• $10,000 -

    A huge thank you to everyone for your support!

    Forever Lungs

    Two women. Two bikes.

    One epic relay cycle across Canada for Pulmonary Fibrosis.


    All donations are greatly appreciated.





  • Over 17,000 Canadians Affected

    Pulmonary Fibrosis Research Can Help People Catch Their Breath Before its Too Late!

    Idiopathic pulmonary fibrosis (IPF) is a progressive and chronic lung disease with a poor

    long-term prognosis. It affects 17,000 Canadians yearly, yet often gets misdiagnosed.

    Over time, lung tissue becomes scarred and changes the lung's ability to function normally. This makes it progressively difficult to breathe and deliver oxygen to the body.

    The exact cause is unknown and while there are treatments that can slow down the progression, there is no cure.

  • Who We Are

    Julie Ann and Olivia

    University teammates and roommates, we first met playing soccer at a University in Pennsylvania at the age of 19. Despite living in different countries after graduation, we have been close friends ever since. The idea to cycle across Canada to raise money for IPF, came to us back in 2006. At the time however, it was not possible to make this a reality. Since then, the idea has always been on our minds. After the passing of Ettore Mendicino in 2014 and the diagnosis of friends and family members with IPF, we knew that the time was now! Splitting the distance to cycle from Vancouver to Toronto, we decided we could make this a reality.

    Julie Ann Chiodo

    Julie Ann Chiodo is an elementary school teacher and sports enthusiast. She is excited to be doing her part to raise awareness about Pulmonary Fibrosis.

    Olivia Mendicino

    Cycling had to be put on the back burner for a while after moving back to Ontario and having two children, but Olivia never forgot her passion for the sport. Above is a photo of a cycling day tour in Ontario of 2012.

    True Friends Breathe Joy Into Your Life

    We hope that you'll help us to do the same for the thousands of individuals and families struggling with Pulmonary Fibrosis.

  • Who We're Riding For

    Carmen Ragno

    Julie Ann's Uncle

    Carmen was first diagnosed with IPF in 2014. In February of 2018, Carmen received a lung transplant. He is currently recovering and doing well. Carmen says that he now has a new birthday on February 7th, 2018 and so many reasons to celebrate!

    Ettore Mendicino

    In loving memory of Olivia's father

    Ettore passed away from IPF in October of 2014. He was first diagnosed in 2009, however his quality of life began to decline a year before his death. He was a hard working, humorous family man, who loved carpentry, soccer, wine making as well as spoiling his two granddaughters.

  • Facts About Our Ride

    2, 300km each

    Distance to travel


    Number of Days to Cycle


    Money to raise for IPF research


    Number of Provinces to Cross

    160 km

    Distance to bike daily


    Estimated calories burned per person, per day.

  • Research Project

    The money we are raising will fund research into investigating the cells that activate IPF. It is an exciting project with lots of potential. Here is a brief summary of the proposed research. 



    Idiopathic pulmonary fibrosis (IPF) is an irreversible fibrotic disorder that is characterized by a progressive decline in lung function. Recent information suggest that a specific cell population called “alternatively activated macrophages” are the ones critically involved in the activation of scar-producing cells in lungs. We have already shown that a biological process increasing the size of an internal organelle in these cells are required for the activation of scarproducing cells – and when the activation is stopped - no further scarring can occur. These data were established in experimental models and have not yet been validated in the human lung, which will be our focus for this project. We will not only investigate the specific mechanisms involved in the activation of these cells, but also set up a translational platform that will allow us to address any biological mechanism involved in the progression of the disease in human lung. To do this, we will examine these processes in blood and in tissues taken from lungs of patients to help diagnose IPF, that is no longer used for clinical purposes.


  • Thank you so much for helping us reach our goal!

    Each Donation Makes a Differnece

    Let’s keep going!!

  • Disclaimer

    If we for any reason cannot complete the distance of our trip, we will contact every donor individually and give them the opportunity for a complete refund. As 100% of the proceeds will be going to support Pulmonary Fibrosis Research, donors will also be given the option to maintain their desired dontation amount.

  • What is Pulmonary Fibrosis?

    Wound healing and scarring: A physiological fibrotic process?

    Every wound would be an immediate threat of death to the human body if its repair system was not rapid and effective. A non-healing wound would allow pathogens to intrude the body and it might hamper proper organ function. Therefore, it’s essential for survival to remove pathogens and debris and close the wound with scar tissue.

    Upon tissue injury, blood vessel cells, platelets and the blood coagulation system induce a first seal of the injured site and transmit “danger signals” to attract immune cells. Those immune cells attack invading pathogens, remove tissue debris and activate fibroblasts. Fibroblasts are parenchymal cells that release collagens and other extracellular matrix proteins upon activation. Collagens finally make up solid scar tissue to restore the integrity of the human body.

    Scar tissue functions as a patch that closes wounds but it does not replace all of the functions of the original tissue. To better understand this fact, one just needs to remember the feeling when touching one’s own scars. Does the scar tissue feel the same as the surrounding skin and does it elicit the same tactile sensations? Probably not!

    And there is still another aspect one can understand when examining one’s own scares. Scar tissue usually changes over time: A relatively new scar might appear protruding and prominent, while old scar tissue becomes thinner and finer, adapting more closely to the surrounding tissue. This process is called remodeling.

    So, how does wound healing and scarring relate to fibrosis? 

    Fibrosis is an uncontrolled scarring process that escapes spatial and temporal control of a normal wound healing. To be more exact, fibrosis seems to be an uncontrolled scarring process since it exhibits many, if not most, of the molecular mechanisms that are also observed during normal wound healing and scarring.

    As seen in wound healing and scarring, fibroblasts are activated in fibrosis to produce and release collagens and other extracellular matrix proteins. In addition, the molecular signals that drive fibroblast activation in fibrosis are the same as during normal wound healing. This includes signals from immune cells (e.g., Transforming Growth Factor-β, Interleukin-6), from blood vessel cells (e.g., Vascular Endothelial Growth Factor), and from platelets (e.g., Platelet Derived Growth Factor and serotonin), all of which also play central roles in normal wound healing. And finally, fibrotic tissue exhibits similar remodeling processes as scar tissue.

    But what is the difference between normal wound healing and fibrosis?

    While wound healing is tightly regulated, fibrosis seems to be out of control. In fibrosis, fibroblasts are not de-activated and they constantly release large amounts of collagens that form fibrotic tissue. Through mostly unknown mechanisms, a large number of fibroblasts in an organ or the whole body are activated in fibrotic diseases, while only a limited number of fibroblasts that reside close to the site of injury are activated in normal tissue repair. Therefore, fibroblasts seem to be gone wild in fibrosis.

    Importantly, fibrosis itself is not a disease but a pathological process. Different diseases, pathological conditions and fibrotic stimuli can initiate the activation of fibroblasts and finally result into fibrosis. Fibrosis is the terminal process of a variety of similar, yet different diseases.

    In this regard, fibrosis of the liver may arise from infections with specific pathogens, such as hepatitis viruses or schistosoma. Malignancies, in particular serotonin producing carcinoids of the gut, can cause fibrosis in the intestine and other organs. Toxins, such as olza oil or gadolinium contrast dye, may induce fibrosis of the skin and internal organs. Finally, radiation therapy, asbestos and other volatile substances may lead to lung fibrosis.

    And yet, there are other fibrotic diseases in which the initiating causes remain unknown. This includes systemic sclerosis, which leads to fibrosis of the skin and internal organs, as well as idiopathic pulmonary fibrosis, a specific type of lung fibrosis.

    How does fibrosis finally lead to organ failure and death?

    The architecture of individual tissues and organs is complex. The lungs, for example, are characterized by a multitude of small blebs, so called alveoli, each connecting to both the air and the blood stream. To enable effective gas exchange, the total area of all blebs sums up to an area of the size of a soccer field. In addition, the air-blood barrier of the alveolar septum measures only a few µ-meter, which is extremely thin. Oxygen only needs to cross two to three cell layers composed of alveolar lining cells and vascular cells. Carbon dioxide travels the opposite direction.

    Scar as well as fibrotic tissue does neither restore the complex organ architecture nor replace the original organ function. Considering fibrosis of the lungs, massive release of collagens into the extracellular space results in thickening of the alveolar septi and destruction of healthy alveolar tissue. Consequently, the alveolar gas exchange declines, which results in progressive dyspnea of the patients.

    What to do about fibrosis?

    To treat patients with idiopathic pulmonary fibrosis and other classical fibrotic diseases, immunosuppressants had long been used. These agents are very effective in controlling autoimmune inflammatory conditions. Since only few patients with fibrotic disorders responded to these therapies, inflammation does not seem to be a major driver of fibrosis in most patients. Many researchers then concluded that inflammation might play a role during the initiation of the fibrotic disease. They believed that molecular signals released by immune cells triggered fibroblast activation, which then became autonomous and self-sufficient in their activated state.

    Nevertheless, this concept remains unproven, and new models of fibrosis consider a chronic injury and repair mechanism.

    On a molecular level, wound repair and fibrosis are characterized by the activation of specific signaling pathways in fibroblasts, many of which are involved in tissue and organ development during morphogenesis. Some of the most important signaling pathways are those of Transforming Growth Factor-β (TGF-β), Platelet Derived Growth Factor (PDGF), Vascular Endothelial Growth Factor (VEGF), Serotonin, Interleukin-6 (IL-6), and Wnt. Given the role of these pathways for the fibrotic process, they represent attractive targets for therapy, in particular since they can be drugged relatively easily.

    Both medications, which are currently approved for the treatment of idiopathic pulmonary fibrosis, target those signaling pathways.

    Nintedanib is a multityrosine kinase inhibitor, which blocks tyrosine kinases (i.e., specific enzymes) that promote the activity of pro-fibrotic PDGF and VEGF signaling. Pirfinedone, the second drug to treat idiopathic pulmonary fibrosis, interferes with TGF-β-signaling.

    The beneficial effects of nintedanib and pirfenidone in patients with idiopathic pulmonary fibrosis are relatively small. In most patients, they cannot reverse or stop the fibrotic process, but only slow it down. Nevertheless, they are the first drugs that do have anti-fibrotic effects in idiopathic pulmonary fibrosis. Thus, nintedanib and pirfenidone are considered a breakthrough in fibrosis research and care. Researchers hope that the two drugs might path the way for more effective medications to treat idiopathic pulmonary fibrosis and fibrosis in general.

    Although classical fibrotic diseases, such as idiopathic pulmonary fibrosis, are rare, the impact of effective anti-fibrotic therapies might be huge. Fibrotic processes can be observed in many other diseases, some of which are very common, including coronary artery disease and various forms of malignancies. Thus, effective anti-fibrotic therapies might also revolutionize the management and outcome of a variety of other diseases.


    Although many patients with classical fibrotic diseases still have a poor prognosis, fibrosis research is moving ahead rapidly. Fibroblasts, which fulfill live saving tasks in physiological wound healing, are out of control in fibrotic disease. While the initiating events of many classical fibrotic diseases are still unclear, specific signaling pathways are active in fibroblasts during fibrotic processes and can be drugged by novel therapies.

    Many thanks to Christian Beyer for providing this information so that we can better understand Pulmonary Fibrosis.


    Eming SA, Wynn TA, Martin P. Inflammation and metabolism in tissue repair and regeneration. Science. 2017 Jun 9;356(6342):1026-1030. doi: 10.1126/science.aam7928. Epub 2017 Jun 8. Review.


    Ryu JH, Moua T, Daniels CE, Hartman TE, Yi ES, Utz JP, Limper AH. Idiopathic pulmonary fibrosis: evolving concepts. Mayo Clin Proc. 2014 Aug;89(8):1130-42. doi: 10.1016/j.mayocp.2014.03.016. Epub 2014 May 24. Review.


    Wynn TA, Ramalingam TR. Mechanisms of fibrosis: therapeutic translation for fibrotic disease. Nat Med. 2012 Jul 6;18(7):1028-40. doi: 10.1038/nm.2807. Review.


    Varga J, Abraham D. Systemic sclerosis: a prototypic multisystem fibrotic disorder. J Clin Invest. 2007 Mar;117(3):557-67. Review.