Medical Case Reports

Introduction

Worldwide, autoimmune diseases, such as gastrointestinal chronic inflammatory disorders, pose a significant threat to public health. Celiac Disease (CD) and Inflammatory Bowel Disease (IBD) are two types of these conditions; Crohn's infection and Ulcerative Colitis (UC). The significant reasons for these pathologies remain to a great extent obscure because of the superposition of a few gamble factors like hereditary inclination, epigenetic viewpoints, safe dysregulation, and healthful and natural elements, which gives to outrageous intricacy. In this vein, numerous studies have suggested that people with genetic predispositions to autoimmunity encounter environmental agents, particularly DNA methylation changes that trigger the onset of these disorders. Additionally, nutritional factors are thought to be one of the underlying causes of the onset of gastrointestinal chronic inflammatory diseases. The most well-known example is celiac disease, a systemic autoimmune disorder that occurs in people with genetic predisposition who consume gluten. As a result, nutritional factors may be linked to epigenetic factors, raising the risk of these diseases even more.

Immune System Issues

It has been reported that Histone Methyltransferases (HMTs) and Histone Deacetylases (HDACs) suppress transcription by binding to MBD proteins with methylated DNA. Qualities communicated after histone alterations (methylation and acetylation) altogether influence phenotypic results and early undeveloped turn of events. Given the intricacy of these pathologies, recommended medicines for these immune system issues are as yet missing in light of the fact that the basic components are not yet clarified. In addition, the pharmacological difficulties posed by these diseases have prompted the majority of doctors to recommend palliative treatments and an adaptable lifestyle for patients. In this sense, a few scientists recommend utilizing normal items got from therapeutic plants to give answers for forestalling risk factors and treating IBD.

Drugs and surgery now make up the majority of clinical treatments for inflammatory bowel diseases. The ongoing pharmacological medicines incorporate 5-aminosalicylate (5- ASA), mixtures, for example, sulfasalazine and mesalamine), corticosteroids (like cortisone and budesonide), immunomodulators, (for example, thiopurines and methotrexate), hostile to TNF specialists (like infliximab, adalimumab, and golimumab), against integrins (Vedolizumab), and calcineurin inhibitors (cyclosporine), which are utilized to smother aggravation and instigate mucosal recuperating. However, prolonged use of these medications may result in severe adverse effects and complications, such as gastrointestinal disturbances, systemic immunosuppression, kidney toxicity, diabetes, weight gain, elevated blood pressure, and an increase in infections. Due to the patient's age and physical condition, surgical treatment is limited and may result in complications such as a pelvic infection, extensive bleeding, or intestinal perforation.

In vitro and in vivo studies have demonstrated that some natural substances, such as flavonoids, terpenoids, and phenolic acids, are effective against these inflammatory autoimmune diseases, particularly ulcerative colitis. Natural substances' potential as a pharmacological treatment for Crohn's disease and celiac disease, on the other hand, has only been the subject of sporadic and insufficient research to date. In addition, research showed that natural products found in fruits and vegetables could help prevent chronic inflammatory intestinal diseases by reducing immune response regulation, inhibiting pro-inflammatory cytokines, and inhibiting enzymes. In light of the former conversation, this survey planned to distinguish the different gamble factors engaged with the beginning of ongoing provocative immune system issues influencing the intestinal system and feature the other regular substances that assume a critical part in balancing the components embroiled in the improvement of these pathologies.

The immune system's hyperactivity is what leads to an autoimmune disease. The immune system's goal is to protect the body from harmful or foreign agents like viruses and bacteria, toxins, and cancer cells. The immune system uses cells to identify foreign agents, destroy them, and transmit messages in order to defend it. In addition to these cells, cytokines act as a messenger between antibodies, which are responsible for identifying foreign agents, and various organs or cells. The immune system is able to tell the difference between self (body cells) and non-self (foreign substances) under normal circumstances; Breaking this tolerance leads directly to autoimmunity. In immune system sicknesses, the resistant framework commits errors and obliterates a few self-tissues, thinking of them as non-self. Immune system sicknesses can be recognized into organ-explicit and vague in which a few organs are impacted progressively or at the same time. Notwithstanding the clinical and phenotypic variety of organexplicit and non-organ-explicit immune system illnesses, there are various immunological instruments that lead to injury autoimmunity.

Multiple Cell Types

Multiple cell types are involved in tolerance processes, which take place either centrally (thymus and bone marrow) or peripherally (secondary lymphoid organs). Disappointments of these resistance processes are at the focal point of immune system infections; they are numerous and frequently not recognized. The reasons for immune system infections remain generally obscure; however, a number of studies have demonstrated that they combine genetic predisposition with environmental factors. In addition, having a positive family history of an autoimmune disease is quite common. The risk of transmission from parents to children remains low and varies depending on the disease, and recent studies have confirmed that genetic inheritance and epigenetic factors are significant but far from sufficient to explain the development of the autoimmune disease. Humans have the same number of genes, all of which are arranged in the same way on the DNA. Each gene can take many different forms, making each person unique, but some genes make people more likely to get other autoimmune diseases; therefore, these genes promote autoimmunity rather than a specific disease. HLA, PTPN22, and IRF5 are the genes that are most frequently studied.

Autoimmunity is thought to develop when genetically predisposed individuals come into contact with the diseasecausing environmental agents, particularly DNA methylation changes. In this regard, recent research suggested that individuals with a genetic predisposition to the autoimmune disease may develop autoimmunity as a result of interactions between epigenetic and genetic elements. Additionally, the majority of autoimmune diseases are more prevalent in women, leading some researchers to speculate that the X chromosome may be to blame for this high prevalence. Th1-mediated immune responses and altered T cell localization were cited as reasons for this female dominance in other studies.