Chapter 15: Resistance and immunity Flashcards
Specific defense mechanisms
•These are grouped together under the term immunity. Resistance is directed against only one specific invader. In addition, immunological memory develops, which confers long-term immunity to specific infections. An antigen is anything that stimulates an immune response.
Non-specific defense mechanisms
•These are the first lines of general defense; they prevent entry and minimize further passage of microbes and other foreign material into the body.
•There are five main non-specific defense mechanisms:
-defense at body surfaces
-phagocytosis
-natural antimicrobial substances
-the inflammatory response
-immunological surveillance.
Defense at body surfaces
- Healthy, intact skin and mucous membranes provide an efficient physical barrier protecting the body’s exposed surfaces. Few pathogens can establish themselves on healthy skin. Sebum and sweat secreted onto the skin surface contain antibacterial and antifungal substances.
- Epithelial membranes lining body cavities and passageways exposed to the external environment (e.g., the respiratory, genitourinary, and digestive tracts) are more delicate but are also well defended. Epithelia produce antibacterial secretions, often acidic, containing antibodies and enzymes, as well as sticky mucus for trapping passing microbes.
- Hairs in the nose act as a coarse filter, and the sweeping action of cilia in the respiratory tract moves mucus and inhaled foreign materials towards the throat. Then it is coughed up (expectorated) or swallowed.
- The one-way flow of urine from the bladder minimizes the risk of infection ascending through the urethra into the bladder. In the female, the acidity of vaginal secretions discourages microbial growth.
Phagocytosis
Process by which certain living cells called phagocytes ingest or engulf other cells or particles. The phagocyte may be a free-living one-celled organism, such as an amoeba, or one of the body cells, such as a white blood cell.
Hydrochloric acid
This is present in high concentrations in gastric juice and kills most ingested microbes.
Lysozyme
This antibacterial enzyme is present in granulocytes, tears, and other body secretions, but not in sweat, urine, or cerebrospinal fluid. It destroys bacterial cell walls but does not affect viruses or other pathogens.
Antibodies
These protective proteins are found coating membranes and in body fluids, and inactivate bacteria
Saliva
This is secreted into the mouth and washes away food debris that may otherwise encourage bacterial growth. It contains antibodies, lysozyme, and buffers to neutralize bacterial acids that promote dental decay.
Interferons
These chemicals are produced by T-lymphocytes, macrophages, and body cells that have been invaded by viruses. They prevent viral replication within infected cells and the spread of viruses to healthy cells.
Complement
Complement is a system of about 20 proteins found in the blood and tissues. It is activated by the presence of immune complexes (an antigen and antibody bound together) and by foreign sugars on bacterial cell walls. Complement:
- binds to, and damages, bacterial cell walls, destroying the microbe
- binds to bacterial cell walls, stimulating phagocytosis by neutrophils and macrophages
- attracts phagocytic cells such as neutrophils into an area of infection, i.e. stimulates chemotaxis.
The inflammatory response
This is the physiological response to tissue damage and is accompanied by a characteristic series of local changes. Its purpose is protective: to isolate, inactivate and remove both the causative agent and damaged tissue, so that healing can take place. The cardinal signs of inflammation are redness, heat, swelling, and pain.
Causes of inflammation
Any form of tissue damage stimulates the inflammatory response, even in the absence of infection. The wide range of causative agents includes extremes of temperature, trauma, corrosive chemicals including extremes of pH, abrasion, and infection by pathogens.
Acute inflammation
- Acute inflammation is typical of short duration, e.g., days to a few weeks, and may range from mild to very severe, depending on the extent of the tissue damage. Most aspects of the inflammatory response are hugely beneficial, promoting the removal of the harmful agent and setting the scene for healing to follow.
- The acute inflammatory response is described here for convenience as a collection of separate events: increased blood flow, accumulation of tissue fluid, migration of leukocytes, increased core temperature, pain, and suppuration. These events significantly overlap and develop together.
Increase blood flow
- Following injury, both the arterioles supplying the damaged area and the local capillaries dilate, increasing blood flow to the site.
- This is caused mainly by the local release of several chemical mediators from damaged cells, e.g., histamine and serotonin. Increased blood flow to the area of tissue damage provides more oxygen and nutrients for the increased cellular activity that accompanies inflammation. Increased blood flow causes the increased temperature and reddening of an inflamed area and contributes to the swelling (edema) associated with inflammation.
Increased tissue fluid formation
- This is partly due to increased capillary permeability caused by inflammatory mediators such as histamine, serotonin, and prostaglandins, and partly due to elevated pressure inside the vessels because of increased blood flow. Most of the excess tissue fluid drains away in the lymphatic vessels, taking damaged tissue, dead and dying cells, and toxins with it.
- Plasma proteins, normally retained within the bloodstream, also escape into the tissues through the leaky capillary walls; this increases the osmotic pressure of the tissue fluid and draws more fluid out of the blood. These proteins include antibodies, which combat infection, and fibrinogen, a clotting protein. Fibrinogen in the tissues is converted by thromboplastin to fibrin, which forms an insoluble mesh within the interstitial space, walling off the inflamed area and helping to limit the spread of any infection. Some pathogens, e.g., Streptococcus pyogenes, which cause throat and skin infections, release toxins that break down this fibrin network and promote the spread of infection into adjacent, healthy tissue.
Migration of leukocytes
- Loss of fluid from the blood thickens it, slowing the flow and allowing the normally fast-flowing white blood cells to contact, and adhere to, the vessel wall. In the acute stages, the most important leukocyte is the neutrophil, which adheres to the blood vessel lining, squeezes between the endothelial cells and enters the tissues (diapedesis) where its main function is in phagocytosis of antigens. Phagocyte activity is promoted by the raised temperatures (local and systemic) associated with inflammation.
- After about 24 hours, macrophages become the predominant cell type at the inflamed site, and they persist in the tissues if the situation is not resolved, leading to chronic inflammation. Macrophages are larger and longer-lived than neutrophils. They phagocytose dead/dying tissue, microbes and other antigenic material, and dead/dying neutrophils. Some microbes resist digestion and provide a possible source of future infection
Chemotaxis
This is the chemical attraction of leukocytes, including neutrophils and macrophages, to an area of inflammation.
Increased temperature
- The increased temperature of inflamed tissues has the twin benefits of inhibiting the growth and division of microbes, whilst promoting the activity of phagocytes.
- The inflammatory response may be accompanied by a rise in body temperature (fever, pyrexia), especially if there is a bacterial infection.
- Pyrexia increases the metabolic rate of cells in the inflamed area and, consequently, there is an increased need for oxygen and nutrients.