Inflammation
Presented by
Armin Borhan, MD
Pathologist (AP/CP)
What is inflammation?!
- A response of vascularized tissues to infections & tissue damage brings cells &
molecules of host defense from the circulation to the sites eliminate the
offending agents basically a protective response not harmful reaction (but also
may cause tissue damage)
- The suffix -itis means inflammation of
Inflammation
Without inflammation infections would go unchecked & wounds would never
heal
Inflammation
Typical inflammatory reaction steps
• The offending agent (in extravascular
tissues) recognized by host cells & molecules
• WBCs & plasma proteins recruited
from the circulation to the site
• The WBCs & proteins activated & work
together to eliminate the offending substance
• The reaction is controlled & terminated
• The damaged tissue is repaired
Inflammation
- Inflammation two types acute & chronic
- When chronic ?! if the initial response fails to clear the stimulus
Causes of inflammation
- Infections (bacterial, viral, fungal, parasitic)
- Tissue necrosis
- Foreign bodies (splinters, tattoo, sutures, fillers)
- Immune reactions (AKA hypersensitivity)
Reactions of Blood Vessels in Acute Inflammation
- Vasodilation induced by inflammatory mediators (e.g. histamine) erythema
- Increased vascular permeability by histamine & endothelial injury passage of
fluids
- Fluid leak from blood vessels edema (either exudate or transudate)
Reactions of Blood Vessels in Acute Inflammation
Principal mechanisms of increased vascular permeability
Leukocyte recruitment to sites of inflammation
WBC recruitment is a multistep process
1. Margination toward the vessel walls (depends on physical features of the blood cells)
2. Loose attachment to & rolling on endothelium (mediated by selectins)
3. Firm (stable) attachment to endothelium (mediated by integrins)
4. Migration through interendothelial gaps (CD31 homotypic interaction)
Leukocyte recruitment to sites of inflammation
Nature of leukocyte infiltrates in inflammatory reaction in a case of MI
WBC activation, removal of microbes & dead cells
- Leukocytes eliminate microbes & dead cells by phagocytosis destruction in
phagolysosomes (free radicals e.g. ROS, NO or granule enzymes)
- Anti-inflammatory mediators terminate the acute inflammatory reaction when it
is no longer needed (TGF-β & IL-10)
- Otherwise, damage to normal tissues by the same mechanisms is likely
Mediators of inflammation
- They are the substances that initiate & regulate inflammatory reactions
- Understanding the role of chemical mediators in inflammatory process is important
most anti-inflammatory drugs target specific mediators
Morphologic patterns of acute inflammation
- Although mentioned general features are characteristic of most acute
inflammatory reactions (lead to 5 cardinal signs), special morphologic patterns are
often superimposed on them, depending on the severity, specific cause &
particular site involved
- Examples are Suppurative Inflammation & Ulcer
Purulent (Suppurative) Inflammation, Abscess
- Characterized by the production of pus, an exudate consisting of neutrophils, the
liquefied debris of necrotic cells & edema fluid
- Mostly infection with bacteria that cause liquefactive necrosis e.g. staphylococci
(AKA pyogenic or pus-producing bacteria)
- A common example of an acute suppurative inflammation is acute appendicitis
Purulent (Suppurative) Inflammation, Abscess
Abscess is localized collections of pus caused by implantation of pyogenic microbes
in a tissue or an organ (image lung abscesses in a case of pneumonia)
Purulent (Suppurative) Inflammation, Abscess
In time the abscess may become walled off and ultimately replaced by connective
tissue. When persistent or at critical locations (e.g. the brain), abscesses may have
to be drained surgically
Ulcer
- A local defect, or excavation, of the surface of an organ or tissue that is produced
by the sloughing (shedding) of inflamed necrotic tissue
- It is most commonly seen in:
(1) mucosa of the mouth, stomach, intestines or GU tract
(2) skin of the lower extremities in older persons (due to circulatory disturbances)
Morphologic features of chronic inflammation
In contrast to acute inflammation, chronic inflammation is characterized by:
(1) Infiltration with mononuclear cells
(2) Tissue destruction (persistent offense)
(3) Attempts at healing (angiogenesis & fibrosis)
Eosinophils as a cellular component of chronic inflammation
Eosinophils are abundant in immune reactions mediated by IgE & in parasitic
infections as well as allergies
Granulomatous Inflammation
- A form of chronic inflammation, shows collections of activated macrophages
(epithelioid histiocytes), often with T cells & sometimes central necrosis
- Granuloma is a cellular attempt of IS to wall off an offending agent that is difficult
to eradicate
Granulomatous Inflammation
There are two types of granulomas:
(1) in case of persistent microbe (e.g. Mycobacterium tuberculosis)
Granulomatous Inflammation
(2) in case of Foreign body (e.g. sutures and cosmetic fillers)
Granulomatous Inflammation
Foreign body granuloma (suture)
Granulomatous Inflammation
Foreign body granuloma (lip filler)
Granulomatous Inflammation
Foreign body granuloma (breast silicone leak)
Granulomatous Inflammation
Foreign body granuloma (tattoo)
Systemic effects of inflammation
The acute-phase response consists of several clinical & pathologic changes:
(1) Fever is caused by prostaglandins production in hypothalamus
(2) Acute-phase proteins (e.g. CRP & Fibrinogen) production in liver elevation of
plasma levels ESR rise
(3) Leukocytosis (neutrophilia vs lymphocytosis)
