Journal of Clinical Trials
Open Access

Phenotyping of Inflammatory Bowel Disease by Multi Omics Analysis

John Ming^* and Robert Sammy ^*Correspondence: John Ming, Department of Medical Sciences, St. Joseph Medical Center, Stockton, California, USA, Email:

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Description

Inflammatory Bowel Disease (IBD) known as Ulcerative Colitis (UC) is characterized by ascending large intestine inflammation with sporadic cycles of active inflammation and asymptomatic periods. UC is becoming an increasingly serious health danger for millions of people due to its early illness onset at roughly 30 years of age and rising incidence rates in developed nations (24.3/100,000 in Europe and 19.2/100,000 in North America). Patients with UC have a higher chance of developing colorectal cancer and thromboembolic problems because of the persistent inflammation. As patients are managed according to symptom subsets and their intensity in an iterative scheme, which has not fundamentally changed for the past 20 years, the chronicity of UC coupled with lifelong non-curative therapy of symptoms presents a challenge.

Numerous clinical observations, both invasive and non-invasive, as well as patient compliance with subjective assessments in the form of patient-reported outcomes are required by commonly used metrics like the Ulcerative Colitis Disease Activity Index (UCDAI) and MAYO-score. Genome-wide association studies and other extensive research were used to elucidate the genetic elements that underlie disease, but, as far as we are aware, no clear causal relationships have yet been found. The multidrug resistance gene MDR1 and 15 MHC locus HLA Class II alleles have both been mentioned as potential genetic risk factors.

In contrast to UC, studies focusing on the genetic landscape of the second most common type of IBD, Crohn's Disease (CD), discovered evidence of causal effects of single nucleotide polymorphisms with biological plausibility and dose response effects that were independently confirmed by numerous studies. The aforementioned arguments support the hypothesis that environmental factors are involved, along with other potential post-genomic influence elements such the general makeup and functionality of the proteome, metabolome, and microbiome. Post-genomic analysis technologies can offer greater insights into the molecular underpinnings of progression and escalation even for malignant diseases where genetic instability controls disease development.

The activation of the innate immune system observed on a proteome wide scale, the influence of the microbiome and its compositional alterations before and after diagnosis with UC, or general compositional changes in the metabolome or microbiome dependent co-metabolome, are just a few examples of recent studies that shed light on potential pathophysiologic mechanisms of UC. There are still pathophysiological processes that need to be discovered, even though these findings are moving UC-related research in a more molecularly focused direction. Studies concentrating on post hoc analysis of serological markers for the discrimination of clinically relevant cohorts indicated the need for thorough screening and the combining of data on several omics levels, as well as the limitations of existing marker molecules.

We provide a comprehensive, spatially resolved investigation of intra-individual colonic proteome changes during active UC. By combining a wide range of biomolecules, from amino acids to lipids, including eicosanoids and plasma proteins, the parallel analysis of plasma samples, which allowed uncovering systemic disease associated modifications, was carried out. Thus, we show that certain colitis-related biomarkers were still altered even when no new symptoms were recorded, suggesting potential chronicity drivers. In-depth molecular phenotyping of the UC illness manifestation is provided by the current multi omics analysis, which also hints to potential new treatment targets and potential biomarker candidates.