CHRONIC

INFLAMMATION
Pathology and Microbiology – 1 (PMB-201)

Presented by: Dr. Naila Tariq

 Bacterial products, immune complexes,
Toxins, physical injury, other cytokines

Macrophage (and other cell activation)

IL-1/TNF

ACUTE PHASE REACTIONS ENDOTHELIAL EFFECTS FIBROBLASTIC EFFECTS

Fever Leukocyte adherence Proliferation
Sleep PGI synthesis Collagen synthesis
Appetite PAF Collagenase
Acute phase proteins Procoagulant activity Protease
Hemodynamic (shock) Anticoagulant PGE synthesis
Neutrophilia IL-1
 CHRONIC INFLAMMATION
► Under conditions in which the inflammatory response is unable to
eliminate the injurious agent or restore injured tissue to its normal
physiologic state of chronic inflammation. The primary cellular
components of the chronic inflammatory response are macrophages,
plasma cells, lymphocytes and in certain conditions, eosinophils.
► Chronic inflammation is mediated by both immunologic and
nonimmunologic mechanisms and is frequently observed in
conjunction with granulation tissue.
► The macrophage is the pivotal cell in regulating these reactions
because it function as a source of both inflammatory and
immunologic mediators.
The histologic hallmarks of chronic inflammation are:
► Infiltration by mononuclear cells principally macrophages,
lymphocytes and plasma cells
► Proliferation of fibroblast and in many instances, small blood vessels
► Increased connective tissue (fibrosis)
Infiltration by monocyte/macrophages is a particularly important
component of chronic inflammation. Other types of cells present in
chronic inflammation are plasma cells, lymphocytes, eosinophils and
mast cells.
Plasma cells produce antibody, directed either against persistent antigen
in the inflammatory site or against altered tissue components.
Lymphocytes are called for in both antibody and cell mediated
immunological reaction, but also for unknown reasons, in non
immunologic inflammation.
Eosinophils are characteristic of immunologic reactions mediated by IgE
and of parasitic infections, but also are often present for obscure
reason.
 CHRONIC INJURY

BACTERIAL AND TISSUE- ACTIVATED T-

TISSUE DERIVED MITOGEN
DERIVED MONOCYTE LYMPHCOYTE
CHEMOTACTIC FACTORS

CHEMOTACTIC GROWTH
FACTORS FACTORS

RECRUITMENT OF PROLIFERATION OF
CIRCULATING TISSUE
MONOCYTE MACROPHAGES

INCREASED
MACROPHAGES
LONG-LIVED TISSUE EPITHILOID CELLS
MACROPHAGES

MULTI-
► The accumulation of macrophages in chronic inflammation NEUCLATED
GIANT CELLS
 WAYS OF CHRONIC
INFLAMMATION
Clinically chronic inflammation in various organs occurs in
three ways:
► It may follow acute inflammation because of the
persistence of the inciting stimulus.
► It may be due simply to repeated bouts of acute
inflammation.
► More curiously, it may begin insidiously as a low-grade,
smoldering response that never acquires the classic
features of acute inflammation (it may start initially as a
chronic inflammation)
 ACCUMULATION OF
MACROPHAGES
Accumulation of macrophages occur in three ways, each predominating
in different types of infection.
► Continued recruitment of monocyte from the circulation results from
the steady release of chemotactic factors. This is numerically the
most important source for macrophages.
► Local proliferation(by mitotic division) of macrophages after their
immigration from the blood stream. We have no idea what triggers
this division, but no more than two cycles of division occur.
► Prolonged survival and immobilization of macrophages with in the site
of inflammation. His is specially evident when the irritants such as
inert lipids and carbon particles are of low virulence
 GRANULOMATOUS INFLAMMATION
The following types of granulomatous inflammation may be recognized:
► Diffuse granulomatous reaction such as is seen in lepromatous leprosy.
► Tuberculoid granulomatous reaction.
Three variants of this occur:
► Non-caseating tuberculoid reaction, as seen in sarcoidosis, lupus
vulgaris and tuberculoid leprosy.
► Caseating tuberculoid reaction, as commonly seen in tuberculosis.
► Suppurative tuberculoid reaction, in which small abscesses filled with
many polymorphs are formed, and are surrounded by a mantle of
epithiloid cells. This type of reaction occurs in lymphogranuloma
venerum, tularemia, coccidioidomyeosis, sportrichosis, and cat-scratch
disease.
Non-caseating Caseating Suppurative
Granuloma Granuloma Granuloma
 GRANULOMATOUS INFLAMMATION

DISEASE CAUSE
TUBERCLOSIS MYCOBACTERIUM TUBERCLOSIS

SARCOIDOSIS UNKNOWN

CERTAIN FUNGAL INFECTIONS CRYPTOCOCCUS NEOPHARM

BLASTOMYCES DERMATITIDIS
COCCIDIODES IMMITIS
SYPHILIS TREPONEMA PALLIDUM
CAT SCRATCH FEVER VIRUS ?
CHLAMYDIAE ?

ACTINOMYCOSIS ACTINONYMYCES BOVIS

 MAJOR GRANULOMATOUS INFLAMMATION
DISEASE CASE TISSUE REACTION
Certain fungal infections Cryptococcus Neopharm ___________
Blastomyces Dermatitidis ___________
Coccidiodes Immitis ___________

Syphilis Treponema Pallidum Gumma: microscopic to grossly visible lesion, enclosing

wall of histocytes, fibroblastand lymphocytes, plasma
cells infiltrate, center cells are necrotic without loss of
cellular outline

Cat-scratch fever Unknown Rounded or stellate granuloma containg central granular

debris and recognizable neutrophils, giant cell
uncommon.

Actinomycosis Actinonymyces Bovis Granulomatous rim enclosing necrotic and viable

polymorphonuclear leukocytes as well as sulfur
granulus.
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