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Inflammation is defined as the local response of living mammalian tissues to injury due to any agent. It is body defense reaction in order to eliminate or limit the spread of injurious agent. The agents causing inflammation may be as under: Physical agents like heat, cold, radiation, mechanical trauma.



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Lecture 8

Inflammation (Pg 114)

DEFINITION AND CAUSES. Inflammation is defined as the local response of living mammalian tissues to injury due to any agent. It is body defense reaction in order to eliminate or limit the spread of injurious agent.

The agents causing inflammation may be as under:

1. Physical agents like heat, cold, radiation, mechanical trauma.

2. Chemical agents like organic and inorganic poisons.

3. Infective agents like bacteria, viruses, parasites.

4. Immunological agents like cell-mediated and antigen-antibody reactions.

Although the inflammation involves 2 basic processes with some overlapping, viz. early inflammatory response and later followed by healing, but for the purpose of description, the two are considered separately.

SIGNS OF INFLAMMATION. The Roman writer Celsus in 1st century A.D. named the famous 4 cardinal signs of inflammations as:

rubor (redness);

tumor (swelling);

color (heat); and


To these, fifth sign functio laesa (loss of function) was later added by Virchow. The word inflammation means burning. This nomenclature has its origin in old times but now we know that burning is only one of the signs of inflammation.

TYPES OF INFLAMMATION. Depending upon the defense capacity of the host and duration of response, inflammation can be classified as acute and chronic.

I. Acute inflammation is of short duration and represents the early body reaction and is usually followed by repair.

II. Chronic inflammation is of longer duration and occurs either after the causative agent of acute inflammation persists for a long time, or the stimulus is such that it induces chronic inflammation from the beginning.


The changes in acute inflammation can be conveniently described under the following 2 headings:

I. Vascular events; and

II. Cellular events.

I. Vascular Events

Alteration in the microvasculature (arterioles, capillaries and veins) is the earliest response to tissue injury. These alterations include: hemodynamic changes and changes in vascular permeability.


The earliest features of inflammatory response result from changes in the vascular flow and caliber of small blood vessels in the injured tissue. The sequence of these changes is as under:

1. Irrespective of the type of injury, immediate vascular response is of transient vasoconstriction of arterioles. With mild form of injury, the blood flow may be re-established in 3-5 seconds while with more severe injury the vasoconstriction may last for about 5 minutes.

2. Next follows persistent progressive vasodilatation which involves mainly the arterioles, but to a less extent, affects other components of the microcirculation like venules and capillaries. This change is obvious within half an hour of injury. Vasodilatation results in increased blood volume in micro vascular bed of the area, which in turn, may elevate the local hydrostatic pressure resulting in transudation of fluid into the extra cellular space.

3. Slowing or stasis of microcirculation occurs next. Slowing is attributed to increased permeability of microvasculature due to increased hydrostatic pressure

4. Stasis or slowing is followed by leucocytic margination or peripheral orientation of leucocytes (mainly neutrophils) along the vascular endothelium. The leucocytes stick to the vascular endothelium briefly, and then move and migrate through the gaps between the endothelial cells into the extra vascular space. This process is known as emigration (discussed in detail later).

II. Cellular Events

The cellular phase of inflammation consists of 2 processes:

1. exudation of leucocytes; and

2. phagocytosis.


The escape of leucocytes from the blood vessels is the most important feature of inflammatory response. In acute inflammation, polymorphonuclear neutrophils (PMNs) comprise the first line of body defense, followed later by monocytes and macrophages.


Phagocytosis is defined as the process of engulfment of solid particulate material by the cells (cell-eating). The cells performing this function are called phagocytes. There are 2 main types of phagocytic cells:

(i) Polymorphonuclear neutrophils (PMNs) which appear early in acute inflammatory response, also called as microphages.

(ii) Circulating monocytes and fixed tissue mononuclear phagocytes called as macrophages.

The process of phagocytosis is similar for both polymorphs and macrophages and involves the following 3 steps:

1. Attachment stage (Opsonisation)

2. Engulfment stage

3. Killing or degradation stage.


Also called as permeability factors or endogenous mediators of increased vascular permeability, these are a large and increasing number of endogenous compounds which can enhance vascular permeability. However, currently many chemical mediators have been identified which partake in other processes of acute inflammation like vasodilatation, chemotaxis, fever, pain and cause tissue damage.

The substances acting as chemical mediators of inflammation may be released from the cells, the plasma, or damaged tissue itself. They are broadly classified into 2 groups:

I. Mediators released by cells; and

II. Mediators originating from plasma.


1. Vasoactive amines (Histamine, 5-hydroxytryptamine)

2. Arachidonic acid metabolites

(i) Metabolites via cyclo-oxygenase pathway (prostaglandins, thromboxane A2, prostacyclin)      (ii) Metabolites via lipo-oxygenase pathway (5-HETE, leukotrienes)

3. Lysosomal components

4. Platelet activating factor

5. Cytokines (interleukin 1, tumor necrosis factor)


(PLASMA PROTEASES): These are products of:

1. The kinin system

2. The clotting system

3. The fibrinolytic system

4. The complement system


The cells participating in acute and chronic inflammation are circulating leucocytes, plasma cells and tissue macrophages.


Although acute inflammation is typically characterized by vascular and cellular events with emigration of neutrophilic leucocytes, not all examples of acute inflammation show infiltration by neutrophils, and vice versa, some chronic inflammatory conditions are characterized by neutrophilic infiltration. For example, typhoid fever is an example of acute inflammatory process but the cellular response in it is lymphocytic; osteomyelitis is an example of chronic inflammation but the cellular response in this condition is mainly neutrophilic.

The morphologic variation in inflammation depends upon a number of factors and processes. These are discussed below:

1. Factors Involving the Organisms

(i) Type of injury and infection. For example, skin reacts to herpes simplex infection by formation of vesicle and to streptococcal infection by formation of boil; lung reacts to pneumococci by occurrence of lobar pneumonia while to tubercle bacilli it reacts by granulomatous inflammation.

(ii) Virulence. Many species and strains of organisms may have varying virulence e.g. the three strains of C. diphtheriae (gravis, intermedius and mitis) produce the same diphtherial exotoxin but in different amount.

(iii) Dose. The concentration of organism in small doses produces usually local lesions while larger dose results in more severe spreading infections.

(iv) Portal of entry. Some organisms are infective only if administered by particular route e.g. Vibrio cholerae is not pathogenic if injected subcutaneously but causes cholera if swallowed.

(v) Product of organisms. Some organisms produce enzymes that help in spread of infections e.g. hyaluronidase by Cl. welchii, streptokinase by Streptococci, staphylokinase and coagulase by Staphyhcocci

2. Factors Involving the Host

(i) General health of host. For example, starvation, hemorrhagic shock, chronic debilitating diseases like diabetes mellitus, alcoholism etc render the host more susceptible to infections.

(ii) Immune state of host. Immunodeficiency helps in spread of infections rapidly e.g. in AIDS.

(iii) Leukopenia. Patients with low WBC count with neutropenia or agranulocytosis develop spreading infection.

(iv) Site or type of tissue involved. For example, the lung has loose texture as compared to bone and thus both tissues react differently to acute inflammation.

(v) Local host factors. For instance, ischemia, presence of foreign bodies and chemicals cause necrosis and are thus harmful.

3. Type of Exudation

The appearance of escaped plasma determines the morphologic type of inflammation. These are:

(i) Serous, when the fluid exudates resembles serum or is watery e.g. pleural effusion in tuberculosis, blister formation in burns, chickenpox, smallpox.

(ii) Fibrinous, when the fibrin content of the fluid exudates is high e.g. in pneumococcal and rheumatic pericarditis.

(iii) Purulent or suppurative exudates is formation of creamy pus as seen in infection with pyogenic bacteria e.g. abscess, acute appendicitis.

(iv) Hemorrhagic, when there is vascular damage e.g. acute hemorrhagic pneumonia in influenza.

(v) Catarrhal, when the surface inflammation of epithelium produces increased secretion of mucus e.g. common cold.

4. Cellular Proliferation

Variable cellular proliferation is seen in different types of  inflammations.

  1.  There is no significant cellular proliferation in acute bacterial infections except in typhoid fever in which there is intestinal lymphoid hyperplasia.
  2.  Viral infections have the ability to stimulate cellular proliferation e.g. epidermal cell proliferation in herpes simplex, chickenpox and smallpox.
  3.  In glomerulonephritis, there is proliferation of glomerular capsular epithelial cells resulting in formation of 'crescents'.
  4.  In chronic inflammation, cellular proliferation of macrophages, fibroblasts and endothelial cells occurs.

5. Necrosis

The extent and type of necrosis in inflammation is variable.

  1.  In gas gangrene, there is extensive necrosis with discolored and foul smelling tissues.
  2.  In acute appendicitis, there is necrosis as a result of vascular obstruction.
  3.  In chronic inflammation such as tuberculosis, there is characteristic caseous necrosis.


Inflammation of an organ is usually named by adding the suffix- 'itis' to its Latin name e.g. appendicitis, hepatitis, cholecystitis, meningitis etc. A few morphologic varieties of acute inflammation are described below:

1. PSEUDOMEMBRANOUS INFLAMMATION. It is inflammatory response of mucous surface (oral, respiratory, bowel) to toxins of diphtheria or irritant gases. As a result of denudation of epithelium, plasma exudes on the surface where it coagulates, and together with necrosed epithelium, forms false membrane that gives this type of inflammation its name.

2. ULCER. Ulcers are local defects on the surface of an organ produced by inflammation. Common sites for ulcerations are the stomach, duodenum, intestinal ulcers in typhoid fever, intestinal tuberculosis, bacillary and amoebic dysentery, ulcers of legs due to varicose veins etc. In the acute stage, there is infiltration by polymorphs with vasodilatation while long-standing ulcers develop infiltration by lymphocytes, plasma cells and macrophages with associated fibroblastic proliferation and scarring.


When acute bacterial infection is accompanied by intense neutrophilic infiltrate in the inflamed tissue, it results in tissue necrosis. A cavity is formed which is called an abscess and contains purulent exudates or pus and the process of abscess formation is known as suppuration. The bacteria which cause suppuration are called pyogenic.

Pus is creamy or opaque in appearance and is composed of numerous dead as well as living neutrophils, some red cells, fragments of tissue debris and fibrin. In old pus, macrophages and cholesterol crystals are also present.

An abscess may be discharged to the surface due to increased pressure inside or may require drainage by the surgeon. Due to tissue destruction, resolution does not occur but instead healing by fibrous scarring takes place.

Some of the common examples of abscess formation are as under:

(i) Boil or furuncle which is an acute inflammation via hair follicles in the dermal tissues.                                                                     

(ii) Carbuncle is seen in untreated diabetics and occurs as a loculated abscess in the dermis and soft tissues of the neck.

4. CELLULITIS. It is a diffuse inflammation of soft tissues resulting from spreading effects of substances like hyaluronidase released by some bacteria.

5. BACTERIAL INFECTION OF THE BLOOD. This includes the following 3 conditions:

(i) Bacteremia is defined as presence of small number of bacteria in the blood which do not multiply significantly. They are commonly not detected by direct microscopy. Blood culture is done for their detection e.g. infection with Salmonella typhi, Escherichia coli, Streptococcus viridans,

(ii) Septicemia means presence of rapidly multiplying, highly pathogenic bacteria in the blood e.g. pyogenic cocci, bacilli of plague etc. Septicemia is generally accompanied by systemic effects like toxaemia, multiple small hemorrhages, neutrophilic leucocytosis and disseminated intravascular coagulation (DIC).

(iii) Pyaemia is the dissemination of small septic thrombi in the blood which cause their effects at the site where they are lodged. This can result in pyaemic abscesses or septic infarcts.

(a) Pyaemic abscesses are multiple small abscesses in various organs such as in cerebral cortex, myocardium, lungs and renal cortex, resulting from very small emboli fragmented from septic thrombus. Microscopy of pyaemic abscess shows a central zone of necrosis containing numerous bacteria, surrounded by a zone of suppuration and an outer zone of acute inflammatory cells.

(b) Septic infarcts result from lodgement of larger fragments of septic thrombi in the arteries with relatively larger foci of necrosis, suppuration and acute inflammation e.g. septic infarcts of the lungs, liver, brain, and kidneys from septic thrombi of leg veins or from acute bacterial endocarditis.


The account of acute inflammation given up to now above is based on local tissue responses. However, acute inflammation is associated with systemic effects as well. These include fever, leucocytosis and lymphangitis-lymphadenitis.

1. Fever occurs due to bacteremia. It is thought to be mediated through release of factors like prostaglandins, interleukin-1 and tumor necrosis factor in response to infection.

2. Leucocytosis commonly accompanies the acute inflammatory reactions, usually of the range of 15,000-20,000/l. When the counts are higher than this with 'shift to left' of myeloid cells, the blood picture is described as leukemoid reaction. Usually, in bacterial infections there is neutrophilia; in viral infections lymphocytosis; and in parasitic infestations, eosinophilia. Typhoid fever, an example of acute inflammation, however, induces leucopenia with relative lymphocytosis.

3. Lymphangitis-lymphadenitis is one of the important manifestations of localized inflammatory injury. The lymphatics and lymph nodes that drain the inflammed tissue show reactive inflammatory changes in the form of lymphangitis and lymphadenitis. This response represents either a nonspecific reaction to mediators released from inflammed tissue or is an immunologic response to a foreign antigen. The affected lymphnodes may show hyperplasia of lymphoid follicles (follicular hyperplasia) and proliferation of mononuclear phagocytic cells in the sinuses of lymphnode (sinus histiocytosis).


The acute inflammatory process can culminate in one of the following 4 outcomes:

  1.  Resolution
  2.  Healing by scarring

3.   Progression to suppuration

4.   Progression to chronic inflammation.

1. RESOLUTION. It means complete return to normal tissue following acute inflammation. This occurs when tissue changes are slight and the cellular changes are reversible e.g. resolution in lobar pneumonia.

2. HEALING BY SCARRING. This takes place when the tissue destruction in acute inflammation is extensive so that there is no tissue regeneration but actually there is healing by fibrosis.

3. SUPPURATION. When the pyogenic bacteria causing acute inflammation result in severe tissue necrosis, the process progresses to suppuration. Initially, there is intense neutrophilic infiltration. Subsequently, mixture of neutrophils, bacteria, fragments of necrotic tissue, cell debris and fibrin comprise pus which is contained in a cavity to form an abscess. The abscess, if not drained, may get organized by dense fibrous tissue, and in time, get calcified.

4. CHRONIC INFLAMMATION. The acute inflammation may progress to chronic inflammation in which the processes of inflammation and healing proceed side by side.



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