Engineered organism could diagnose Crohn’s disease flareups

Engineered organism could diagnose Crohn’s disease flareups

Bioengineers create pH-sensing gut bacteria to diagnose inflammatory bowel disease.

By Jade Boyd

In an important step toward the clinical application of synthetic biology, Rice University researchers have engineered a bacterium with the necessary capabilities for diagnosing a human disease.

The engineered strain of the gut bacteria E. coli senses pH and glows when it encounters acidosis, an acidic condition that often occurs during flareups of inflammatory bowel diseases like colitis, ileitis and Crohn’s disease.

Researchers at the University of Colorado (CU) School of Medicine used the Rice-created organism in a mouse model of Crohn’s disease to show acidosis activates a signature set of genes. The corresponding genetic signature in humans has previously been observed during active inflammation in Crohn’s disease patients. The results are available online in the Proceedings of the National Academy of Sciences.

Study co-author Jeffrey Tabor, whose lab engineered the pH-sensing bacterium, said it could be reprogrammed to make colors that show up in the toilet instead of the fluorescent tags used in the CU School of Medicine experiments.

“We think it could be added to food and programmed to turn toilet water blue to warn patients when a flareup is just beginning,” said Tabor, an associate professor of bioengineering in Rice’s Brown School of Engineering.

Over their 3.5 billion-year history, bacteria have evolved countless specific and sensitive genetic circuits to sense their surroundings. Tabor and colleagues developed a biohacking toolkit that allows them to mix and match the inputs and outputs of these bacterial sensors. The pH-sensing circuit was discovered by Rice Ph.D. student Kathryn Brink in a 2019 demonstration of the plug-and-play toolkit.

PNAS study co-authors Sean Colgan, the director of the CU School of Medicine’s mucosal inflammation program, and Ian Cartwright, a postdoctoral fellow in Colgan’s lab, read about the pH sensor and contacted Tabor to see if it could be adapted for use in a mouse model of Crohn’s disease.

“It turns out that measuring pH within the intestine through noninvasive ways is quite difficult,” said Colgan, the Levine-Kern Professor of Medicine and Immunology in the CU School of Medicine.

So Brink spent a few weeks splicing the necessary sensor circuits into an organism and sent it to Colgan’s lab.

“Normally, the pH in your intestines is around seven, which is neutral, but you get a lot of inflammation in Crohn’s disease, and pH goes to something like three, which is very acidic,” Tabor said.

Colgan and colleagues have studied the genes that are turned on and off under such conditions and “needed a tool to measure pH in the intestine to show that the things they were observing in in vitro experiments were also really happening in a live animal,” Tabor said.

“Colonizing this bacterial strain was the perfect biological tool to monitor acidosis during active inflammation,” Colgan said. “Correlating intestinal gene expression with the bacterial pH sensing bacteria proved to be a useful and valuable set of biomarkers for active inflammation in the intestine.”

Tabor said he believes the pH-sensing bacterium could potentially be advanced for human clinical trials in several years.

Original source here.

A gut feeling

Scientists link genetic makeup of bacteria in the human gut to several human diseases.

By Jen A. Miller

We are truly never alone, not even within our own bodies. Human beings play host to trillions of bacteria, fungi, viruses, and other microorganisms that make up the human microbiome. In recent years, the mix of these resident bacteria, and the presence of specific bacterial species, has been linked to conditions ranging from obesity to multiple sclerosis.

 Now, going a step farther, researchers at Harvard Medical School and Joslin Diabetes Center have gone beyond microbial species. Analyzing the genetic makeup of bacteria in the human gut, the team has successfully linked groups of bacterial genes, or “genetic signatures,” to multiple diseases.

The work brings scientists closer to developing tests that could predict disease risk or identify disease presence based on a sampling of the genetic makeup of a person’s microbiome.  

The findings, to be published May 18 in Nature Communications, link sets of bacterial genes to the presence of coronary artery disease, cirrhosis of the liver, inflammatory bowel disease, colon cancer, and type 2 diabetes. The analysis indicates that three of these conditions — coronary artery disease, inflammatory bowel disease, and liver cirrhosis — share many of the same bacterial genes. In other words, people whose guts harbor these bacterial genes seem more likely to have one or more of these three conditions.  

The work represents a significant advance in the current understanding of the relationship between microbes residing in the human gut and specific diseases, the team said. If confirmed through further research, the results could inform the design of tools that could gauge a person’s risk for a range of conditions based on analysis of a single fecal sample, they added.     

“This opens a window for the development of tests using cross-disease, gene-based indicators of patient health,” said first author Braden Tierney, a graduate student in the biological and biomedical sciences program at HMS. “We’ve identified genetic markers that we think could eventually lead to tests, or just one test, to identify associations with a number of medical conditions.”  

The researchers caution that their study was not designed to elucidate exactly how and why these microbial genes may be linked to different diseases. Thus far, they said, it remains unclear whether these bacteria are involved in disease development or are mere bystanders in this process. 

The goal of the study was to determine whether groups of genes could reliably indicate the presence of different diseases. These newly identified microbial genetic signatures, however, could be studied further to determine what role, if any, the organisms play in disease development.  

“Our study underscores the value of data science to tease out complex interplay between microbes and humans,” said study senior author Chirag Patel, associate professor of biomedical informatics in the Blavatnik Institute at HMS. 

The researchers started out by collecting microbiome data from 13 groups of patients totaling more than 2,500 samples. Next, they analyzed the data to pinpoint linkages between seven diseases and millions of microbial species, microbial metabolic pathways, and microbial genes. By trying out a variety of modeling approaches — computing a total of 67 million different statistical models — they were able to observe what microbiome features consistently emerged as the strongest disease-associated candidates. 

Of all the various microbial characteristics — species, pathways, and genes — microbial genes had the greatest predictive power. In other words, the researchers said, groups of bacterial genes, or genetic signatures, rather than merely the presence of certain bacterial families, were linked most closely to the presence of a given condition. 

“This opens a window for the development of tests using cross-disease, gene-based indicators of patient health.”— Braden Tierney

Some of the main observations included:

In a previous study, the HMS team used massive amounts of publicly available DNA-sequencing data from human oral and gut microbiomes to estimate the size of the universe of microbial genes in the human body. The analysis revealed that there may be more genes in the collective human microbiome than stars in the observable universe.

Given the sheer number of microbial genes that reside within the human body, the new findings represent a major step forward in understanding the complexity of the interplay between human diseases and the human microbiome, the researchers said. 

“The ultimate goal of computational science is to generate hypotheses from a huge swath of data,” said Tierney. “Our work shows that this can be done and opens up so many new avenues for research and inquiry that we are only limited by the time, people, and resources needed to run those tests.” 

Original source here.

Gene-level-metagenomic-architectures-across-diseases-yield-high-resolution-microbiome-diagnostic-indicators

Support Groups- Do I or Don’t I

From the very time Support Groups were introduced as a means of peer support, the decision facing people whether to the meeting has been the source of many unwanted ‘butterflies’…to go or not to go!

The first thing for people to understand is that this is a normal human response.

Here’s a scenario any support group attendee has lived through at some point:

You decide to go along to a meeting, mainly comprised of total strangers. You get in the door without talking, and then find a seat in the last row of the room in the furthest corner from where the ‘action’ is. You find something to read before you sit down so you don’t have to look up before things start.

Of course, there is no eye contact, because if you look at someone then you might have to talk to them. Talking could lead to conversation, and you’re not there to make conversation – you’re here to listen and then get the hell out of there.

If you’ve been in this situation as described you’ll understand the scenario.

With this in mind, how can we make participating in a Support Group a much less daunting experience than it may seem from the outside?

Each Facilitator, Group or members of the Group may look at introducing some of these for their meeting; some may already run similarly along these lines. At the end of the day, how friendly and welcoming you make your meeting, the safer and more willing people will be to return.

What are your thoughts on welcoming first timers to a meeting?

What steps do you take to make your Support Group a supportive, welcoming and caring environment?

Diet–microbiota interactions in inflammatory bowel disease

Accumulating evidence suggests that the gut microbiota plays pivotal roles in the regulation of intestinal homeostasis and IBD pathogenesis.

By Kohei Sugihara and Nobuhiko Kamada 

Diet-microbiota-interactions-in-inflammatory-bowel-disease paper download below

Inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn’s disease (CD), is a chronic and relapsing inflammatory disorder of the gastrointestinal tract. The prevalence of IBD has been increasing worldwide, affecting about 3 million people in the United States and 2.5 million people in Europe.

Although the precise etiology of IBD has not yet been defined, it is widely accepted that the confluence of multiple factors, including genetic and environmental factors, is associated with its pathogenesis.

Genetic studies have identified over 200 host genetic loci associated with the risk of IBD, and mostly related to immunological pathways, including innate and adaptive immune responses and autophagy.

The prevalence of IBD is high in Western countries; however, the rates of IBD are also rising in many newly industrialised countries as they become more westernised. For example, the number of IBD patients has increased approximately 20-fold in the past 30 years in Japan. This exponential increase suggests that environmental exposures also play critical roles in the development of IBD.

Among environmental factors, diet, smoking, stress, sleep patterns, hygiene, and antibiotic usage are considered to contribute to the risk of IBD. In particular, diet is widely thought to have a pivotal role in the pathogenesis of IBD. It is well-known that diet shapes the composition of the gut microbiota. Gut microbes use diet-derived nutrients for their growth and colonisation in the gut. In contrast, host cells use microbial metabolites as energy sources and immunomodulatory agents to maintain intestinal homeostasis.

This symbiotic relationship between the gut microbiota and the host is crucial for human health. However, the intake of certain diets, such as the westernised diet characterised by high fat and low fibre, results in gut dysbiosis, thereby disrupting intestinal homeostasis and promoting inflammation of the gut. Gut inflammation, in turn, influences the composition and function of the gut microbiota.

In this review, we discuss the complex reciprocal interactions between diet and the gut microbiota in the context of IBD. In particular, we focus on the metabolic reprogramming of host and microbial cells during inflammation and how these metabolic changes may optimise dietary interventions. We also highlight the future direction of microbiota-targeted dietary interventions to develop precision nutrition for the treatment of IBD.

Original source here.

Podcast: Perivascular nerve dysfunction in inflammatory bowel disease

What is the effect of vascular function in the pathogenesis of Inflammatory Bowel Disease (IBD)?

Find podcast here.

IBD patients are at greater risk for developing cardiovascular disease compared to age-matched peers. Listen as Consulting Editor Camilla Wenceslau (University of Toledo) interviews senior author Erika Boerman (University of Missouri) and expert Pooneh Bagher (Texas A&M Health Science Center) about this novel study by Norton et al. Decreased blood flow to the gut is a diagnostic hallmark of IBD, and sensory neurotransmitters calcitonin gene-related peptide (CGRP) and substance P are considered biomarkers of IBD.

Using pressure myography to study mesenteric arteries in an interleukin-10 knockout mouse model, Boerman and collaborators investigated the activation of perivascular sensory nerves, which control gastrointestinal tract blood flow. When Boerman and co-authors first blocked substance P receptors and then stimulated sensory nerves, sensory vasodilation was rescued in the IBD vessels.

A surprising finding was that the substance P pathway seemed to interfere with the CGRP pathway, preventing normal sensory vasodilation. Does Boerman estimate that an influx of immune cells into the gut, interacting with sensory neurotransmitters, is a factor in IBD pathogenesis? Listen as these experts discuss the mechanisms that impact reduced blood flow and tissue ischemia which leads to IBD, and the unanswered questions which may help to unravel the link between IBD and cardiovascular disease.

Patients’ experiences and challenges in living with inflammatory bowel disease

The purpose of this study was to explore patient experiences in living with IBD and uncover factors that contribute to psychological distress.

Download Patients-Experience-and-Challenges-in-Living-with-Inflammatory-Bowel-Disease_A-Qualitative-Approach paper below

Purpose

Inflammatory bowel disease (IBD) significantly impacts patients’ quality of life and imposes a considerable psychological, social, and financial burden. While the relationship between disease activity and quality of life is well established, the subjective challenges of living with IBD are more difficult to assess, and suggestions for improving patient experiences are lacking. The aim of this paper was to explore the various challenges patients encounter in living with IBD and to propose suggestions for overcoming them.

Patients and Methods

This study utilized a qualitative descriptive design with thematic content analysis. Patients were recruited from the Gastroenterology Clinic at McMaster University Medical Centre from December 2014 to April 2015. Data were collected over the course of 5 focus group interviews using a semi-structured interview guide.

Results

Seventeen patients aged 25 to 77 years old (mean age 43 years, SD 17 years) were interviewed. Fifteen patients were diagnosed with Crohn’s disease and 2 patients were diagnosed with ulcerative colitis. Findings were categorized into 18 subthemes which were grouped into 4 broader themes: awareness factor, psychosocial impacts, financial burden, and quality of care.

Conclusion

IBD is associated with complex personal challenges across various demographics. Identifying and meeting the unique needs of individual patients may be achieved through improving communication between patients and their healthcare providers. Family-based education approaches, individualized psychotherapy with therapists familiar with IBD, awareness initiatives addressed to important stakeholders, and patient involvement in community support groups may improve overall IBD care.

Full research here.

The arthritis connection to inflammatory bowel disease (IBD): why has it taken so long to understand it?

Inflammatory bowel disease (IBD) associated arthritis is a subgroup of spondyloarthritis (SpA) that has suffered from lack of recognition in rheumatology clinical and research circles for over 100 years.

Download The-arthritis-connection-to-inflammatory-bowel-disease-IBD_why-has-it-taken-so-long-to-understand-it below.

Introduction

The initial description of a potential cause and effect relationship between arthritis and inflammatory bowel disease (IBD) likely goes back to well over 100 years ago in 1895 where William H White wrote, ‘among twenty-three cases of ulcerative colitis… two had urate of soda in their joints’.1 Almost 30 years later and into the next century, in 1922, Rea Smith, a surgeon based in Los Angeles, noted alleviation of swelling, pain and joint immobility in multiple patients with chronic arthritis on the conclusion of various bowel operations. Although he made mention of ‘ileocaecal coil’ changes on some of his patient’s X-rays, it is difficult to tell if his patients had true IBD or another intestinal affliction; the full characterisation of the various features of IBD phenotypes were not generally appreciated throughout the USA at that time. He then stated, quite prophetically, that ‘no study of a case of arthritis is complete without a careful investigation of the gastro-intestinal tract’.2

A decade later at the Mayo Clinic, where quite a few patients with ulcerative colitis (UC) had assembled for patient care, Arnold Bargen in 1929 and Philip Hench in 1935, in separate publications, drew the attention to peripheral arthritis manifestations in their patients with UC.3 4 They had observed and studied 1500 patients with chronic UC; 60 had arthritis which they felt was the most common complication of the colitis except for polyposis. They went further in their review and expanded the descriptions which became the beginning of an appreciation of the heterogeneric nature of arthritis in IBD. Bargen and Hench described four types of arthritis: (1) Arthritis preceding UC for a fairly long time, resembling the atrophic variety (‘atrophic arthritis’ was the prior description of rheumatoid arthritis (RA)), and considered unrelated to colitis, (2) Atrophic arthritis and colitis occurring at the same time but progressing independently, (3) Arthritis resembling atrophic arthritis that occurs during colitis remission and not during exacerbation of the bowel disease, and (4) The more common type, a subacute arthritis that flares with colitis exacerbations and experiences relief with colitis remission; all of this latter type showing a striking conformity with remissions and exacerbations of both occurring simultaneously. They considered the first three types as the unrelated coincident associations between RA and IBD, and these investigators concluded the fourth and more common type was a specific complication of the colitis itself rather than a coincident association of another disease.

The rheumatism reviews published in 1936 commented that the foregoing data from Bargen and Hench were admittedly incomplete to establish a new condition, referring to a specific colitis-arthritis entity.5 However, the review authors did comment about certain points that did distinguish this entity from garden variety atrophic arthritis (which was clearly progressive and relentless) and these included facts that the clinical relationships among the appearance, activity and recovery from the colitis and arthritis were similar, and most importantly, there was a greater tendency to periodicity as well as to complete remissions in the arthritis compared with what is typically seen in usual atrophic (rheumatoid) arthritis.

The rheumatism reviews’ authors clearly were wrestling with this newly recognised association between the gut and the joints. They were sceptical of those colleagues who were ‘glibly incriminating more or less symptomless intestines as the cause of atrophic arthritis’. They stated that “Those who blame the bowels may find some comfort in the evidence which shows that arthritis and intestinal diseases can be causally related by the hematogenous route, but the rarity of a proved relationship should give one pause”. The authors of the reviews stated quite specifically (and possibly presciently in the editorial comments section of the reviews) that there is a need for complete open-mindedness on this difficult problem of a symptomless gastrointestinal infection playing a role either as a primary or an underlying predisposing cause of arthritis.5

In retrospect, it is highly likely that the type of arthritis of large joints that occurs during colitis remission and not during exacerbation (Hench and Bargen type 3) reflects the now known association between colitis and the peripheral arthritis of ankylosing spondylitis (AS). This issue is examined in detail below; however, since AS was not recognised by Hench and Bauer (and particularly, by Bauer) as a separate entity from RA, it is very likely that it was assumed to be just another part of RA that, on occasion, was called rheumatoid spondylitis.6

There is a distinct literature gap from the late 1930s until the 1950s for arthritis-IBD associations. Why did this happen?

We are unable to find IBD-arthritis descriptions in the literature for the next decade or during the World War II postwar years; neither was a connection mentioned or referenced in the standard nomenclature of diseases approved by the American Rheumatism Association of 1952. For example, the first two editions in 1950 and in 1954 of the textbook Harrison’s Principles of Internal Medicine did not contain text, reference or discussion of IBD-related arthritis.6 Investigators who observed and commented on this information gap later in the century opined that the gap could be in part due to the attribution of these disease manifestations to be simply the coincidence of an association with RA.7 8

However, an alternate view of this literature gap is possibly related to a distraction caused by the description of a newly recognised arthritis syndrome potentially triggered by an exogenous infectious agent. The tenth rheumatism review published in 1953 describes a recently characterised condition called Reiter’s Syndrome where the statement is made that ‘Numerous reports on this syndrome had appeared’ referring to the American and English literature reports from the preceding years.9 The very first actual description of Reiter’s syndrome was made by the English physician Benjamin Brodie over a century earlier in 1818 where he observed a 45-year-old man with arthritis, urethritis and conjunctivitis.10 In 1916, Reiter in Germany and Fiessinger-Leroy in France described postdysenteric cases of urethritis-arthritis-conjunctivitis combinations occurring in soldiers living in close quarters during World War I.11 The initial characterisation of the syndrome in USA was performed by Walter Bauer and Ephraim Engleman in 1942, describing the Reiter’s triad in a 23-year-old man with no history of preceding diarrhoea or venereal disease; these investigators acknowledged ‘until the aetiology is established, this symptom complex should be referred to as a syndrome rather than a disease’.12

More comprehensive descriptions of this form of acute and subsequent chronic arthritis related to an infectious agent did occur during the intervening World War II years primarily from descriptions by Paronen et al in Finland where prevalent close-quarters living conditions promoted the spread of bacillary dysentery across populations of civilians.13 American publications describing this condition also could have contributed to distracting investigators from further studies characterising IBD-arthritis, although it was prophetically stated in the tenth rheumatism review that postdysenteric arthritis can be clinically indistinguishable from Reiter’s syndrome.9 Further, it is clearly mentioned in this 1953 rheumatism review that a possible relationship to bacillary dysentery should be considered under the discussion of the section called Aetiology of Reiter’s Syndrome.

Bringing the gut-arthritis connection to the forefront of critical thinking was a result of an unintentional experiment of nature, again related to the war effort. A shipboard epidemic of bacillary dysentery took place immediately after an American naval vessel left port from somewhere in Europe in 1962, where Dr Rolf Noer carefully documented the clinical sequelae of this epidemic from the beginning to its conclusion. He found 9 cases of Reiter’s syndrome out of 602 cases of bacillary dysentery, findings which could not be explained by chance. He then stated, “It appeared that our cases of Reiter’s disease were sequelae of bacillary dysentery”.14 Later and well after the genetic association between HLA-B27 and spondyloarthritis (SpA) was discovered, Calin and Fries were able to locate, examine, and clinically and genetically characterise five of the original nine Noer cases; they discovered an 80% positivity rate for HLA-B27 in these former navy enlisted men, all of whom had subsequently experienced severe, progressive destructive SpA. Calin and Fries concluded that B27 had an effect on both the incidence and severity of postdysenteric Reiter’s syndrome.15

Ahvonen et al in 1969 studied various arthritis manifestations associated with Yersinia enterocolitica infection and wrote, ‘transient non-purulent (reactive) arthritis with acute onset has been occasionally reported in association with bacterial infections such as those caused by BrucellaShigella, and Salmonella typhimurium’. They introduced the term ‘reactive arthritis’ for the first time in rheumatology literature.16 A clear and convincing separation between RA and what appeared to be an infectious agent (either from the gut or the genitourinary tract) triggering an acute and then a chronic disease most assuredly required the widespread recognition of the clinical and research importance of what later tuned out to be rheumatoid factor.17 18 The discovery and characterisation of the antibody nature19 of rheumatoid factor (and its absence in the patients with IBD-arthritis) is likely to be a major reason for the subsequent rejuvenated and focused interest in IBD-arthritis20 as a separate and distinguishable entity.

When was RA finally separated from the arthritis of IBD?

Luis Fernandez-Herlihy, an influential practitioner from the Lahey Clinic in Boston, summarised in 1959 his opinion describing (from a database of over 500 cases) the range of articular manifestations in patients with UC. He employed the following five categories: rheumatoid spondylitis, RA, erythema nodosum, arthralgias and acute toxic arthritis. Among these, acute toxic arthritis had the closest relationship with colitis; he noted that this category became clinically evident only with the exacerbation of colitis and relieved on colitis remission without any residual deformity. He then postulated ‘it is possible that acute toxic arthritis constitutes a milder, earlier, or perhaps an atypical form of Rheumatoid Arthritis’.21

However, clarity from Verna Wright and Geoffrey Watkinson whose observations were published in the same year as Fernandez-Herlihy nevertheless made a point of distinguishing ‘colitic arthritis’ from RA; this was based on the negative results from the (newly recognised) agglutination test for RA, and the recognition of asymmetrical joint involvement, lack of joint deformity and the absence of rheumatoid nodules in those with colitic arthritis.22 At around the same time, rheumatologists along with gastroenterologists began emphasising the presence of axial involvement in patients with IBD. Steinberg and Storey in 1957 made what appears to be the first association between AS and Crohn’s disease.23 Eric Bywaters and Barbara Ansell in the following year (1958) reported a case series of 37 patients with UC and arthritis, 6 of whom had sacroiliitis. They distinguished these patients from typical AS without colitis, from reactive arthritis (known at the time as Reiter’s syndrome), and from RA in three ways based on more female patients in the colitis group, absence of urethritis, and negative agglutination tests, respectively.7 The first US scholarly and scientifically controlled observation revealing a relationship between UC and AS was performed by Zvaifler and Martel in 1960; 100 cases of UC were chosen at random from a coded Roentgen database for UC. These investigators observed a 6% prevalence of AS when these imaging studies were reread.24 They stated that the concurrence of spondylitis with UC was too frequent to be explained by chance.

Read full research here.

You’ve Got Guts – May Is Crohn’s & Colitis Awareness Month

By 2022, it’s expected that more than 100,000 people will be living with Crohn’s disease and ulcerative colitis in Australia. As the rate of these inflammatory bowel diseases (IBD) continue to rise, Crohn’s & Colitis Australia (CCA) is urging people to share what it’s like to live with these life-long illnesses as part of Crohn’s and Colitis Awareness Month this May.

It takes guts to live with Crohn’s and colitis – and to speak about it.

Known as “invisible illnesses”, a person may look completely well on the outside, but can be suffering from abdominal pain, cramping, bleeding, diarrhoea, inability to eat, or severe urgency to find a toilet. These diseases affect every aspect of a person’s life, such as career or study plans or choices about when to start a family. For every person diagnosed, not only is their life changed forever, but so too are the lives of their family and friends.

Leanne Raven, Chief Executive of CCA, the peak support body for people living with Crohn’s disease and ulcerative colitis, is encouraging people with inflammatory bowel disease to reach out for support and share their experiences, particularly during Crohn’s and Colitis Awareness Month.

“Too often, people with an inflammatory bowel disease won’t share their problems or experiences with others or ask for help when they need it because of the stigma surrounding the diseases. At CCA, we create safe places, such as our Support Groups, so that people will no longer have to face these diseases alone.

“Many well-known diseases are understood with just a single word, but most Australians are still not familiar with the terms inflammatory bowel disease, Crohn’s disease or ulcerative colitis. The burden of explaining these diseases repeatedly to people who may not understand should be a problem of the past,” she said.

Crohn’s and Colitis Awareness Month offers an opportunity for people living with Crohn’s or ulcerative colitis to courageously speak up and share the obstacles they overcome daily to increase the wider public’s understanding of the diseases. Those living with the diseases can get involved in CCA’s ‘You’ve Got Guts’ campaign and share their brave stories and comments on social platforms.

“We are so fortunate to have our Ambassadors, including Justan Singh, Jacinta Parsons and Flic Manning, sharing their own stories during the Awareness Month. We hope their courage will inspire others with the confidence to share their own experiences with Crohn’s or colitis, even if it is just with one trusted person or an online post and be their own IBD Champion!

“CCA encourages people living with an inflammatory bowel disease to build a strong support network of health professionals, friends, family and work mates around them, to talk to when some extra support is needed. We hope that the more people living with these illnesses feel supported to share their experiences, the greater awareness we can raise,” Ms Raven said.

Anyone diagnosed with Crohn’s or colitis can join CCA, a community that understands. To learn more or to donate to support CCA’s outreach programs, visit https://www.crohnsandcolitis.org.au/awareness-month-2021/ or call 1800 138 029.

– ENDS –

For media enquiries contact Rachel Gemmell on 0428 998 279 or at [email protected].