Talk:2016 Group 5 Project
|Group Projects - Blood Cell Biology - Updated 21 April|
|This year's main topic is Blood Cell Biology. Each group should discuss with group members the specific sub-topic that will be covered by their project.
Here is a list of some of the cell types (Structure and Function)
Embryology - content cannot be reused but a useful resource about cell development.
Histology - images these can be reused in your projects.
|Group Assessment Criteria|
Group Assessment Criteria
Z5015719 (talk) 18:14, 22 March 2016 (AEDT) hey guys! so does anyone have any preferences for which topic to do? I feel like they'd all be quite good, the options from red blood cell to monocyte/ macrophage look particularly good to me in terms of the marking criteria and so does the mast cell but again they all look pretty good to do. Thoughts?
- Cell surface specialisations
- History of the cell and research
These two articles are review articles but they're a good place to star for background info and to find primary articles.
Ok, so here is the brainstormed list of suggested subtopics: ○ Introductory paragraph ○ History § Current research § Future research ○ Morphology/structure ○ Physiology ○ Biochemistry ○ Pathology ○ CNS/ autism ○ Staining----- ○ glossary
By week 5, let's all have read the wikipedia page on mast cells, read those 4 research articles and decide which sections we're going to write!
- content - correctly cited and referenced: referenced source, copyright info, student image template, reference appears with the image
- don’t cite review article as original research- there is no new information here
- element of teaching to peer level
- citation of literature, put to date research in area (published in the last 2 years etc) - current areas of research about the cell
- Identify key research labs that are researching on the topic: external links that is researching something specific about the cell
- feedback in the group discussion (positive criticism)
- animations, videos (yt) (insert link),
- At least one image is a student drawn image
Lab 3 Assessment
Four article summaries on one selected sub-section
Role of Mast Cells in disease and examples of diseases.
The aim of this article was to analyse the relationship between mast cells and the glycoslphosphatidylinositol-anchored molecule CD48, and the role of this relationship in the recognition (and immune response) of pathogenic E. coli via FimH. Malaviya et.al. demonstrated that CD48 binding to E. coli that expressed FimH could be inhibited by pretreatment of mast cells with CD48 antibodies. It was further shown that FimH-expressing E. coli effectively binds to recombinant CD48 in a cell free system and that the insertion of cDNA encoding rat CD48 into CHO (Chinese Hamster Ovary) cells resulted in CD48 acting as functional FimH receptors. Additionally, they found that pretreatment of Bone Marrow mast cells with increasing concentrations of phospholipase C resulted in a significant reduction in mast cell ability to release TNF-a (therefore decreasing neutrophil chemotaxis) after exposure to FimH-expressing E. coli. Therefore, it was shown that mast cells TNF-a response to FimH expressing bacteria is mediated by CD48 molecules which could be clinically significant in the immune response to pathogenic E. coli in the immunocompromised. 
This article would be useful when talking about the role of mast cells in disease as it talks about the relationship between mast cells and the FimH expressing bacteria (specifically E. coli). An understanding of the mechanisms of recognition and the immune response to bacterial pathogens is an important section of the cells role in disease. This study also explains the implications of the environment surrounding the mast cell on their ability to efficiently carry out normal functions and the effects that would have on the pathogenesis of a disease. Finally, the study also provides an explanation of the clinical significance of its findings and a possible treatment for the immunocompromised.
This study analyses the quantity of mast cell infiltration into colon tissues identified with different pathologies, including colonic polyps, well-differentiated colonic adenocarcinoma and poorly-differentitated colonic adenocarcinoma. The analysis of mast cell infiltration aimed to understand the relationship between mast cell presence and the development of colorectal cancer. Bone Marrow mast cells were co-cultured with colon cancer cells for 24-48 hours and the increase in the rate of colon cancer cell proliferation in the co-cultutred group compared to a control group indicated that colon cancer cell proliferation is significantly promoted by mast cells. It was also identified that colon chance cell migration occurred quicker in the co-cultured group where mast cells were present. After confirming that mast cell play a significant role in colon cancer cell proliferation and migration, both in vivo and in vitro, regulatory pathways of this process were analysed. It was demonstrated that mast cells promote colon cancer cell invasion and angiogenesis through MAPK/Rho-GTPase/STATs pathways. Finally, it was determined that colon tumour development can be significantly controlled via Fcε-PE40 chimeric toxin, killing mast cells without inducing degranulation and anaphylactic reaction. 
The major benefit and relevance of this article to the sub-section of the role of mast cells in disease, is that it demonstrates and explains an example of the negative role of mast cells in the pathogenesis of a disease. This study provides an interesting perspective on the role of mast cells in disease as they are typically thought to be cells that aid the hosts defence system rather than a stimulant of the pathogen. This article also provides an explanation of the clinical significance on their findings and suggests a possible treatment in reducing colon tutor development.
In this study, the underlying mechanisms of extracellular anti-microbal activity and mechanisms of mast cells was analysed using the bacteria S. pyogenes to exclude influence of mast cell phagocytic function. Results demonstrated that extracellular anti-microbal activity was carried out through the production of extracellular traps. It was observed that S. pyogenes growth was inhibited by human mast cells when in close proximity in a co-culture, but phagocytosis of the pathogen did not occur. Fluorescent staining of the human mast cell DNA, S. pyogenes and cathelicidin LL-37 (release by mast cells) depicted the entrapment of the pathogen in a highly defined structure containing DNA. This structure was associated with the extracellular presence of LL-37. Histones and tryptase were also recognised to be other structural components of the mast cell extracellular trap. Mast cell extracellular trap formation was demonstrated to be a result of mast cell death, a process dependent on the production of reactive oxygen species which indicated that mast cell extracellular trap formation was an active and controlled process in response to specific stimuli. This study is the first to demonstrate the formation of extracellular traps by immune cells other than neutrophils. 
This article is beneficial to the understanding of the role of mast cells in disease because it provides information on additional ways that mast cells influence immune response. The study outlines the formation of extra-cellular traps, a mechanism initially thought to be exclusion to neutrophils, and their role in the response to pathogens. Furthermore, it broadens the knowledge and understanding of the physiology of mast cells by presenting it as a complex cell with many mechanisms in the immune response.
The effect of histamine release, by mast cells, on the maturation of immature dendritic cells and the subsequent differentiation of naive CD4+ T cells into either Th1 or Th2 phenotypes and cytokine release was analysed in the above study. It is already known that histamine plays a major role in atopic diseases such as allergy, anaphylaxis and even asthma, however, this study demonstrates that histamines direct action on immature dendritic cells can influence the development of adaptive responses. This was supported by the observation that dendritic cells matured in a histamine rich culture polarised naive CD4+ T cells towards the Th2 phenotype. It was observed that the histamine secretion by mast cells was able to regulate the secretion of cytokines and chemokines, particularly down regulating the production of IL-12, a cytokine crucial for the development of Th1 responses. The data collected in the study also demonstrated that histamine can upregulate the expression of CD86 within dendritic cells (a component necessary for Th2 phenotype responses). Therefore, this study proposes that elevated levels of IgE and Th2 cells often present in atopic diseases could be established by a positive feedback loop of mast cell histamine release promoting Th2 phenotype differentiation and therefore IgE production, ultimately resulting in further histamine production and the positive feedback loop. 
Similarly to the above article, this study produces another mechanism that mast cells utilise to aid in the body's response to pathogens. This article is particularly interesting because it presents mast cells as a complex mediator of T cell maturation (towards the Th2 phenotype) through the establishment of a positive feedback loop of histamine secretion.