammalian cells, particularly HEK293 cells, which have been shown to provide relevant and reproducible results in preclinical research.

Outlook
Given Prof. Kurreck's research and his focus on replacing animal testing with more accurate models, we are now considering the following steps:

• Investigating established alternatives to animal testing in clinical trials, particularly focusing on human-relevant in vitro models.
• Further exploring the challenges, benefits, and limitations of both animal experiments and alternative methods to make more informed decisions moving forward.

First Meeting

Purpose
Prof. Dr. Burkhard Tümmler, Coordinator of the Disease Area Cystic Fibrosis at the German Centre for Lung Research, specializes in cystic fibrosis research. We sought his expertise in lung research, particularly regarding the effects of P. aeruginosa infections in the lung. Given his current role and specialization, Prof. Tümmler provides valuable insights for our project. The purpose of our meeting was to present our project to Prof. Tümmler and identify potential weaknesses. We unveiled our graphic abstract for the first time to assess its effectiveness in presentations. Additionally, our aim was to understand how CAPTURE affects the body and lungs, focusing on the specificity and safety of our plasmid carriers.

Contribution
Right at the beginning of our conversation, Prof. Dr. Tümmler recommended exploring Bob Hancock's work, highlighting its foundational role in global peptide research. He emphasized that while AMPs hold promise, their short half-life poses a challenge for effective delivery to the lungs. Additionally, AMPs can be hazardous to humans due to their ability to fuse with mammalian cells. Prof. Tümmler expressed concerns that our approach of using lectins to enhance liposome specificity might not be sufficient. However, he acknowledged that our strategy of specifying our OMVs with phage tail proteins to target P. aeruginosa is promising, albeit challenging due to the vast diversity of phages and bacterial strains. The likelihood of identifying the correct phage tail protein is low but achievable with extensive research. Prof. Tümmler conducted an in-depth scrutiny of CAPTURE, questioning our understanding of the chemical composition and its effects on both the body and the pathogen. He encouraged us to broaden our research by reviewing publications from various authors to improve CAPTURE.

Implementation
For the next steps, we intend to read more publications to better understand the individual components of CAPTURE and to describe them in more detail. Our goal is to expand our knowledge and explore ways to make our system more specific and efficient. As Prof. Tümmler pointed out, we currently lack sufficient understanding to effectively improve the system. Additionally, we suspect that during the meeting and through our graphical abstract, it may not have been clear to Prof. Tümmler that our aim is to deliver the AMP encoded on a plasmid. To address this, we intend to place greater emphasis on the plasmid in our graphical abstract. To facilitate this process, we will dedicate the next two weeks to exchanging ideas with Prof. Tümmler.

Second Meeting

Purpose
The second meeting with Prof. Tümmler was held to address specific questions regarding our plasmid, targeting system, and the biofilm of P. aeruginosa.

Contribution
Prof. Tümmler highlighted several factors contributing to the instability of AMPs, including the presence of ions, salt, microbial and host proteases, bacterial polysaccharides, etc. He noted that a plasmid is inherently more stable than synthesized AMPs, eliminating production costs since the bacteria synthesize the peptide themselves. He reviewed our arguments for using a plasmid instead of a synthesized AMP. In terms of choosing a specific AMP, he recommended selecting a peptide that inhibits transcription or translation. This is because the Sushi AMP creates pores in the outer membrane, so once synthesized in the bacteria, it would require a secretion signal. He theorized that using an AMP with synthesis inhibition would prevent the bacteria from developing resistance due to the fast and efficient mechanism. When we asked about the possibility of cross-resistance to our AMP, he indicated that he could not provide a definitive answer. He addressed the anticipated challenge of P. aeruginosa biofilm presence, assuring us that the biomass in lungs infected with this pathogen is primarily composed of goblet cell mucus, with only a small percentage formed by Pseudomonas. Concerning our targeting mechanism for OMVs, he noted that the longer P. aeruginosa remains in the lung, the greater the chance of degrading the phage receptors and developing resistance. However, he emphasized that the diversity of phages provides a high probability of identifying one effective against Pseudomonas.

Implementation
Following the discussion with Prof. Tümmler, we decided to incorporate a secretion signal, HSTII, to transport our AMP to the outer membrane where it would target the membrane of the pathogen. We also plan to finish our experiments related to biofilm formation, as the pathogenesis derives from the mucus already present in the lung.

Outlook
To gain a deeper understanding of cross-resistance and its impact on P. aeruginosa developing AMP resistance, we decided to contact Prof. Dr. Rieg, an expert in antibiotic resistance and a professor at the University Hospital.

Purpose
With CAPTURE gaining recognition as a novel advancement in drug research, we sought advice on patenting and market implementation. We consulted Prof. Dr. Ralf Reski, a patent expert at the University of Freiburg, known for his research on mosses and his experience in filing multiple patents.

Contribution
Prof. Reski, who attended our Faculty Day presentation, affirmed that CAPTURE is innovative and recommended securing a patent, as no similar treatments for P. aeruginosa exist. He outlined the patenting process in three phases: preparing an application, contacting the Central Office for Technology Transfer, and working with a patent attorney to secure validation at various levels (national or global). Prof. Reski offered to assist us with future inquiries or applications.

Implementation
We are considering patenting CAPTURE and may consult Prof. Reski for guidance. However, we are unsure if a patent is the best step due to uncertainties about the project’s future after the Jamboree. Additionally, we are planning to publish an abstract in BioSpektrum, but may delay it if we pursue a patent.
Key steps:

• Decide as a team whether to pursue a patent.
• Draft the patent application if necessary.
• Coordinate with BioSpektrum on publication timing.

Purpose
Prof. Dr. Hajo Grundmann has a background in clinical tropical medicine, medical microbiology, hygiene, and environmental medicine. He was the project leader of the European surveillance system for antimicrobial resistance. Through this meeting, we hope to get a general assessment of our project and gain insight into hospital work worldwide, including potential differences and their significance. With his background in microbiology, we want to know whether our targeting methods are effective and marketable.

Contribution
He opened by noting that the CAPTURE idea is a new method for treating P. aeruginosa. He believes that CAPTURE can be effective because our method intervenes from the inside. Resistance develops in the periplasmic space, so CAPTURE seems to him to intervene precisely in the patient. He also mentioned that P. aeruginosa is a very important and difficult-to-control pathogen that has many variants and can develop multiple resistances, which is supported by its large genome. The pathogen protects itself with a biofilm, which makes it even harder to combat. Thanks to Prof. Dr. Walentek, we know that the biofilm does not play a major role, as it forms in the lungs as the tunica mucosa respiratoria. A well-known and insidious disease is cystic fibrosis, which produces thick mucus in the lungs.
Based on Grundmann's many years of clinical experience, he drew attention to the problem that chronically ill patients, such as CF patients, are often victims of this pathogen. Not only is the individual perspective on pathogens important, but also the systemic one. Such patients are very costly for hospitals and healthcare systems, both in time and money. Current treatment options are lengthy and inefficient, making patients a burden on the healthcare system for better or worse.
According to Grundmann, this is our selling point. With CAPTURE, we use specific targeting options for the bacterium P. aeruginosa. In contrast to previous antibiotic therapy methods, CAPTURE can specifically find and kill the bacterium. Cells in the surrounding environment are not affected. In order to prove this experimentally, we suggested using the lung organoids created by Walentek. Grundmann thought this was a good idea for testing CAPTURE. Administration via nebulizer is also a good option, says Grundmann. For intensive care patients, he could imagine an adapter that administers CAPTURE during artificial respiration in addition to ventilation.
He drew our attention to hospitals worldwide through his experience in several hospitals in the Global South and North. He emphasized that there is far too little research on hospital conditions in the Global South, so it is not possible to conclude that hospitals in the Global South are less hygienic. According to Grundmann, this is a myth and an important point in the debate. The significance of a new P. aeruginosa treatment method cannot, therefore, be fully understood, as there is simply too little research on this topic.

Implementation
We want to highlight the fact that research on infections in the Global South is often neglected. The focus is placed on infections in the Global North, and infection figures in the South are simply forgotten. We have also become even more confident about administering CAPTURE by inhalation, now that we also know how to administer CAPTURE to intensive care patients in a compliant manner. We are also considering ordering lung organoids from Prof. Dr. Walentek, if time permits, to test CAPTURE's effect on lung cells.

Outlook

• Research on infection studies in the Global South.
• Planning experiments with lung organoids.

Purpose
Prof. Rieg is a specialist in internal medicine at Freiburg University Hospital, focusing on host-pathogen interaction and systemic therapy in humans. His expertise is particularly in sexual and vector-borne diseases affecting humans. With CAPTURE, we aim not only to achieve a proof of concept but also to progress towards clinical application. Talking to Prof. Rieg, we seek to identify potential challenges and problems with CAPTURE at an early stage and develop solution strategies.

Contribution
Prof. Rieg has significantly enriched our understanding of P. aeruginosa infections, emphasizing the risks faced by patients who acquire this infection during hospital stays. He highlighted the importance of hospitalization duration as a critical factor in the likelihood of contracting P. aeruginosa. This means that people with lung infections, such as those during the coronavirus pandemic, have a "natural" probability of becoming infected with the pathogen. Patients with prolonged hospital stays also have a higher risk of infection, especially those in facilities with similar patient profiles and diseases, as noted by Prof. Donker. He also underscored that P. aeruginosa infections are a growing global challenge. This pathogen thrives in aqueous environments and requires no special conditions to grow, making it a worldwide threat. Furthermore, Prof. Rieg considers a dual protection system for our project, as proposed by Prof. Tuemmler, to be an effective and adaptive clinical solution. This would involve using ICE (Integrative and Conjugative Elements) in conjunction with our phage tail proteins on the outer membrane vesicles. The primary challenge is to develop the most effective therapy for as many infected patients as possible. An additional specification, such as the aforementioned ICE, is an optimal extension for CAPTURE. Prof. Rieg supports our idea of using an inhalation device, like our nebulizer, as a gentle treatment for people with lung infections. He is now our second expert, alongside Dr. Tuemmler, to verify this application.

Implementation
This meeting helped us recognize two key aspects of our project. First, the importance of minimizing the hospital stay of high-risk patients with lung disease to reduce their risk of infection with P. aeruginosa. Second, as Prof. Rieg pointed out, our AMP could have a synergistic effect when used in combination with antibiotics, and the mechanism of action of AMPs helps prevent the development of drug resistance.

Outlook
Our conversation highlighted that P. aeruginosa is far more than a typical pathogen. While people with a healthy immune system can easily withstand this pathogen, it poses a significant threat to vulnerable patients. Those with compromised health, such as cystic fibrosis patients who are already dependent on artificial ventilation, are particularly at risk. Their intensive hospital treatments elevate them to high-risk status, making them more susceptible to severe and potentially fatal P. aeruginosa infections.

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