Essay On Cecal Tonsil

Normally, tonsils limited to its area, but the growth of the tonsils can be expanded as a result of prolonged or repeated infections or enlarged tonsils. Tonsil microscopy structure is closely related to its function as an immune organ. Kripte-epithelium works as the immune system to antigens entering through the respiratory air, and what is eaten by a person.

Signaling proteins that alert the immune system an infection is present and that sometimes directly fight pathogens are the:

Inflamed tissues from Ulcerative Colitis (UC) patients show increased oxidative and nitrosative damage, leading to accumulation of mutations and dysplastic progression27,28. Infiltrating leukocytes from these patients have increased ROS production in basal conditions and in response to different ligands29. Since TLR4 mediates ROS production in leukocytes22, it is easy to speculate that immune cells drive pro-tumorigenic effects of TLR4. However, bone marrow-transfer experiments in our lab demonstrate that non-immune TLR4 participates in development of neoplasia8. Furthermore, we have shown that epithelial TLR4 activation predisposes to colitis and CAC6. To understand the role of epithelial TLR4 in neoplasia, our research has focused on the

Despite the wide-range of microbes affected by the innate immune system, the activity of peptides associated with the immune response seem to be highly sequence specific. The peptides specifically target areas of the membrane with high curvature. (Mark, 601)

Tonsillitis can be described as the inflammation of the non-encapsulated lymphoid structures, lingual and palatine tonsils. These lymphoid tissues are part of the immune system and are the first line of defence against pathogens in the oral cavity. The palatine and lingual tonsils are located underneath the stratified squamous epithelial mucosa of the tongue and oropharynx. The tonsils’ response to bacterial or viral infections of the epithelial mucosa, e.g. streptococci and the Epstein-Barr virus (EBV), is inflammation and enlargement of the tonsils and antibody responses, largely IgA. Symptoms of tonsillitis include Sore throat and fever.

By cloning the LPS locus, he was able to identify a ‘toll-like receptor’ (TLR4) which acted sense the presence of invading microbes bearing LPS. Receptors of the same family, ten of which are now known to exist in humans, each ‘tuned’ to detect different kinds of microbes, also initiate inflammation to combat infection, but sometimes shock as well. It was for this work that Beutler won the Nobel Prize, and his team at the University of Texas Southwestern Medical Center continues to search for proteins that protect mammals against defined infections. In the process, they have identified genes required for other functions, including the regulation of iron absorption, hearing and the development of embryos

The specific aims for Experiment 1 was to study the efficiency of phagocytosis analyzing the macrophages’ abilities to engulf Nile Red beads. We also looked at the impacts of effectors on their abilities and also different concentrations of resolvin. For Experiment 2A, we studied the efficiency of efferocytosis by analyzing the macrophages’ abilities to engulf and digest apoptotic cells under various effectors and concentrations. In Experiment 2B, we studied the efficiency of efferocytosis by analyzing the macrophages’ abilities to engulf and digest apoptotic cells under effectors and cytokines. We hypothesized that having an effector (resolvin D-2 and lipoxin) and a pro-resolving cytokine (IL-13) would increase efferocytosis than having either one alone or having neither one.

To address this issue, we will be using NARSA (Nebraska Transposon Mutant library) library consisting of single transposon insertion mutants covering almost 90% of S. aureus USA 300 genome. We will use a translational reporter line of C. elegans, in which HLH-30 has a GFP tag to monitor nuclear accumulation. Identification of the S. aureus genes involved in HLH-30 activation will allow us to pinpoint the PAMP/DAMP which is recognized by the host. Achieving this aim will allow us to manipulate this conserved innate signaling pathway and further our fundamental understanding of how the host detects pathogen.

Pharyngitis (a sore throat) is considered to be an infection of the back of the throat which include the tonsils and is caused by streptococcal (Fine, Nizet, & Mandl, 2013). During the winter months, more than 12 million people are seen in the ED complaining of a sore throat (Fine, Nizet, & Mandl, 2013). The pharyngitis can be caused by group A streptococcal (GAS) or acute pharyngitis (viral). The symptoms of streptococcal and viral pharyngitis are so similarity that the two cannot be differentiated by their clinical signs and symptom. An adequate distinction should be made between the two according to the American College of Physicians and Center for Disease Control and Prevention, and clinical scores were applied to classify risk for GAS

Immunity depends on the recognition of pathogen components by innate receptors expressed on immune and non-immune cells against microbial pathogens. Innate receptors are conserved germ-line-encoded proteins and include TLRs (toll-like receptors), RLRs [RIG-1 like receptors (retinoic acid-inducible gene-1)] and NLRs (nod-like receptors). Receptors recognize pathogens or pathogen-derived products in different cellular compartments, for instance plasma membrane, endosomes or the cytoplasm, and induce the expression of cytokines, chemokines and co-stimulatory molecules to eliminate molecules to eliminate pathogens and instruct pathogen specific adaptive immune response.

pylori’s expression of a Type IV secretion system suggests it utilizes horizontal gene transfer to uptake DNA to and from host cells or other bacterial cells in its environment. H. pylori uses its T4SS to inject the highly pathogenic cagA protein into the gastric epithelial cells of the human host which then phosphorylates and interferes with human host signaling cascades related to cell differentiation, proliferation, motility and cytoskeletal rearrangement causing H. pylori induced proinflammatory responses via IL-8 activation and NF-κB stimulation. This sequence of events results in the elongation of infected host epithelial cells, characteristic of H. pylori illness, termed the “hummingbird phenotype (2).” It has been shown that almost 100% of all Eastern Asian strains express the cagA protein while only about 60-70% of the Western strains express a functional cagA protein. It is clear to see that geographical regions have dramatic differences in virulence and pathogenicity of H. pylori strains further proving the vast diversity in the genetics of the bacteria. The H. pylori T4SS can be assessed in three different clusters of genes. The first is the protein type IV secretion system (pT4SS) whose primary function is to translocate the cagA protein. The cag pathogenicity island uses 18 out of its 27 genes to translocate cagA into the host cells and 14 genes are used in

1) [4-6, 2, 7]. Maintaining a delicate balance between tolerance and responsiveness in the intestinal mucosal immune system is very important and disruption of this balance leads to chronic intestinal inflammation [53, 4]. A properly functioning mucosal immune system, the mucosal barrier, and the presence of endogenous microbiota are the main elements in the maintenance of intestinal homeostasis [54]. The occurrence of an aberrant immune response to endogenous microbiota has been proposed to play an important role in the disease pathogenesis of CE in dogs [8, 2, 7]. Thus, phagocyte activation and their biomarkers may represent potential and useful markers of inflammation in dogs with

These patterns, which appear to be regulated via toll-like receptors (TLRs)9, promote and exacerbate the inflammatory response acting as endogenous danger signals after trauma. This relationship between injury and the innate immune system characterizes a vital part of The Danger Theory proposed by Matzinger, which suggests that the role of danger signaling recognized by pattern recognition receptors (PRRs) is to protect the body from harm and as such, propagates an immunoinflammatory response10. For example, we have recently demonstrated that γδ T-cells can be activated in vitro by mitochondrial DAMPs, leading to increased TLR-2 and TLR-4 expression and resultant cytokine production11. Our lab has also shown that circulating monocytes are activated as early as 24 hrs after burn in mice subjects via increased expression of TLR-212. These findings suggest that elevations in circulating DAMPs may result in activation of the innate immune system and lead to inflammatory complications in severely injured human

The best characterised signalling PRRs are the Toll-like receptors (TLRs). They are present in plants, invertebrates and vertebrates, and represent a primitive host defence mechanism against bacteria, fungi and viruses.

Tonsillitis is inflammation of the tonsils, with particular reference to the palatine tonsils , two ovoid bodies of about 2,5 - 3,5 cm in length and two in width consist of lymphoid tissue and placed at the sides of the throat, immediately behind and above the base of the tongue. The tonsils are exposed to inflammation, usually viral, bacterial, more rarely, resulting in enlargement of themselves and with referred pain in the throat and in some cases ear.