Does anyone know their microbiology?

I have a few questions that I can't answer myself. Anyone know anything about microbiology?

 

Ask Google...

 

Google can suck my mom because it isn't helping me.

 

ask jeeves...

 

It would be helpful to know what the questions are.

 

Genes for antibiotic resistance are often found on these structures in bacteria: (I have plasmids but I am worried because not all cells have plasmids afterall it is the bonus DNA)

Cell-mediated immunity is important in fighting these kinds of infection: (I have nothing because t-cells fight against cancer and cancer is not a infection....)

Two different proteins, one a part of adaptive immunity and one a part of the innate defenses, that defend the blood from bacterial infection are: (I want to say immunioglobulin..... I have no idea for the other)

 

I've got no fucking clue.

Was gonna research but I'm feeling too lazy now.

 

Ahhhh thanks for nothing but some hope with a burnt out candle bud.

 

Many of the antibiotic-resistance genes of staphylococci are carried on plasmids (see Agrobacterium for discussion of this) that can be exchanged with Bacillus spp. and Streptococcus spp., providing the means for acquiring additional genes and gene combinations. Some are carried on transposons - segments of DNA that can exist either in the chromosome or in plasmids.

http://helios.bto.ed.ac.uk/bto/microbes/penicill.htm

 

http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/C/CMI.html

 

Thanks Hacker I figured out those questions and I am on a new set of questions


If the antibody-producing cells are located in a lymph node some distance away from the skin lesion, how did the antibody-producing cells "find out" about the infection?

Give two examples of disease where loss of health is caused by toxin production. Name the disease, the pathogen, and briefly describe the toxin.

 

http://www.cat.cc.md.us/courses/bio141/lecguide/unit2/innate/bloodcells.html

 

Cell-mediated immunity is an immune response that does not involve antibodies but rather involves the activation of macrophages and natural killer cells, the production of antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen. Cellular immunity protects the body by:

activating antigen-specific cytotoxic T-lymphocytes that are able to lyse body cells displaying epitopes of foreign antigen on their surface, such as virus-infected cells, cells with intracellular bacteria, and cancer cells displaying tumor antigens;
activating macrophages and natural killer cells, enabling them to destroy intracellular pathogens; and
stimulating cells to secrete a variety of cytokines that influence the function of other cells involved in adaptive immune responses and innate immune responses.
Cell-mediated immunity is directed primarily at microbes that survive in phagocytes and microbes that infect non-phagocytic cells. It is most effective in removing virus-infected cells, but also participates in defending against fungi, protozoans, cancers, and intracellular bacteria. It also plays a major role in transplant rejection.

 

http://www.cdc.gov/ncidod/dbmd/diseaseinfo/marinetoxins_g.htm

 

According to Sigma product information "Pertussis toxin is released from B. pertussis in an inactive form. When the pertussis toxin B oligomer binds to the cell membrane, the S1 subunit of its A protomer becomes activated, perhaps through the action of glutathione and ATP. Pertussis toxin catalyzes the ADP-ribosylation of the α subunits of the heterotrimeric guanine nucleotide regulatory proteins Gi, Go, and Gt. This prevents the G protein heterotrimers from interacting with receptors, thus blocking their coupling and activation. Since the Gα subunits remain in their GDP-bound, inactive state, they are unable to inactivate adenylyl cyclase or open K+ channels

Botulin toxin is the toxic compound produced by the bacterium Clostridium botulinum. It is a protease that attacks one of the fusion proteins at a neuromuscular junction, preventing vesicles from anchoring to the to the membrane to release acetylcholine . By inhibiting acetylcholine release, the toxin interferes with nerve impulses and causes paralysis of muscles in botulism. The toxin is a two-chain polypeptide with a 100-kDa heavy chain joined by a disulphide bond to a 50-kD light chain.
It is possibly the most toxic substance known, with a lethal dose of about 200-300 pg/kg, meaning that somewhat over a hundred grams could kill every human living on the earth. It is also remarkably easy to come by: Clostridium spores are found in soil practically all over the earth, and can easily grow in a can or jar of poorly-preserved food.

 

Hippypaul you are my hero!!!

 

Activation of naïve helper T cells
Following T cell development, matured naïve (meaning they have never been exposed to the antigen they target) T cells leave the thymus and begin to spread throughout the body, including in the lymph nodes. Like all T cells, they express T antigen receptors (also known as the T cell receptor or TcR), which in the case of CD4+ T cells have an affinity with Class II MHC molecules. Class II MHC proteins are found specifically on the surface of professional antigen-presenting cells (APCs). Professional antigen presenting cells are primarily dendritic cells, macrophages and B cells. The antigens that bind to MHC proteins are almost always peptides.

Following an infection, professional antigen-presenting cells with processed antigen travel from the site of infection to the lymph nodes and begin to present various antigenic peptides, which bind to either MHC Class I and Class II. Depending on the APC, some also express unprocessed antigen (e.g. for use in antibody class switching), such as follicular dendritic cells, however unprocessed antigens do not interact with T cells. T cells are then exposed to these APCs and those T cells with T cell receptors (TcRs) that are capable of binding with antigen-bound MHC begin to activate. It should be noted that memory T cells are also activated this way if the body is re-infected with the same antigen.

CD4 is believed to be important for TH cell stabilisation during activation, possibly by binding to specific portions of the Class II MHC molecule. This stabilises the binding between the two cells, allowing for activation. CD4 is believed to determine which MHC class the T cell will interact with (in this case MHC Class II), and it appears that CD4+ T cells almost always have a pre-defined role in the immune system.

Once the naïve T cell has been exposed to antigen (a high affinity interaction between the TcR and the antigen-bound Class II MHC has occurred), the cell produces a potent T cell growth factor called interleukin-2 (IL-2). The IL-2 that is produced binds to the same (or other) activated T cells (only activated T cells produce all the subunits of the IL-2 receptor), resulting in auto-regulation and self proliferation. After many cell generations, these progenitors can differentiate into effector TH cells, memory TH cells, or suppressor TH cells.

Effector TH cells secrete cytokines, proteins or peptides that stimulate or interact with other leukocytes, including TH cells.
Memory TH cells retain the TcR affinity of the originally activated T cell, and will be called upon if needed for a secondary immune response.
Suppressor TH cells do not activate or promote immune function following proliferation, but decreases it instead. This is essential for limiting and shutting down an immune response, and the prevention of auto-immune disease.
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Determination of the helper T cell response
Helper T cells are capable of influencing the actions of a variety of immune cells, and the response (the signals, such as cytokines, helper T cells give other cells) that is generated can be essential for a successful outcome from infection. Before they are able to help other cells, they must determine which cytokines will be the most effective or useful in the event of an infection (or other immune system challenge).

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TH1/TH2 Model for helper T cells
Proliferating helper T cells which develop into effector T cells can differentiate into two major subtypes of cells known as TH1 and TH2 cells (also known as Type 1 and Type 2 helper T cells respectively). These subtypes are defined on the basis of the specific cytokines they produce. TH1 cells produce interferon-gamma (or IFN-gamma) and lymphotoxin (also known as tumor necrosis factor-beta or TNF-beta), while TH2 cells produce interleukin-4 (IL-4), interleukin-5 (IL-5) and interleukin-13 (IL-13), among numerous other cytokines. The TH1/TH2 model also states that interleukin-12 (IL-12) plays an essential role during TH1 development, but IL-12 is not produced by helper T cells, but rather by certain professional APCs, such as activated macrophages and dendritic cells. Interleukin-2 is associated with TH1 cells, and its production by helper T cells is necessary for the proliferation of cytotoxic CD8+ T cells, but this association with TH1 may be misleading; IL-2 is produced by all helper T cells early in their activation.

Given the relative specificity of the cytokines released by either response on particular sections of the immune system it has been suggested that both TH groups play separate roles during an immune response. That is; TH1 cells are necessary in maximising the killing efficacy of the macrophages and in the proliferation of cytotoxic CD8+ T cells, therefore their primary role during an immune response is to activate and proliferate these cells. TH2 cells express many cytokines, many of which are essential in stimulating B-cells with antibody class switching and increased antibody production; TH2 cells are therefore considered necessary for the full maturation of the humoral immune system.

This primary assocation between the cytokines of TH responses and the cells mentioned in the previous paragraph does not define all of the effects activated helper T cells can have on the immune system. Some cytokines also act on helper T cells themselves (or on other immune cells, such as interleukin-5 upon eosinophils). Some of the cytokines in either group act to preserve the development of the TH profile that was selected during the initial determination of the T cell response.

For example, the Type 2 response not only promotes its own response via the action of interleukin-4 on helper T cells (which increases the production of TH2 cytokines including itself), but also expresses interleukin-10 (IL-10), which inhibits a variety of cytokines including interleukin-2 and interferon-gamma in helper T cells, and IL-12 in dendritic cells and macrophages. The TH2 response promotes both the production of its own cytokines while inhibiting the establishment of the TH1 response.

There is a similar phenomenon with the Type 1 response. The Type 1 cytokine interferon-gamma increases the production of interleukin-12 by dendritic cells and macrophages, and via positive feedback by IL-12, promotes the TH1 response. IFN-gamma also inhibits the production of cytokines such as interleukin-4, an important cytokine associated the Type 2 response, and thus it also acts to preserve its own response.

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Complexities surpassing the TH model
The interactions between cytokines from the TH1/TH2 model can be more complicated in some animals. For example, the TH2 cytokine IL-10 inhibits the cytokine production of both TH subsets in humans. As human IL-10 (coded hIL-10) suppresses T cell proliferation and cytokine production but ensures that plasma cells continue to produce high levels of antibodies, it has been proposed that hIL-10 protects the immune system from the over-stimulation of helper T cells while still maximising antibody production.

There are also other T cells that can also influence the expression and activation of helper T cells, such as natural suppressor T cells, as well as the TH3 subset of helper T cells. Terms such as "regulatory" and "suppression" have become ambiguous after the discovery that helper CD4+ T cells are also capable of regulating their own response outside of dedicated suppressor cells.

The major difference in definition of "suppressor" (or "natural regulatory") T cells is that they do not undergo change in cytokine function and are always immuno-supressant, while other groups produce inhibitory cytokines later in its repertoire. The latter is a feature of TH3 cells, which transform into a suppressor subset after its initial activation and cytokine production.

Both suppressor T cells and TH3 cells produce the cytokine transforming growth factor-beta (TGF-beta) and IL-10. Both cytokines are inhibitory to helper T cells, TGF-beta being inhibitory to the majority of immune cells.

Considering many of the cytokines discussed above are also expressed by other immune cells (see individual cytokines for details) it is obvious that while the original TH1/TH2 model is enlightening and potentially gives insight into the functions helper T cells have, it is far too simple to define the entire role of helper T cells throughout a response.

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Movement of activated helper T cells
Once helper T cells have proliferated and the response determined, the activated TH cells leave the lymph node and transport through the lymphatic system and into the bloodstream. These cells then spread throughout the body, moving to inflammed tissues or other lymph nodes via chemotaxis. The mechanism by which immune cells cross the endothelium (lining of the blood vessels) is called diapedesis.

Once in the site of infection/lymph nodes, helper T cells may bind to APCs expressing MHC Class II, and if it recognises the antigen bound to the MHC molecule, reactivates. Once reactivated, the T cell releases various products including cytokines discussed above, although it is likely that the cytokines it produces depends on its location, the cells it is interacting with, the presence of other cytokines, as well as other factors that are not yet understood. Considering most infections involve most, or even all of the cell types CD4+ T cells interact with, the role of the helper T cell during infection is complex and yet to be fully elucidated.

 

Always knew that nursing license would pay off some day. That and Wikipedia go at once and give them money.

 

Hahaha well I am glad it ould help some pathetic college student in a bind with microbiology.

 

So basically the cytokines are what allow for APC to find out about the infection....