Inflammation and immunity
Inflammation is a mechanism through which the body system reacts to injury or infection. The features of inflammation include soreness, warmth, redness, and enlargement. Inflammation, therefore, is classified under nonspecific immune responses. On the other hand, immunity is the mechanism of resistance involving the immune system or all physiological mechanisms that endow the host with the capacity to recognize antigens and to neutralize, eliminate, or metabolize them without causing injury to their tissues (Stvrtinova and Hulin, 1995). It is, therefore, a state in which the body system has an effective defense system against the antigens which cause diseases. The immunity is divided into both nonspecific and specific immunity.
The nonspecific components can eliminate a broad range of pathogens irrespective of their antigenic specificity. Specific immunity generates pathogenic specific immunity against new diseases encountered by the body. The macrophages and leucocytes are exited from the blood circulation and migrate to the site of inflammation. The bone marrow produces recruits of phagocytes which engulfs the pathogens rendering them harmless before they are eliminated out of the body. The number of macrophage precursor cells is increased by the monocytes produced by the bone marrow (Stvrtinova and Hulin, 1995). The macrophages, monocytes, and dendritic cells are examples of antigen-presenting cells.
Inflammation isolates and destroys injurious agents in the preparation of tissue repair by cell division to replace lost cells in regenerative tissues like skin, while in non-regenerative ones like muscles. The lost cells are replaced by scar tissues and fibroblast produces protein collagen to refill these lost cells. Immunity involves the B-lymphocytes and the T-lymphocytes which are produced by the pluripotent stem cells. And their activation leads to the production of antibodies, while inflammation is the activation of the white blood cells to destroy the antigens causing infections. Immunity protects in the initial stages of the infection only while inflammation is the healing process through the activation of the white blood cells to clear the antigens causing infections and damage to the tissues. Inflammation is activated after the injury while immunity is before any injury or any kind of damage to the tissues.
Haemopoiesis is the production of blood cellular components mainly leucocytes. The undifferentiated stem cells give rise to progenitors committed to either lymphoid or myeloid lineage pathways of differentiation. The lymphoid lineage pathway gives rise to thymus-derived (T-cells) and bone marrow-derived/Bursa of Fabricius-derived (B-cells). The myeloid lineage pathway generates mononuclear phagocytoses that are monocytes and macrophages and gives rise also to polymorphonuclear leucocytes. Myeloid stem cells also generate mast cells, erythrocytes, and platelets.
Hypersensitivity definition
Hypersensitivity is the extreme, detrimental reaction formed by the normal immune system. Hypersensitive reactions are mainly divided into four types: type i, type ii, type iii, and type iv. This is based on their mechanisms of action and the period of the reactions. These reactions can cause damage leading to the death of the host. Such immune responses may increase cell-mediated immunity (Hoskin, 2005). Humoral immune responses include types I to III, while type iv is classified under cell-mediated immune response.
Types of hypersensitivity
Type I hypersensitivity is called immediate or anaphylactic hypersensitivity. Here an allergen stimulates the production of the Th2 cells leading to the production of IgE by the plasma cells to mediate this reaction. Basophils and mast cell surfaces are bound by the receptors of the IgE, thus is believed to clear parasitic infections from the body. These responses take place at the mucous membranes and the reactions can be systematic or localized to a specific target. These reactions may involve skin, nasopharynx, and the eye (Stvrtinova and Hulin, 1995)
Type II hypersensitivity is commonly referred to as cytotoxic hypersensitivity (Stvrtinova and Hulin, 1995). This involves cell destruction by lysis, the complement is activated by the IgM or IgG through a process called phagocytosis. This involves the opsonization of the antigen by phagocytes leading to cell lysis. Examples of such reactions are hemolytic disease and transfusion reactions. Type III is immune complex-mediated hypersensitivity. This is dependent on the quantity and location of immune complexes (Hoskin, 2005). This takes place in the blood vessel walls in the kidney. Its effects are restricted near the site of antigen entry or systemic. The major cause of such reactions is incomplete clearance of immune complexes from the tissues by phagocytes leading to activation of the complement system (Hoskin, 2005). Some of the examples are serum sickness and post-streptococcal glomerulonephritis.
Type IV Delayed-type is commonly referred to as (cell-mediated) hypersensitivity (Stvrtinova and Hulin, 1995). This type of hypersensitivity involves two phases mainly: the effector and sensitization phases. In the sensitization phase, the dendritic cells and macrophages secrete interleukin 12 (IL-12) in lymph nodes to provoke the development of Th1 cells (Stvrtinova and Hulin, 1995). This later releases cytokine and chemokines to attract and activate macrophages. Activated macrophages elevate the oxygen radical, class II MHC molecules, nitric oxide, and tumor necrosis factor receptors. They defend intracellular pathogens but can cause allergens like contact dermatitis.
Reference
Hoskin, D. (2005). Hypersensitivity (Allergic) reactions. Web.
Stvrtinova, V. and Hulin, J. J. (1995). Inflammation and fever from pathophysiology Principles of disease. New York, NY: Macmillan Press.