**2. Inflammatory bowel diseases**

#### **2.1 Etiology and pathophysiology**

The etiology of IBD is not fully elucidated, but it seems that it often occurs in genetically susceptible individuals after an inappropriate immune response to the microbiota; so, the key to the pathogenesis of IBD is represented by the intestinal immune system. Typically, the gut epithelium prevents antigen or bacteria entry into the circulation by sealed intracellular junctions. In IBDs, because of the inflammation or the loss of the primary barrier function, these intracellular junctions are defective. The Goblet cells produce mucus as an additional protective mechanism [4].

Crohn's disease is a patchy inflammatory disease affecting any part of the digestive tract, from the mouth to the anus and perianal area. Ulcerative colitis is a disease of continuity involving the rectum and colon in a centripetal manner and associating extraintestinal involvement of the skin, bones, or eyes [5].

#### **2.2 Histopathology**

In the active form of IBD, the microscopic evaluation reveals the infiltration of lamina propria with a mix of macrophages, dendritic cells, neutrophils, and natural killer T cells. Because of the increased activation and number of these cells, there is also an increasing level of cytokines, interleukin 1b, tumor necrosis factor-alpha, and interleukin 23-TH 17 [6–8].

#### **2.3 Clinical manifestations**

Patients with ulcerative colitis describe tenesmus, abdominal pain, and a sensation of incomplete evacuation. Still, the most upsetting symptom is represented by bloody diarrhea with or without mucus. The physical exam reveals predominantly left upper or left lower quadrant abdominal pain [1].

Patients with Crohn's disease have different clinical manifestations, depending on the region of gastrointestinal involvement. Symptoms like right lower quadrant pain, non-bloody diarrhea, and weight loss are the most common in Crohn's disease [9].

#### **2.4 Diagnosis**

When diagnosing IBD, the clinician has to combine inflammatory laboratory markers, clinical findings, endoscopic biopsies, and imaging findings. The guiding

**131**

*Is a Fecal Microbiota Transplant Useful for Treating Inflammatory Bowel Disease?*

despite medical treatment, having a poor quality of life [14–16].

person. This therapy procedure was firstly documented in 1958 [17].

except the cecum, where aerobic bacteria achieve high frequencies [21].

*Ruminococcus*, *Eubacterium*, and *Faecalibacterium* [22, 23].

transplantation had positive outcomes [18–20].

laboratory tests are represented by leukocytosis, microcytic anemia, thrombocytosis, and elevated levels of C-reactive protein and erythrocyte sedimentation rate [10–12]. The imagistic methods that are useful when diagnosing IBD or assessing complications are ultrasound, magnetic resonance imaging (e.g., rectal fistulas), and computed tomography (e.g., perforation or bowel obstruction). But to confirm a diagnosis of IBD biopsies obtained via colonoscopy or esophagogastroduodenos-

There are many conventional and novel drug treatments that have proven efficacy in IBDs (aminosalicylates, steroids, biological therapies, and immunosuppressants). However, many patients become refractory to standard management of the disease, some of them presenting significant side effects that even require surgery. There are an increasing number of patients that live with mild active symptoms,

The gastrointestinal microbiota has a dominant role in driving inflammation in IBD; that is why medications that manipulate the microbiota have been investigated

Alternative treatment in IBD management is fecal microbiota transplantation (FMT) consisting of the transfer of gut microbiota from a healthy donor, via infusion of a liquid stool suspension, to restore the intestinal microbiota of a diseased

The reports concerning the patients that have been subjected to fecal microbiota

In humans, the gut microbiota varies across the digestive tract. There are relatively few bacterial species present in the stomach and small intestine, compared to the colon, which is the habitat of the highest microbial density—up to 1012 cells per gram of intestinal content. Ninety-nine percent of the bacteria are anaerobes,

Although many species in the human gut have not been studied because they cannot be cultured by the ways yet discovered, there are four dominant phyla: *Proteobacteria*, *Bacteroidetes*, *Actinobacteria*, and *Firmicutes*. Most bacteria belong to the genera *Bifidobacteria*, *Clostridium*, *Peptostreptococcus*, *Bacteroides*, *Peptococcus*,

The gut microbiota is still intensively studied. Besides metabolizing indigestible food compounds, it stimulates the gut immune system, directly defending against pathogens. It has a substantial role in developing and maintaining the intestinal epithelium and inducing antibody production. Also, studies focused on its action in

The intestinal barrier provides protection against pathogenic invasion through many defense mechanisms, including butyrate and other metabolically protective products, the commensal bacteria competitively preventing pathogenic bacteria's

(e.g., probiotics, prebiotics) with variable evidence of their efficacy [15, 16].

*DOI: http://dx.doi.org/10.5772/intechopen.91444*

copy is necessarily needed [12, 13].

**2.5 Options of treatment**

**3. Microbiota**

**3.1 Normal functions**

the gut-brain axis [23, 24].

*3.1.1 Direct inhibition of pathogenic bacteria*

#### *Is a Fecal Microbiota Transplant Useful for Treating Inflammatory Bowel Disease? DOI: http://dx.doi.org/10.5772/intechopen.91444*

laboratory tests are represented by leukocytosis, microcytic anemia, thrombocytosis, and elevated levels of C-reactive protein and erythrocyte sedimentation rate [10–12].

The imagistic methods that are useful when diagnosing IBD or assessing complications are ultrasound, magnetic resonance imaging (e.g., rectal fistulas), and computed tomography (e.g., perforation or bowel obstruction). But to confirm a diagnosis of IBD biopsies obtained via colonoscopy or esophagogastroduodenoscopy is necessarily needed [12, 13].

#### **2.5 Options of treatment**

*Human Microbiome*

mucosal adherent bacteria are increased [1, 2].

include the entire colon into the cecum [1–3].

**2. Inflammatory bowel diseases**

**2.1 Etiology and pathophysiology**

**2.2 Histopathology**

and interleukin 23-TH 17 [6–8].

left upper or left lower quadrant abdominal pain [1].

**2.3 Clinical manifestations**

pathogenesis of IBD is increasing; this fact results from an inappropriate immune response towards components of the commensal microbiota. In IBD, the diversity of luminal microbiota is reduced. *Firmicutes* (bifidobacteria, lactobacillus, and *Faecalibacterium prausnitzii*) are especially decreased. On the opposite side, the

Both ulcerative colitis and Crohn's disease share many common features like bloody stools, diarrhea, fever, and abdominal pain, but each of them also has unique features. There are many differences between the two entities, the most important being the depth of involvement in the bowel wall and their location. Crohn's disease results in transmural ulceration of any portion of the gastrointestinal tract, but it affects most often the colon and terminal ileum; at the opposite side, ulcerative colitis affects the rectum, but it may extend beyond the sigmoid and into the sigmoid or

The etiology of IBD is not fully elucidated, but it seems that it often occurs in genetically susceptible individuals after an inappropriate immune response to the microbiota; so, the key to the pathogenesis of IBD is represented by the intestinal immune system. Typically, the gut epithelium prevents antigen or bacteria entry into the circulation by sealed intracellular junctions. In IBDs, because of the inflammation or the loss of the primary barrier function, these intracellular junctions are defective. The Goblet cells produce mucus as an additional protective mechanism [4]. Crohn's disease is a patchy inflammatory disease affecting any part of the digestive tract, from the mouth to the anus and perianal area. Ulcerative colitis is a disease of continuity involving the rectum and colon in a centripetal manner and

In the active form of IBD, the microscopic evaluation reveals the infiltration of lamina propria with a mix of macrophages, dendritic cells, neutrophils, and natural killer T cells. Because of the increased activation and number of these cells, there is also an increasing level of cytokines, interleukin 1b, tumor necrosis factor-alpha,

Patients with ulcerative colitis describe tenesmus, abdominal pain, and a sensation of incomplete evacuation. Still, the most upsetting symptom is represented by bloody diarrhea with or without mucus. The physical exam reveals predominantly

Patients with Crohn's disease have different clinical manifestations, depending on the region of gastrointestinal involvement. Symptoms like right lower quadrant pain, non-bloody diarrhea, and weight loss are the most common in Crohn's disease [9].

When diagnosing IBD, the clinician has to combine inflammatory laboratory markers, clinical findings, endoscopic biopsies, and imaging findings. The guiding

associating extraintestinal involvement of the skin, bones, or eyes [5].

**130**

**2.4 Diagnosis**

There are many conventional and novel drug treatments that have proven efficacy in IBDs (aminosalicylates, steroids, biological therapies, and immunosuppressants). However, many patients become refractory to standard management of the disease, some of them presenting significant side effects that even require surgery. There are an increasing number of patients that live with mild active symptoms, despite medical treatment, having a poor quality of life [14–16].

The gastrointestinal microbiota has a dominant role in driving inflammation in IBD; that is why medications that manipulate the microbiota have been investigated (e.g., probiotics, prebiotics) with variable evidence of their efficacy [15, 16].

Alternative treatment in IBD management is fecal microbiota transplantation (FMT) consisting of the transfer of gut microbiota from a healthy donor, via infusion of a liquid stool suspension, to restore the intestinal microbiota of a diseased person. This therapy procedure was firstly documented in 1958 [17].

The reports concerning the patients that have been subjected to fecal microbiota transplantation had positive outcomes [18–20].
