inflammation lecture 2

Lecture 2 Inflammation
Dr.Ahmed Raji
Special Morphologic Patterns of Acute Inflammation
The morphologic features of all acute inflammatory reactions are dilation of small
blood vessels, slowing of blood flow, and accumulation of leukocytes and fluid in the
extravascular tissue.
However, special morphologic patterns are seen depending on:
The severity of the inflammation.
The specific cause.
The particular tissue involved.
The importance of recognizing the gross and microscopic patterns is that they often
provide valuable clues about the underlying cause.
Serous inflammation:
Serous inflammation is characterized by the accumulation of a thin fluid that is derived
from the plasma or from the secretions of mesothelial cells lining the peritoneal,
pleural, and pericardial cavities.
Accumulation of fluid in these cavities is called an effusion.
The skin blister resulting from a burn or viral infection represents an accumulation of
serous fluid, beneath the epidermis of the skin.
Fibrinous inflammation:
When there is great increase in vascular permeability, large molecules such as
fibrinogen pass the vascular barrier, and fibrin is formed and deposited in the
extracellular space.
A fibrinous exudate is characteristic of inflammation in the lining of body cavities, such
as the meninges, pericardium and pleura. Histologically, fibrin appears as an
eosinophilic threads.
Suppurative or Purulent Inflammation:
This type of inflammation is characterized by the production of large amounts of pus
or purulent exudate consisting of neutrophils, liquefactive necrosis, and edema fluid.
Certain bacteria (e.g., staphylococci) produce this localized suppuration and are
therefore referred to as pyogenic (pus-producing) bacteria.
Abscesses are localized collections of purulent inflammatory tissue.
Abscesses have:
A central necrotic focus that composed of necrotic leukocytes and tissue cells.
A zone of preserved neutrophils around the necrotic focus.
A zone of vascular dilation and fibroblastic proliferation, indicating chronic
inflammation and repair.
Chronic Inflammation
Chronic inflammation is inflammation of prolonged duration (weeks or months) in
which inflammation, tissue injury, and attempts at repair coexist, in varying
combinations.
Etiology:
• Persistent infections by microorganisms that are difficult to eradicate, such as
mycobacteria, and certain viruses, fungi, and parasites. These organisms often
evoke an immune reaction called delayed-type hypersensitivity, the
inflammatory response sometimes takes a specific pattern called a
granulomatous reaction.
• Immune-mediated inflammatory diseases. Chronic inflammation plays an
important role in a group of diseases that are caused by excessive and
inappropriate activation of the immune system. Such as autoimmune diseases
and allergic diseases.
• Prolonged exposure to potentially toxic agents, either exogenous or endogenous.
An example of an exogenous agent is particulate silica, a nondegradable
inanimate material that, when inhaled for prolonged periods, results in an
inflammatory lung disease called silicosis.
Morphologic Features:
In contrast to acute inflammation, which is manifested by vascular changes, edema, and
predominantly neutrophilic infiltration, chronic inflammation is characterized by:
• Infiltration with mononuclear cells, which include macrophages, lymphocytes,
and plasma cells.
• Tissue destruction.
• Healing by connective tissue replacement of damaged tissue.
Cells of chronic inflammation:
Macrophage
The macrophage is the dominant cellular player in chronic inflammation, and it is one
component of the mononuclear phagocyte system.
From the blood, monocytes migrate into various tissues and differentiate into
macrophages. The half-life of blood monocytes is about 1 day, whereas the life span of
tissue macrophages is several months or years.
Monocytes begin to emigrate into extravascular tissues quite early in acute
inflammation, and within 48 hours they may constitute the predominant cell type.
Extravasation of monocytes is governed by the same factors that are involved in
neutrophil emigration, that is, adhesion molecules and chemical mediators with
chemotactic and activating properties.
When a monocyte reaches the extravascular tissue, it undergoes transformation into a
larger phagocytic cell, the macrophage. Macrophages may be activated by a variety of
stimuli, including microbial products, cytokines (e.g., IFN-?) secreted by sensitized
T lymphocytes and by natural killer cells, and other chemical mediators.
The products of activated macrophages will eliminate injurious agents such as
microbes and initiate the process of repair.
Other cell types involved in chronic inflammation include:
• Lymphocytes
Lymphocytes use various adhesion molecule pairs (selectins, integrins and their
ligands) and chemokines to migrate into inflammatory sites.
Lymphocytes and macrophages interact in a bidirectional way, macrophages
display antigens to T cells and produce cytokines (notably IL-12) that stimulate
lymphocyte responses.
Activated lymphocytes produce cytokines, some of which recruit monocytes
from the circulation and IFN-?, which is a powerful activator of macrophages.
• Plasma cells
Develop from activated B lymphocytes and produce antibodies directed either
against persistent foreign or self-antigens in the inflammatory site or against
altered tissue components.
• Eosinophils
Are abundant in immune reactions mediated by IgE and in parasitic infections.
A chemokine that is especially important for eosinophil recruitment is eotaxin.
Eosinophils have granules that contain major basic protein that is toxic to
parasites.
Granulomatous Inflammation
Granulomatous inflammation is a distinctive pattern of chronic inflammation that is
seen in a limited number of infectious and some noninfectious conditions.
Granulomatous inflammation is a cellular attempt to contain an offending agent that is
difficult to eradicate.
In this attempt there is often strong activation of T lymphocytes leading to macrophage
activation, which can cause injury to normal tissues.
Tuberculosis is the prototype of the granulomatous diseases, but sarcoidosis, catscratch
disease, lymphogranuloma inguinale, leprosy, brucellosis, syphilis, some
mycotic infections, berylliosis, reactions of irritant lipids, and some autoimmune
diseases are also included.
A granuloma is a focus of chronic inflammation consisting of a microscopic
aggregation of macrophages that are transformed into epithelium-like cells (epithelioid
cells), surrounded by a collar of lymphocytes and occasionally plasma cells.
Older granulomas develop an enclosing rim of fibroblasts and connective tissue.
Frequently, epithelioid cells fuse to form giant cells in the periphery or sometimes in
the center of granulomas. They have a large mass of cytoplasm containing 20 or more
small nuclei arranged either peripherally (Langhans-type giant cell) or haphazardly
(foreign body–type giant cell).
There are two types of granulomas:
1- Foreign body granulomas are caused by relatively inert foreign bodies. Typically,
foreign body granulomas form around material such as sutures, or other fibers that are
large enough to preclude phagocytosis by a single macrophage.
2- Immune granulomas are caused by a variety of agents that are capable of inducing
a cell-mediated immune response. This type of immune response produces granulomas
usually when the causative agent is poorly degradable, in such responses macrophages
engulf foreign protein antigen, process it, and present peptides to antigen-specific T
lymphocytes, causing their activation. The responding T cells produce cytokines, such
as IL-2, which activates other T cells, and IFN-?, which is important in activating
macrophages and transforming them into epithelioid cells and multinucleate giant cells.
The prototype of the immune granuloma is that caused by infection with
Mycobacterium tuberculosis.