The Inflammatory Response

The body is designed to defend itself against invading bacteria, and transmitting. The skin and mucous membranes argon the first take out of defence, the invasion of foreign bacteria apprize pass this first line of defence and immediately triggers the second line of defence. The second line of defence is the subversive solution (McCance & Huether, 2009). The mechanism of the insurgent response is to protect the injured aim by putting to death the mover responsible, limiting its effects on the rest of the body and initiating the healing mathematical process (Porth, 2007).According to Botwinski (2001), during contagious disease bacteria grow and divide, and release potent toxins that wee-wee damage to the bodys cells. These toxins trigger the initiation of the unhealthy response. The channelizes that cash in ones chips are initiated by the interactions between bacterial products and inflammatory mediators. Inflammatory mediators are chemicals that are released by protect ive cells or plasma when harmful agents use up the body. Inflammatory mediators include histamine, prostaglandins, and leukotrienes (Kumar, Abbas, Fausto, Robbins, & Cotran, 2005).The main cells involved are the mast cells and are laid in connective meander in close contact with credit line vessels. Mast cells play a key role in the inflammatory response, when bear on by infection they release a potent substance called histamine. When histamine leaks into the tissues it engenders changes in the surrounding rail line vessels. The two changes that occur in the tune vessels is simple eye vessel distension and increase capillary permeability. The changes are designed to exploit the movement of plasma proteins and circulating cells out of the crosscurrent flow and into the send of infection (McCance & Huether, 2009).At the onset of injury the histamine that is released causes the blood vessels at the situation to constrict for a short time then dilate (Nair, 2009). This tu rnout of the blood vessels increases blood flow, and therefore increases the amount of oxygen, nutrients, and albumin blood cells existence de followred to the site of injury (Botwinski, 2001). New blood vessels can also circularize up at the site and the area becomes flooded with blood. This increase in blood flow produces the characteristics of redness and warmth and are the earliest symptoms seen in the inflammatory response (Porth, 2007).The blood vessel wall confines blood products and cells in the circulation and prevents it from leaking out into the surrounding tissues of the body. This is done by cells called endothelial cells that tightly line the walls (von Braun & Anderson, 2006). The chemicals that are released at the site of injury bind with receptors on the endothelial cells and causes them to retract producing gaps in their walls. This structural change allows healing fluid and cells to escape out into the affect area (Porth, 2007). Braun & Anderson (2006) describ e that the harmful bacteria are diluted by this increased amount of fluid.The increased fluid and pressure produces the swelling seen at the site of infection. Nerve endings can also be stimulated as a result from the increasing pressure and this is what can cause the pain associated with infection (Nair, 2009). An important part of the inflammatory response is to send circulating white blood cells to the infected area. They are attracted in large numbers to the injection of injury as a result from blood vessel dilation and the release of bacteria substances and inflammatory mediators (Kumer et al. 2005). The white blood cells rail line is to abide a defence by killing invading bacteria, and getting disengage of doomed tissue. The main white blood cell in the inflammatory response is the neutrophil and arrives first at the site of inflammation virtually six to twelve hours after the initial injury (McCance & Huether, 2007). Macrophages are cells that live in various tissue loc ations and like the neutrophils they are released in the blood stream and attracted to the substances released at the site of infection.Macrophages and neutrophils are called phagocytes, and share the same job in the inflammatory response, which is to clean up the damage by ingesting and killing the invading bacteria (McCance & Huether, 2005). According to Sherwood (2009), the phagocytes floating in the circulation stick to the intimate of the blood vessel wall, this process is called mirgination. Diapedesis then occurs, in this process the phagocytes thrust through the gaps of capillary walls that were formed earlier on in the inflammatory response.Chemical mediators called chemotaxins accumulate at the site of infection and attract the phagocytes. once inside the surrounding tissue the phagocytes make their way through the tissue to areas where there are higher concentrations of chemotaxins, this process is called chemotaxis (Roitt & Delves, 2001). Once at the affected area the neutrophils and macrophages eliminate the invading bacteria from the inflammation site by a process called phagocytosis. Phagocytosis is cell-eating and is a three stage process placid of recognition and attachment, engulfment, and killing and degradation (Kumar et al. , 2005).Phagocytes have receptors on their surface that change them to recognise and attach to the receptors on the surface of the microorganism, this attachment prevents the bacteria from getting-away. In the process of engulfment the phagocytes stretch two surface like projections called pseudopods around the microorganism until it completely surrounds it, the microorganism is then trapped inside. Potent chemicals and enzymes are released inside the phagocyte and these break down and kill the invading microorganism. The pus that forms at the infected site is the accumulation of these phagocytic cells both living and dead (Sherwood, 2009).McCance & Huether (2009) describe that there are three protein systems that are also initiated during the inflammatory response. They are the complement, clotting and kenin systems, and consist of protein enzymes. These systems work along side the protect cells and help them carry out their roles. The complement system consists of potent en garde proteins that help in the destruction of invading bacteria. The clotting system produces fibrinous tissue that acts as a boundary by trapping the bacteria and maximising the activity of the phagocytic cells.The clot that is formed also minimizes blood loss and prevents spread of infection (Botwinski, 2001). The kenin system consists of mainly bradykinin a protein that causes dilation of vessels, vascular permeability, and pain (McCance & Huether, 2009). The protective mechanisms of the inflammatory response prepare the site for healing and regeneration of the destructed tissue. Depending on the severity of infection and damage this can be a long process and is washed-up when structure and function is returned to normal (McCance & Huether, 2009).