Other Cells in Chronic Inflammation

Slide 1 · Other Cells in Chronic Inflammation

Eosinophils • Mast cells • Persistent neutrophils

Cell-specific recruitment, activation and tissue effects

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

By the end of the lecture, interpret the contribution of three additional inflammatory cell types.

Explain how a chronic inflammatory infiltrate varies with the inciting stimulus.

Trace Th2-associated recruitment and effector activity of eosinophils.

Describe IgE receptor signaling and chronic functions of mast cells.

Recognize why neutrophils may persist in chronic lesions.

Slide 3 · Chronic inflammation is a continuing process

Inflammation, tissue injury and attempted repair coexist over weeks or months.

A chronic process may follow acute inflammation or begin insidiously.

The inflammatory population changes according to persistent stimuli and local mediators.

Eosinophils, mast cells and neutrophils may join the mononuclear infiltrate.

Slide 4 · Morphology: The baseline and the exceptions

Typical chronic pattern

Macrophages, lymphocytes and plasma cells

Tissue destruction

Angiogenesis and fibrosis

Additional cells

Eosinophils in selected immune responses

Mast cells in acute and chronic reactions

Neutrophils may remain prominent

Do not equate “chronic” with complete absence of neutrophils.

Slide 5 · The offending stimulus influences the infiltrate

Persistent or repeated stimulus

Type 2 immune response

Eosinophils

IgE-linked response

Mast-cell activation

Persistent microbes or tissue signals

Neutrophils

Cell composition is a clue to the underlying inflammatory mechanism.

Slide 6 · Why “other cells” matters

Macrophages are dominant in most chronic lesions—but the infiltrate is not uniform.

Specific immunologic stimuli favor recruitment of additional leukocytes.

Their mediators can protect against a threat and damage host tissues.

A mixture of cell types can be present at the same time.

Slide 7 · CD4⁺ helper subsets provide context

Th1

IFN-γ secretion

Classical macrophage activation

Th2

IL-5 → eosinophils

IL-4 / IL-13 → IgE production

Th17

IL-17 and other cytokines

Chemokines recruit neutrophils and monocytes

Th2 and Th17 links explain two major patterns covered in this lecture.

Slide 8 · T helper signals are an upstream switch

Antigen-driven T-cell response

Cytokine environment

Selective leukocyte recruitment

Dominant effector activity

Local cytokines help determine which “other” cells accumulate.

Slide 9 · Three additional cellular contributors

Eosinophil

Helminth defense and epithelial injury

Mast cell

IgE-associated mediator release and cytokines

Neutrophil

Persistent recruitment in selected chronic lesions

Different cells imply different dominant mechanisms—not a unique diagnosis.

Slide 10 · Eosinophils: Stimulus-specific abundance

Eosinophils are particularly abundant in Th2-mediated immune reactions.

Parasitic infections are a core example.

Some allergic disorders show the same type of cellular enrichment.

Their presence reflects immune polarization rather than duration alone.

Slide 11 · Two settings with eosinophils

Parasitic infection

Th2-associated response

Eosinophil recruitment

Granule protein can harm helminths

Allergic reaction

Th2-associated response

Eosinophil recruitment

Granule protein can injure epithelium

The same cell population may be protective or injurious depending on the setting.

Slide 12 · Th2-mediated eosinophil recruitment

Th2 lymphocyte

IL-5 secretion

Eosinophil recruitment and activation

Local effector activity

IL-5 as an important Th2 signal for eosinophils.

Slide 13 · Recruitment requires adhesion and chemotaxis

Eosinophils reach inflamed tissue using both vascular and directional signals.

Their recruitment uses adhesion molecules similar to those used by neutrophils.

Specific chemokines, including eotaxin, provide recruitment signals.

Chemokines can originate from leukocytes and epithelial cells.

Slide 14 · From blood to an inflamed site

Circulating eosinophil

Adhesion molecule–dependent recruitment

Chemokine-directed movement

Eosinophil-rich focus

The same multistep recruitment principle applies to several leukocyte classes.

Slide 15 · Eotaxin: A local directional cue

Eotaxin (chemokine)

Leukocytes

Potential producer

Epithelial cells

Potential producer

Eosinophils

Recruited cells

The local tissue participates in shaping its own inflammatory infiltrate.

Slide 16 · Two recruitment signal classes

Adhesion molecules

Permit interaction with the vascular wall

Similar in principle to neutrophil recruitment

Part of arrival at tissue

Chemokines

Provide directional recruitment cues

Eotaxin is a named example

Produced locally by tissue and immune cells

Adhesion and chemotactic signaling are complementary, not alternative, steps.

Slide 17 · Eosinophil granules are effectors

Eosinophils contain cytoplasmic granules with major basic protein.

Major basic protein is strongly cationic.

It is toxic to helminths.

It can also injure the host’s epithelial cells.

Slide 18 · Major basic protein: Protective pathway

Helminthic infection

Eosinophil-rich Th2 response

Major basic protein release / action

Injury to helminth

Eosinophil antimicrobial benefit is linked to its granule protein.

Slide 19 · Major basic protein: Collateral injury

Allergic inflammation

Eosinophil accumulation

Major basic protein exposure

Epithelial cell injury

Effector molecules do not inherently distinguish pathogen from host tissues.

Slide 20 · One granule product; Two outcomes

Benefit

The target is a helminth

Toxic granule content assists defense

Potential clearance of persistent parasite

Cost

Host epithelium is exposed

The same protein can damage host cells

Inflammation may amplify tissue injury

Explain both outcomes when interpreting eosinophil-rich inflammation.

Slide 21 · Th2 cells connect eosinophils and IgE

Th2 cytokines coordinate more than one downstream effector.

IL-5 recruits and activates eosinophils.

IL-4 and IL-13 stimulate IgE antibody production.

IL-4 and IL-13 also support alternative macrophage activation.

Slide 22 · An integrated Th2-associated response

Th2 lymphocyte

IL-5 / IL-4 / IL-13

Eosinophils / IgE responses

Tissue inflammation or protection

The precise outcome depends on the antigen and host tissue.

Slide 23 · Application: Eosinophils in parasite defense

A chronic inflammatory focus occurs during a persistent helminthic infection. Eosinophils are conspicuous.

Which eosinophil product best explains the host-defense function?

Major basic protein in eosinophil granules.

Its toxicity to helminths provides benefit; The same protein may damage nearby epithelium.

Slide 24 · Application: Eosinophils in allergy

A chronic allergic lesion contains abundant eosinophils near an epithelium.

Why can this infiltrate contribute to tissue damage, despite its role in host defense?

Major basic protein can injure epithelial cells.

Th2-associated recruitment can bring an effector optimized for helminth toxicity into host tissue.

Slide 25 · Interpreting eosinophils: A necessary caution

An eosinophil-rich infiltrate indicates a possible mechanism—not a final diagnosis.

Parasitic infection and some allergic diseases as key contexts.

The source does not provide a numerical eosinophil threshold.

Use the tissue context and clinical setting before attributing a cause.

Slide 26 · Mast cells: Tissue distribution

Mast cells are widespread in connective tissues.

They are situated where local responses can be initiated.

Them in both acute and chronic inflammation.

They should not be treated as exclusive to immediate allergy.

Slide 27 · Mast cells participate in two time scales

Immediate response

IgE-dependent activation

Degranulation

Histamine and prostaglandins

Chronic context

Persist within inflammatory tissues

Can produce multiple cytokines

May promote continuing inflammation

Acute mediator release and chronic immune modulation are distinct roles.

Slide 28 · FcεRI is a high-affinity IgE receptor

Mast-cell surfaces express FcεRI.

FcεRI binds the Fc portion of IgE antibodies.

Bound IgE confers antigen-specific recognition in immediate hypersensitivity.

Antigen engagement initiates mast-cell activation.

Slide 29 · IgE links antigen recognition to mast cells

IgE antibody

Fc portion binds FcεRI

Antigen recognized by bound IgE

Mast-cell response

The mast cell senses antigen through its surface-bound IgE.

Slide 30 · Two different roles in the same receptor system

Mast cell with FcεRI

IgE Fc portion

Receptor binding

IgE antigen-binding site

Antigen specificity

Receptor engagement

Cellular activation

Fc binding anchors antibody; Antigen recognition provides specificity.

Slide 31 · Immediate mast-cell activation

Antigen engages bound IgE

Mast-cell receptor engagement

Degranulation

Mediator release

This is the described pathway in immediate hypersensitivity reactions.

Slide 32 · Mast-cell mediator release

Histamine and prostaglandins among the products released.

They are associated with mast-cell activation in immediate reactions.

Degranulation is an important mechanism in this response.

The extracted section does not enumerate every mediator or downstream effect.

Slide 33 · Receptor, stimulus and output

Recognition

FcεRI expressed on mast-cell membrane

IgE bound by its Fc region

Antigen engages cell-bound IgE

Response

Mast cell becomes activated

Degranulation follows receptor engagement

Histamine, prostaglandins and other mediators

Recognition and effector phases should be taught as separate events.

Slide 34 · Immediate hypersensitivity settings

IgE-mediated mast-cell activation has recognizable clinical contexts.

Food-triggered allergic reactions.

Reactions to insect venom.

Drug-associated allergic reactions.

Slide 35 · Severity can extend to anaphylaxis

Specific allergic trigger

IgE-dependent mast-cell activation

Release of inflammatory mediators

Potential anaphylactic shock

The severe outcome is possible, not inevitable.

Slide 36 · Why mast cells matter in chronic disease

Their contribution is not confined to degranulation during a single exposure.

Mast cells can remain present in chronic inflammatory lesions.

They can secrete a broad range of cytokines.

These cytokines may promote inflammation in different settings.

Slide 37 · Two mast-cell functions, one cell

Acute allergic episode

Surface-bound IgE recognizes antigen

Rapid mediator-release response

Can be clinically severe

Chronic inflammation

Mast cells remain among local immune cells

Cytokines influence inflammatory milieu

Contribution varies by context

Do not infer chronic activity solely from a history of an immediate reaction.

Slide 38 · Application: Identifying mast-cell activation

After exposure to an insect venom, a patient develops an immediate allergic reaction.

Which antibody-receptor interaction is central to the mast-cell mechanism described here?

IgE binds the mast-cell FcεRI receptor through its Fc region.

Antigen engagement of cell-bound IgE triggers the mediator-release response.

Slide 39 · Application: Chronic mast-cell contribution

A chronic inflammatory lesion contains mast cells without an acute systemic allergic episode.

Can mast cells still plausibly contribute to the ongoing reaction?

Yes—mast-cell cytokine secretion may promote local inflammation.

Mast cells participate in both acute and chronic reactions; Immediate IgE-mediated degranulation is not their only role.

Slide 40 · Eosinophils and mast cells: Linked but not identical

Eosinophils

Enriched by Th2 responses

IL-5 / eotaxin recruit them

Major basic protein may injure tissue

Mast cells

Resident in connective tissue

FcεRI-bound IgE senses antigen

Degranulation and cytokine secretion

A common allergic context does not mean the two cells have identical functions.

Slide 41 · Type 2 inflammatory network

Th2 cytokine profile

Eosinophil recruitment + IgE production

Eosinophil / mast-cell activities

Potential host injury in allergy

This diagram links source-described routes; It is not a complete molecular pathway.

Slide 42 · Neutrophils: A chronic inflammation exception

Neutrophils commonly characterize acute inflammation, but they may persist in chronic processes.

The term “chronic” reflects duration and tissue-response pattern.

It does not exclude neutrophilic exudation.

Robbins provides chronic bone infection and irritant-induced lung damage as examples.

Slide 43 · Persistent microbes sustain neutrophils

Persistent microbial stimulus

Continued inflammatory signaling

Neutrophil recruitment

Neutrophil-rich chronic exudate

Persistence may reflect ongoing recruitment rather than long survival of individual cells.

Slide 44 · Macrophages can recruit neutrophils

Activated macrophages release mediators that favor continuing inflammation.

Robbins explicitly identifies macrophage-derived mediators as a reason for neutrophils in chronic reactions.

Macrophage products include TNF, IL-1 and chemokines in the parent section.

A chronic mononuclear response can therefore recruit a neutrophilic component.

Slide 45 · T lymphocytes can also sustain recruitment

Activated T-cell mediators contribute to persistent neutrophil influx.

Th17 cells secrete IL-17 and related cytokines.

These induce chemokine secretion that attracts neutrophils and monocytes.

The Th17 connection explains one immune route to neutrophil-rich inflammation.

Slide 46 · Th17 pathway toward neutrophil recruitment

Activated Th17 cell

IL-17 and other cytokines

Chemokine production

Neutrophils and monocytes arrive

The pathway helps connect T-cell activity to mixed chronic infiltrates.

Slide 47 · Chronic osteomyelitis: An instructive example

Chronic bacterial infection of bone may maintain neutrophilic exudate for months.

This is an explicit Robbins example of neutrophils in a chronic lesion.

Persistence of infection sustains the exudative component.

Neutrophil-rich material alone does not prove that the process is short-lived.

Slide 48 · Chronic osteomyelitis: The mechanistic chain

Persistent bacterial infection in bone

Continuing inflammatory signaling

Ongoing neutrophilic exudate

Chronic tissue inflammation

A prolonged lesion may retain an acute-type cellular component.

Slide 49 · Smoking-related lung injury: A second example

Neutrophils contribute to chronic lung damage caused by smoking and other irritants.

Persistent irritant exposure differs from persistent microbial infection.

Both may nonetheless favor a neutrophilic inflammatory component.

Interpret cell composition in light of the etiologic setting.

Slide 50 · Two routes to chronic neutrophilic injury

Chronic bone infection

Stimulus: Persistent bacteria

Tissue: Bone

Finding: Months of neutrophilic exudate

Smoking-associated injury

Stimulus: Chronic irritant exposure

Tissue: Lung

Finding: Neutrophil-associated damage

Similar cellular players do not establish the same initiating cause.

Slide 51 · Application: Interpreting neutrophils

A bone sample from long-standing osteomyelitis contains a substantial neutrophilic exudate.

Does neutrophil predominance exclude chronic inflammation?

No. Chronic osteomyelitis may show persistent neutrophilic exudation for months.

Inflammation is categorized by overall duration and tissue response, not by one leukocyte type alone.

Slide 52 · A cellular comparison across mechanisms

Eosinophils

Th2 / parasitic or allergic settings

Eotaxin-mediated recruitment

Major basic protein

Mast cells

IgE-linked and other chronic settings

FcεRI + bound IgE

Histamine / prostaglandins / cytokines

Neutrophils

Persistent microbes or chronic irritants

Macrophage / T-cell mediator support

Exudate and tissue damage

Stimulus → recruitment/activation → effector → tissue response is the shared explanatory framework.

Slide 53 · One tissue can receive multiple immune signals

Chronic inflamed tissue

Th2 mediators

Eosinophils

IgE + antigen

Mast cells

Persistent microbial / cytokine signals

Neutrophils

The diagram is a conceptual map, not a claim that all three are present in every lesion.

Slide 54 · How recruited cells contribute to injury

Persistent inflammatory trigger

Recruitment / activation

Release of effector products

Potential host-tissue damage

Inflammation can protect, but uncontrolled or misdirected effector activity damages host cells.

Slide 55 · Interpret inflammatory infiltrates as patterns

What composition suggests

Potential initiating stimulus

Dominant immune mediator pathway

Likely effector mechanisms

What it cannot establish alone

A single unique etiology

A validated severity threshold

A complete clinical diagnosis

Pattern recognition must be integrated with context; No diagnostic cutoffs are supplied.

Slide 56 · Integrated application: Three specimens

Three chronic lesions are described: (A) helminth-associated tissue inflammation; (B) immediate venom allergy; (C) months-long bacterial bone infection.

Which additional cell or activation pathway best fits each example?

A: Eosinophils; B: IgE–FcεRI mast-cell activation; C: Persisting neutrophils.

Each association is directly; None is exclusive to that diagnosis.

Slide 57 · Five defensible distinctions

The identity of the dominant effector matters more than the generic label “chronic.”

Th2 cytokines recruit eosinophils; Eotaxin contributes chemotactic guidance.

Major basic protein harms helminths and can injure host epithelium.

FcεRI-bound IgE mediates antigen-linked mast-cell degranulation.

Mast-cell cytokines may also contribute to chronic inflammation.

Neutrophils can persist in bone infection and irritant-related lung damage.

Slide 58 · Reference and scope

Robbins, Cotran & Kumar: Pathologic Basis of Disease. 11th edition (2026).

Chapter 3: Inflammation and Repair—Chronic Inflammation and Other Cells in Chronic Inflammation.

Teaching schematics are original editable PowerPoint objects; they are not microscopy or clinical specimens.

Interpret inflammatory cell patterns with the tissue context and the inciting stimulus.