1. SRI PARAMAKALYANI COLLEGE
( Reaccredited with B Grade with a CGPA of 2.71 in the II Cycle by NAAC
Affiliated to Manonmaniam Sundaranar University, Tirunelveli)
ALWARKURICHI 627 412 TAMIL NADU, INDIA
POST GRADUATE & RESEARCH CENTRE - DEPARTMENT OF MICROBIOLOGY
(Government Aided)
II SEM - CORE –IMMUNOLOGY
SUB CODE: ZMBM22
UNIT I
INFLAMMATION
SUBMITTED TO C. SARANYA VELLAIAMMAL
GUIDE: Dr. S.VISWANATHAN, Ph.D, REG NO : 20211232516124
ASSISTANT PROFESSOR & HEAD OF THE DEPARTMENT, I. M.SC.MICROBIOLOGY
SRI PARAMAKALYANI COLLEGE, SRI PARAMAKALYANI COLLEGE
ALWARKURICHI ALWARKURICHI
4. Inflammation is part of the complex biological response of
body tissues to harmful stimuli, such as pathogens, damaged
cells, or irritants.
It is a protective response involving immune cells, blood
vessels, and molecular mediators.
The function of inflammation is to eliminate the initial cause of
cell injury, clear out necrotic cells and tissues damaged from
the original insult and the inflammatory process, and initiate
tissue repair.
5. It is a generic response, and therefore it is considered as a
mechanism of innate immunity, as compared to adaptive
immunity, which is specific for each pathogen.
Its purpose is to localize and eliminate the injurious agent and
to remove damaged tissue components so that the body can
begin to heal.
The response consists of changes in blood flow, an increase in
permeability of blood vessels, and the migration of
fluid, proteins, and white blood cells from the circulation to
the site of tissue damage.
6. Redness
A swollen joint that may be warm to the touch
Joint pain
Joint stiffness
Fever
Chills
Fatigue/loss of energy
Headaches
Loss of appetite
Muscle stiffness
7. Inflammation can be either short-lived (acute) or long-lasting
(chronic).
Acute inflammation goes away within hours or days.
Chronic inflammation can last months or years, even after the
first trigger is gone. Conditions linked to chronic inflammation
include
o Cancer
o Heart disease
o Diabetes
o Asthma
o Alzheimer’s disease
8.
9. Acute inflammation occurs immediately upon injury, lasting
only a few days.
Cytokines and chemokines promote the migration
of neutrophils and macrophages to the site of inflammation.
Pathogens, allergens, toxins, burns, and frostbite are some of
the typical causes of acute inflammation. Toll-like
receptors (TLRs) recognize microbial pathogens.
Acute inflammation can be a defensive mechanism to protect
tissues against injury.
Inflammation lasting 2–6 weeks is designated subacute
inflammation.
10.
11. 1. Vasodilation and Stasis
The first change in the microcirculation is a transient and
insignificant vasoconstriction, which is then followed by
marked, active dilation of arterioles, capillaries, and venules.
This vasodilation causes an initial marked increase in blood
in the area (hyperemia)
Subsequently, as fluid is lost into the exudate, stasis may
supervene, with very sluggish blood flow.
12. The permeability of capillaries and venules is a function of the
intercellular junctions between vascular endothelial cells.
These pores normally permit the passage of small molecules (MW
< 40,000).
Pinocytosis permits selective transfer of larger molecules across
the capillary into the interstitium.
In normal capillaries, fluid passes out of the microcirculation and
into tissues under the influence of capillary hydrostatic pressure
and returns because of plasma colloid osmotic pressure.
13.
14. Increased passage of fluid out of the microcirculation because of
increased vascular permeability is termed exudation.
The composition of an exudate approaches that of plasma, it is rich
in plasma proteins, including immunoglobulins, complement, and
fibrinogen,
Fibrinogen in an acute inflammatory exudate is rapidly converted
to fibrin by tissue thromboplastins.
Fibrin can be recognized microscopically in an exudate as pink
strands or clumps.
15.
16. 1.Formation of Phagosomes
The first step in phagocytosis is recognition of the injurious agent
by the phagocytic cell, either directly or after the agent has been
coated with immunoglobulin or complement factor 3b (C3b)
The coating agents are opsonins.
Op sonin-mediated phagocytosis is the mechanism operating in the
immune phagocytosis of microorganisms.
Both IgG and C3b are effective opsonins.
17.
18. Chronic inflammation is inflammation that lasts for months or
years.
Macrophages, lymphocytes, and plasma cells predominate in
chronic inflammation, in contrast to the neutrophils that
predominate in acute inflammation.
Diabetes, cardiovascular disease, allergies, and chronic
obstructive pulmonary disease (COPD) are examples of diseases
mediated by chronic inflammation.
Obesity, smoking, stress and insufficient diet are some of the
factors that promote chronic inflammation.
19. A granuloma is defined as an aggregate of macrophages.
Two types of granuloma are recognized:
(1) epithelioid cell granuloma, which represents an immune
response in which the macrophages are activated by
lymphokines of specifically stimulated T cells; and
(2) foreign body granuloma, which represents nonimmune
phagocytosis of foreign nonantigenic material by
macrophages.
20. Epithelioid cells are activated macrophages that appear as large
cells with abundant pale, foamy cytoplasm.
It have enhanced abilities to secrete lysozyme.
Granulomas are usually surrounded by lymphocytes, plasma
cells, fibroblasts, and collagen.
A typical feature of epithelioid cell granulomas is the formation
of Langhans-type giant cells that are derived from fusion of
macrophages and characterized by 10–50 nuclei around the
periphery of the cell.
21. Epithelioid cell granulomas form when two conditions are
satisfied:
(1) When macrophages have successfully phagocytosed the
injurious agent but it survives inside them. The abundant pale,
foamy cytoplasm reflects the presence of extensive rough
endoplasmic reticulum (secretory function).
(2) When an active T lymphocyte-mediated cellular immune
response occurs. Lymphokines produced by activated T
lymphocytes inhibit migration of macrophages and cause them
to aggregate in the area of injury and form granulomas.
22.
23. When foreign material that is large, inert, and nonantigenic
enters a tissue and persists there, foreign body granulomas
form.
Nonantigenic material, which includes
sutures, talc particles, and inert fibers, is removed by
macrophages through nonimmune phagocytosis.
Macrophages aggregate around the phagocytosed particles
and form granulomas.
These frequently contain foreign body giant
cells characterized by numerous nuclei dispersed throughout
the cell rather than arranged around the periphery, as occurs
in Langhans-type giant cells.
24. Nongranulomatous chronic inflammation is characterized by
the accumulation of sensitized lymphocytes (specifically
activated by antigen), plasma cells, and macrophages in the
injured area.
These cells are scattered diffusely throughout the tissue,
however, and do not form granulomas.
Scattered tissue necrosis and fibrosis are common.
25. Nongranulomatous chronic inflammation represents a
composite of several different types of immune response due
to different antigenic agents.
Chronic Viral Infections
Chronic Autoimmune Diseases
Chronic Chemical Intoxications
Chronic Nonviral Infections
Allergic Inflammation and Metazoal Infections
