Adaptive Immunity and Antibiotic Resistance

    The immune system of the human body consists of different cells and molecules which play different roles in response to infection. These responses are divided as innate and adaptive immune response. Innate response acts on different infectious agents the same way no matter how often they are encountered. The adaptive immune response has immune recognition to specific invading microorganisms that the body is previously exposed to and that repeated exposure to those particular microorganisms elicits a stronger immune response. There are bacteria, however, that are able to evade not only from the bodys immune system but also from the actions of antibiotics designed to eliminate them. These bacteria are able to develop mechanisms which allow them to become resistant to antibiotics from which they are previously susceptible to. They also have mechanisms by which they are able to confer this antibiotic resistance to their progeny.

The adaptive or acquired immune response has four important features specificity, diversity, memory, and self vs. non-self recognition. Specificity refers to the ability of the immune response to act on specific antigens that it has previously encountered. This ability is due to the presence of receptors on B cells and T cells which recognizes specific antigens present on an invading pathogen. Diversity refers to the ability of the B cells and T cells to randomly generate very large and diverse repertoire of antigen receptors which increase the chances of these cells to recognize offending microorganisms, thereby triggering the immune response. Immunologic memory is a feature of the adaptive immune response wherein previously encountered antigens are recognized by memory cells in order to mount a stronger immune response. The ability of the body to prevent self-antigens from triggering an immune response is because of immunoregulatory mechanisms which discriminate self from nonself antigens mediated by suppressor T cells. These features of the acquire immune response enable vaccinations to generate a protective immunity against a particular disease. Vaccines contain known antigens from a particular pathogen which stimulate specific receptors from the diverse repertoire of antigen-specific on the surface of B cells and T cells. Killer cells and antibodies are elaborated which mount a strong immune response once memory cells are challenge by the same antigens. The artificial immunity is achieved without getting the actual disease since vaccines use killed or live but attenuated pathogens which render these pathogens harmless. Other vaccines contain only the antigens to elicit the immune response without the actual pathogens.

Mycobacterium tuberculosis is the infectious agent which causes tuberculosis. Its route of entry is primarily through the lungs. Once the tubercle bacilli enter the body, the initial response of the system is through the cell known as alveolar macrophage which engulfs the bacilli and inhibits its proliferation. In the event that this process does not effectively kill all bacilli, a type of lymphocyte known as CD4 T cells express specific antigen receptors which recognizes the bacilli and recruits and activates other immune cells such as monocytes and dendritic cells to the site of infection to further amplify the immune response. Immune cells also stimulate the release cytokines and antibodies which provides additional defense and immune against M.tuberculosis Schluger (1998).

When infectious agents elude the immune defense, infection ensues which leads to disease. Although antimicrobial agents are available to eliminate the invading microorganism, there are bacteria capable of eluding them as well. This happens when the bacteria acquires the ability to resist the action of the antibiotics due to gene mutations after repeated exposure to the antibiotics. There are four mechanisms of antibiotic resistance. One mechanism is through drug inactivation or modification which renders the drug ineffective. This is due to enzymes that are elaborated by bacteria which deactivates the drug. Another mechanism is the alteration of the target site where the antibiotic binds with the bacteria. This prevents the drug from binding to the bacteria and allows the bacteria to escape the toxic effects of the drug. Some antibiotics disrupt metabolic pathways critical to the survival of the bacteria. However, there are some bacteria that are able to resist this effect by altering their metabolic pathways an turn to using substrates not inhibited by the antibiotic. Some bacteria also acquire the ability to reduce the permeability of the drug into the bacteria or increase the expulsion of the drug out of the bacteria which effectively reduces the effect of the drug.

Bacteria acquire antibiotic resistance through the transfers of resistant genes from other bacteria with resistant mutations. The transfer of genetic material between bacteria is referred to as horizontal gene transfer. The genetic exchange is possible through several mechanisms. Bacteria can acquire antibiotic resistance through uptake and expression of resistant genes from other bacteria. This process is called transformation. Transduction is another process which transfers resistant genes from one bacterium to another through a bacterial virus known as bacteriophage. Bacteria can also transfer resistant genes through direct cell-to-cell contact mediated by genetic material known as conjugal plasmids or conjugal transposons.


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