1. Inflammation is the body's protective response to injury or infection that involves blood vessels, immune cells, and chemical mediators. 2. Chemical mediators of inflammation include vasoactive amines, peptides, lipid mediators, cytokines, and enzymes that are released from immune cells and damaged tissues. These mediators cause changes like increased blood flow and vascular permeability. 3. The inflammatory response aims to destroy and isolate the injurious agent while facilitating tissue repair. Prolonged inflammation can lead to chronic disease if the trigger persists.

1. Abisha.S.J
FC&RI
Tuticorin

2. Inflammation is an important
protective process for the host.
Inflammation is a stereotyped
response in a living animal to
a variety of injuries that involves
the Vasculature, various
inflammatory cells, and potent
chemical mediators.

3. Inflammation and Healing
Defects in the inflammatory response can lead to chronic illness
as well as death. In addition to its protective function, inflammation
also sets the stage for healing and repair.
The purpose of the inflammatory response is to dilute, isolate, and
destroy the injurious agent, and to facilitate healing.

4. The body only has a limited number of ways to
respond to an injury, hence the pathogenesis of an
inflammatory lesion and the histological
appearance of that lesion can be similar whether
the injury was caused by a bacterial cell, a foreign
body, ionizing radiation, a toxin, or trauma.

5. Agents causing inflammation
Infective
agents
Immunolo
gical
agents
Physical
agents
Chemical
agents
Inert
materials
Bacteria
Viruses and
their toxins,
fungi,
parasites
Cell
mediated
Antigen
antibody
reactions
Heat
Cold
Radiation
Mechanical
trauma
Organic
Inorganic
poisons
Foreign
bodies

6. Inflammatory Cells
The circulating cells includes-
Neutrophils
Monocytes
Eosinophils
Lymphocytes
Basophils
Platelets
The connective tissue cells are-
Mast cells
Fibroblast
Macrophages
Lymphocytes
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9. Signs of Inflammation
Cardinal signs are
• Heat (calor)
• Redness (rubor)
• Swelling (tumor)
additional signs seen in acute inflammation
• Pain (dolor)
• Loss of function (function laesa)

10. Types of inflammation
Inflammation can be divided into acute and
chronic forms which differ histologically as well
as in duration.
Acute inflammatory episodes, characterized by
vascular events and exudation, usually progress over a period of
3 to 10 days, then resolve as the injurious agent is eliminated.
Chronic inflammation, characterized by cellular proliferation,
can extend from weeks to months to the lifetime of the host,
continuing as long as the injurious agent persists.

11. Acute Inflammation
It is a rapid response to
injury or microbes and
other foreign substances
that is designed to
deliver leukocytes and
plasma proteins to sites
of injury

12. Acute inflammation has two major components
• Vascular changes
• Cellular events
Vascular
• Changes in Vascular Caliber and Flow
• Increased Vascular Permeability
Vasodilation
which allow the largest serum protein molecules such as
fibrinogen and immunoglobulins, normally confined within the
circulation, to exude into the tissue.
Vasodilatation- increase blood flow
Increased intravascular hydrostatic pressure

13. Red line appears within seconds resulting from vasodilatation
of capillaries and venules
Flare is a bright reddish
appearance or flush
surrounding the red line
results from vasodilatation
of the adjacent arterioles
Wheal is the swelling or
edema of the skin occurring
from transudation of fluid
in extra vascular space

14. Changes in Vascular Caliber and Flow
• Changes in blood vessels begin rapidly after infection
or injury but may develop at variable rates, depending
on the nature and severity of the original inflammatory
stimulus.

15. 1. Leakage of exudate

16. Cellular Events
• an important function of the inflammatory
response is to deliver leukocytes to the site of injury and
to activate them
Leukocyte recruitment
Sequence consists of:
1. margination, adhesion to endothelium & rolling along the
vessel wall

17. 2. firm adhesion to endothelium

18. 3.transmigration between endothelial cells;
4. migration in interstitial tissues toward a chemotactic stimulus

20. 5.Phagocytosis (recognition, attachment, engulfment, killing)
6.Termination
7.100% resolution, scar or chronic inflammation three
possible outcomes

21. Patterns of acute inflammation
vascular and cellular reactions that characterize acute
inflammation are reflected in the morphologic
appearanceof the reaction
Grossly
• According to principle
constituent of exudates:-SEROUS
FIBRINOUS
NEUTROPHILIC
SUPPURATIVE
ACUTE
INFLAMMATION

22. serous
characterized by:
• the outpouring of a watery
• relatively protein-poor fluid that, depending on the site of
injury
Neutrophilic exudate:
neutrophils are the prominent cellular component; common
with bacterial infections in most animal species, but this type
of exudate is not as prominent in fish as in other species;
e.g. abscess

23. fibrinous
• occurs as a consequence of more
severe injuries,
• resulting in greater vascular
permeability that allows large
molecules (such as fibrinogen) to pass
the endothelial barrier
suppurative
• manifested by the presence of large
amounts of purulent exudate (pus)
consisting of neutrophils, necrotic
cells, and edema fluid

24. Histologcially, these exudates consist of eosinophilic staining
in the intercellular space; fibrin will have the appearance of
eosinophilic strands.
More severe injuries, particularly bacterial infections, will elicit a
cellular component to the exudate.
Histologcially

25. Chronic Inflammation
• is inflammation of prolonged duration (weeks to months
to years) in which active inflammation, tissue injury, and
healing proceed simultaneously.
Characterized by:
• infiltration with mononuclear cells
• plasma cells tissue destruction
• repair
• angiogenesis
• fibrosis

26. Chronic Inflammatory Cells
• fundamental feature of chronic inflammation is its
persistence
• results from complex interactions between the cells that are
recruited to the site of inflammation and are activated
at this site

27. Neutrophils
Neutrophils are the classic hallmarks of acute inflammation,
many forms of chronic inflammation may nevertheless continue
to show extensive neutrophilic infiltrates
Polymorphonuclear
leucocytes
Mediates tissue injury
Phagocytosis of
microorganisms and
tissue debris

28. Macrophages
 dominant cell of chronic
inflammation
 derived from circulating
blood monocytes
 act as filters for particulate
matter, microbes, and
senescent cells, as well as
acting as sentinels
scattered in most connective
tissues,
 also found in organs such as
the liver spleen and lymph
nodes

29. Lymphocytes
 mobilized to the setting of any specific
immune stimulus
 as well as non-immune-mediated
inflammation

30. Eosinophils
• characteristically found in inflammatory sites around
parasitic infections
• or as part of immune reactions mediated by IgE, typically
associated with allergies
 modulates mast cell-mediated reactions

31. Mast cells
• sentinel cells widely distributed in connective tissues throughout
the body,
• participate in both acute and chronic inflammatory responses
• "armed" with IgE antibody specific for certain environmental
antigens

32. Chronic inflammatory response;
Chronic inflammatory lesions can be composed purely of
macrophages, lymphocytes, or plasma cells.
Macrophages provide phagocytic and killing activity, whereas
the other cell types provide antibody and cell-mediated immune
activity.

33. Granulomatous inflammation
is the more commonly observed
form of chronic inflammation in
fish as well as other animals.
It consists of a mixture of
macrophages, lymphocytes,
plasma cells, fibroblasts, and
sometimes neutrophils, all
oriented in and around the site
of injury.
The lesions of BKD and mycobacteria are examples of
this type of inflammatory response.
Multinucleated giant cells or epithelioid macrophages
are often found in these sites as well.

36. According to duration According to fate of inflammation
Per-acute inflammation Hyperplastic inflammation
Acute inflammation Hypertrophic inflammation
Sub-acute inflammation Atrophic inflammation
Chronic inflammation Fibrous inflammation
Adhessive inflammation

37. Healing
The inflammatory response sets the stage for healing.
Healing can occur by regeneration of the damaged tissue or
scar formation.
The form of healing that occurs is determined by the nature of
the injured tissue and its ability to regenerate as well as the
severity and duration of injury.
Tissues composed of cells that can readily divide (e.g.
epithelium) can easily regenerate, replacing cells lost to
inflammation and necrosis.

38. However, for this to occur the infrastructure of the tissue, i.e.
reticular fibers, basement membranes, etc., must remain
intact and provide a scaffold for cell
replacement.
If that infrastructure is lost, fibrosis (scar formation) will likely
occur.

39. Fibrosis also occurs in tissues composed of cells that
cannot regenerate, such as myocardial cells.
Fibrosis is typical of the healing process of gaping
wounds as well, particularly in the skin.
In some cases of extensive tissue loss, a cavity may
simply remain at the site of injury (cavitation). This is most
often seen in the brain

40. Definition
Diffusible molecules that act locally at the site of tissue
damage and infection, and at more distant sites.
They can be divided into exogenous and endogenous
mediators.

41. Inflammatory mediators
Inflammatory mediators can be classified into seven groups
according to their biochemical properties
• Vasoactive amines
• Vasoactive peptides
• Fragments of complement components
• Lipid mediators
• Cytokine
• Chemokines and proteolytic enzymes.
Chemical mediators are released from cells ,plasma, or
damaged tissue

42. Chemical mediators

43. • Cell derived & Plasma derived
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44. VASOACTIVE AMINES
¡) Histamine
 Stored in the granules of
mast cells, basophils and
platelets.
Main actions
Vasodialation, incresed vascular
permeability, itching, pain
Cell derived mediators

45. ARACHIDONIC ACID
METABOLITES
(EICOSANOIDS)
Arachidonic acid (fatty acid) is
released from the cell
membrane by phospholipases.
It is then activated to form
arachidonic acid metabolites or
eicosanoids by one of the
following two pathways: cyclo -
oxygenase and lipo –
oxygenase pathway

46. LYSOSOMAL COMPONENTS
The inflammatory cells
neutrophils and monocytes
contain lysosomal granules
which on release elaborate a
variety of mediators.

47. . PLATELET ACTIVATING
FACTOR (PAF)
Released from IgE sensitised
basophils or mast cells,
leucocytes, endothelium and
platelets.
ACTIONS
Increased vascular
permeability
Vasodialation and
vasoconstiction
Bronchoconstriction
Adhesion of leucocytes to
endothelium
Chemotaxis

48. CYTOKINES
 These are polypeptide substances produced by activated
lymphocytes (lymphokines) and activated monocytes
(monokines)
 Major cytokines- interleukin-1(IL-1), tumour necrosis factor
(TNF)α and β, Chemokines.
ACTIONS
IL-1 and TNF-α, TNF-β
Induce endothelial effects
Increased leucocyte
adherece
Thrombogenicity
Fibroblastic proliferation

49. (1)derived from metabolism of phospholipids and arachidonic acid
(e.g., prostaglandins, thromboxanes, leukotrienes, lipoxins,
platelet-activating factor [PAF])
(2) preformed and stored in cytoplasmic granules (e.g.,histamine,
serotonin, lysosomal hydrolases),
(3) derived from altered production of normal regulators of vascular
function (e.g., nitric oxide and neurokinins).

50. (1) Cycloxigenases (COX1, 2) acts on Arachidonic acid through
cyclooxygenation, production of prostaglandins and thromboxanes
(2) lipoxygenation, to form leukotrienes and lipoxins.

51. Mediators of inflammation
Mediators Principal sources Actions
CELL DERIVED
Histamine Mast cell, basophil,
platelet
Vasodilation , increased vascular
permeability, pain, endothelial
activation
Serotonin Chromaffin cells of GIT,
spleen & platelet
Vasodilation , increased permeability
Prostaglandin Mast cell, leukocyte Vasodilation, pain, fever
Leukotrienes Mast cell, leukocyte Increase permeability, Chemotaxis,
leukocyte adhesion & activation
Platelet- activating factor Leukocyte, mast cell Increase permeability,
bronchoconstriction, chemotaxis
Reactive Oxygen Species Leukocyte Microbicidal, Tissue damage
Nitric Oxide Endothelium,
Macrophages
Vascular smooth muscle relaxation
Cytokine ( TNF, IL-1)
Chemokines
Macrophage, mast cell
leukocyte
Local endothelial activation
Chemotaxis, leukocyte activation

52. These include the various products derived from activation
and interaction of 4 interlinked systems:
kinin,
clotting,
fibinolytic and
complement
Plasma derived mediators
Hageman factor(factor xii) of clotting system plays a key role in
interactions of the 4 systems
oActivation of factor xii in vivo by contact with basement
membrane and bacterial endotoxins, and in vitro with glass or
kaolin leads to activation of clotting, fibrinolytic, and kinin
systems.
oThe end products of the activated clotting, fibrinolytic and
kinin system activate the complement system

53. Hageman factor (clotting factor
XII), generated within the
plasma
Conversion of plasminogen
to plasmin.
Conversion of prekallikrein
to kallikrein.
Activation of the alternative
complement pathway.
Activation of the coagulation
system.

54. Kinins are potent
inflammatory
agents formed in
plasma and
tissue by the
action of serine
protease
kallikreins on
specific plasma
glycoproteins
termed
kininogens

55. THE COMPLEMENT SYSTEM
I. The activation of
complement system can
occur by:
i. Classic pathway via non
immunological agents
ii. Alternate pathway via non
immunological agents
 Complement system on
activation yields activated
products – anaphylotoxins
(C3a, C4a, C5a) and
membrane attack complex
(MAC) – C5b, C6, C7….

56. Mediator Principal source Functions
PLASMA PROTEIN DERIVED
Complement Products
(C5a, C3a, C4a)
Plasma (produced in liver)
Leukocyte chemotaxis and
activation, vasodialation
Increased permeability,
smooth muscle contraction
Vasodilation, pain.
Endothelial activation,
leukocyte recruitment
Kinins Plasma (produced in liver)
Protease activated during
coagulation
Plasma (produced in liver)

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