The Effect Of Iga Antibodies Play A Major Role On Maintaining Homeostasis At Mucosal Surfaces Including The Gastrointestinal Tract ( Brandtzaeg Essay

IgA – antibodies that are secreted across mucus layer to prevent microbes from penetrating cell bodies

binds with the surface IgE and mediators are released (Story, 2012). TH2 cells are involved

IBD is the result of an abnormal innate repsonce to antigens in the intestinal flora, thus activating the adaptive immune repsinse; a process in which genome wide stidues have implicated several genes such as NOD2 and ATG16L1, both involved in the intracellular processing of bacterial antigens. PSC has shown similar mechanisms characterized by Th1 cytokines and structuring. However, PSC has aslo shown close association with classic autoimmune diseases such as type 1 diabetes, rheumatoid arthiritis, and others; has shown a strong association with the human leukocyte antigen(HLA) DRB1*0301 haplotype; and has shown a variety of autoantigens to neutrophils and biliary epithelial cells (BEC). (1) Thus suggesting the immunopathogenesis of PSC is complicated and may have more than one cause.

Lipopolysaccharides (LPS) in their cell wall leads to the monocyte activation and production of RA-associated cytokines interleukin (IL)-1 and IL-33 through the TLR pathways. HLA-B27 has been shown to be a predisposing factor to increases the risk of developing arthritis that is more likely to be severe and prolonged[8]. However, there is strong evidence found between reactive arthritis and Human Leukocyte Antigen (HLA) B27 genotype (Major histocompatibility complex) in humans that are present on the surface of all body cells that contain a nucleus, and high concentrations were found in in leukocytes. HLA-B27 has been shown to be a predisposing factor in individuals with reactive arthritis and also affect the elimination of the infecting bacteria. Despite, HLA-B27 is not trigger the initial infection itself, but it increases the risk of developing arthritis. Overall, burden rates of Salmonella-associated arthritis to vary between 6% and 30% followed by the other enteric infection reported to be between 1 and 4% in adults with Campylobacter or Shigella

Overall Scientific premise: Inflammatory bowel disorder (IBD) affects an estimated 1-1.3 million people in the US alone, according to the Centers for Disease Control and Prevention (CDC). Although immune intolerance in the gut is considered one of the factors driving disease progression, the origins of IBD remain unknown. Enteric infections play a major role and could potentially be an underlying cause of IBD (PMID:15256979). Staphylococcus aureus, an ESKAPE pathogen, one of the major causes of foodborne enteric infections. Nevertheless, there is a considerable knowledge gap as to how S. aureus can cause dysregulation and inflammation at enteric mucosal surfaces that could lead to IBD. Previous studies along these lines led to the

Helicobacter pylori is structurally small, gram negative rods which is microaerophilic in nature and has capability of colonizing regularly in human stomach (Strausbaugh et al., 2002). Due to such colonizing capability, it is regarded as one of the most common bacterial pathogen present in almost 50% of the world’s population (Zhao et al., 2014) and the reason behind such well adaptation or enduring of H.pylori in the Human’s stomach is due to the combined effects of several factors that addresses different challenges or obstacles presented by the nasty environment inside the stomach (Montecucco and Rappuoli, 2001). Helicobacter pylori produce the urease that neutralize the gastric acid or shows the buffering effect around the surroundings within the stomach. Moreover, it has a capacity of crossing the thick mucus lining of the stomach easily and binding itself to the antigen known as Lewis antigen that are basically present in gastric cells and whose function is to secrete different factors associated with stimulating and attracting the inflammatory cells and Toxin VacA that performs the multiple functions and such activities of H.pylori is possible due to its helicoidal shape the mode of action of flagella present. Mainly, the presence of the cag pathogenicity island (Cag-PAI) which is a 40-kb DNA insertion elements containing 32 genes and encoding a type IV secretion system helps in the optimal fitness of the bacteria in the stomach and appearance of pathogenic traits.

Scientists are beginning to recognize the link between gut microbiota and inflammation and the role it plays in the pathogenesis of obesity-related disorders like diabetes (type two). Using animals, scientists have been able to link obesity models of a microbiota composition that is different than what is expected when observed for obesity development and insulin resistance. This means that this altered microbiota composition is linked to the development of obesity and insulin resistance. This can be seen through multiple mechanisms, including “increased energy harvest from the diet, altered fatty acid metabolism and composition in adipose tissue and liver, modulation of the gut peptide YY and glucagon-like peptide (GLP)-1 secretion, activation of the lipopolysaccharide toll-like receptor-4 axis, and modulation of the intestinal barrier integrity by GLP-2”. It is imperative to understand the mechanisms that regulate gut microbiota compositions that produce these various compositions. During infancy, several factors that can affect the gut microbiota include delivery mode, type of feeding, hospitalization, and possible prematurity. The use of antibiotics and the infant’s diet are also becoming increasingly recognized as factors that can affect one’s susceptibility to developing type two diabetes. The typical Western diet has played a significant role in

After H. pylori infection is acquired, the immune system typically reacts by producing IgG against organism-specific antigens. Because the bacterial infection H. Pylori is "silent" and causes no symptoms, many can have this without ever knowing. (Pilotto

In this experiment, the scientists compared the amount of autoantibodies present in the digestive system of BN rats and BNm rats. An extraction of sera from BNm rats revealed the presence of autoantibodies that recognize and attacked wall components of arterioles and venules, as well as muscular layers of the intestine (Chabod et al. 2012). Furthermore, the intestinal tracts of BNm rats were noticeably marked with macroscopic lesions, multifocal infiltration, and granulomas (Chabod et al. 2012). In comparison, BN rats lacked the same autoantibodies found the mutated rats and tended to have less intestinal abrasions and abnormalities (Chabod et al. 2012). To determine whether CD4 T cells contributed to the development of IBD, the researchers experiments with wild type BN rats that were thymectomized and given anti-CD4 treatment (Chabod et al. 2012). The experimented rats showed no signs of IBD, indicating that mutation in the Themis gene is required for the development of IBD seen in BNm rats (Chabod et al. 2012). This further supports the researchers’ notion that a mutated Themis gene, along with subsequent reduction of viable CD4 T cells, is closely related to the occurrence of

This mechanism of defense is called colonization resistance (Sekirov et al. 2010). Resident microbiota and incoming pathogens compete for resources in the intestine. In a healthy intestine, normal microflora establishes mutually beneficial relations with intestinal mucosa and effectively eliminates pathogens. Inflammatory host responses triggered by virulence factors of S. Typhimurium can alter conditions in the intestine and shift the competition between protective microbiota and the incoming pathogen, which is able to survive in and profit from the altered niche (Stecher et al. 2007), whereas to intestinal microbiota host responses are unfavorable (Sekirov et al.

Most of the T cells in the gastric mucosa differentiate into Th1 cytokines, the others become anergic. Anergy of T cells may be brought about by the interaction of T cells with the gastric epithelial cells that express B7-H1. B7-H1 is a costimulatory molecule that increases during H. pylori infection. In gastric epithelial cells the development of Treg cells from naïve T cells is brought about by exposure to H. pylori via induction of BH-71. This suggests that H. pylori might utilise the epithelium to promote the development of Treg cells which play a vital role in suppressing effector T cells. Because of this the existence on Treg cells in H. pylori infection may diminish the adaptive immune

Adheres to human intestinal epithelial cells at “the apical brush boarder of the enterocytic Caco-2 cells” and binds to the muscus produced “by the HT29-MTX musuc secreting cells” (1). This was all mediated by a proteinaceous adhesion-promoting factor that is species specific.

It uses chemotaxis to determine which direction it must travel by sensing the proton gradient within the stomach. It connects to host cells via an array of different adhesins which attach the bacterium to lipid or carbohydrate components on the cell membrane. (2) One of the largest contributors to Helicobacter Pylori’s pathogenicity is its pathogenicity island. This pathogenicity island (type 4) is often absent in asymptomatic carriers and is thought to give the bacterium the ability to cause ulceration of the stomach lining. This pathogenicity island injects peptidoglycan from their cell wall as an inflammatory agent to stimulate the host’s immune response. (2) This response by the immune system is thought to cause the eventual ulceration of the gastric lining. (1) To combat the effects of the highly acidic stomach, a defense mechanism of the body, Helicobacter Pylori produces ammonia to counter the acidity of the hydrogen ions.

Biedermann, L., & Rogler, G. (2015). The intestinal microbiota: its role in health and disease. European Journal Of Pediatrics, 174(2), 151-167. doi:10.1007/s00431-014-2476-2

In fish mucosal immune system is mainly associated with gut, skin and the gill; these are the main mucosal surfaces and immune barriers. Mucosal immune system is a major part that responds and protects against pathogens that enter the body via mucosal surfaces. An inductive site for mucosal immunity possesses organized mucosa-associated lymphoid tissue (MALT) and local and regional draining lymph nodes (LN), while the effector sites have distinctly different histological compartments. In fish hindgut seems to play vital role in antigen uptake (Rombout et al., 1993). Absorption of macromolecules by intestinal epithelial cells and many diffusely distributed leucocytes as well as intraperitoneal lymphocytes (IELs) are described in numerous fish