Overview of Acute Inflammation

Inflammatory Cells

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nflammation is complex. It forms part of the innate immune system and has acute and active chronic stages, but today we’ll just be focusing on ACUTE inflammation. Then there’s the fluid/vascular and cellular phases of the acute inflammatory response. It can get confusing – I was certainly drowning in confusion when I was learning this in my Introduction to Veterinary Pathogenesis unit in second year bachelors. Let's ease into it with a brief overview! Hope it helps…

What is inflammation?

Inflammation, part of the body’s innate immune responses, occurs in response to any injury to a tissue. Being innate, this means inflammation is an in-built response in the body’s immune system and is a regularly available, generalised, non-adaptive line of defence. The suffix '-itis' refers to inflammation e.g. dermatitis, hepatitis.

Inflammation can cause some distinctive signs, known as the 5 cardinal signs:

Heat

Redness

Swelling

Pain

Impaired function

Inflammation starts off as acute and can progress to chronic active if the response is ongoing. Today, we’ll just be discussing ACUTE INFLAMMATION, of which there are two phases: fluid/vascular and cellular.

Acute inflammation begins with the fluid/vascular phase then enters the cellular phase…

FLUID/VASCULAR PHASE

Often described as being in the peracute stage of acute innate inflammation, this phase precedes the cellular phase. This means there is not yet any presence of inflammatory cells. As the name suggests, this phase involves fluids such as blood and interstitial fluid.

In this phase, the pathogen or site of tissue damage is localised and diluted by fluids. The site becomes swollen, which causes the connective tissues to pull apart, thus enabling cells to move more easily through the damaged site. Fibrinogen also enters the site, forming fibrin clots.

Hyperaemia is also a prominent feature of the fluid/vascular inflammatory phase. Hyperaemia means increased blood flow caused by the dilation of arteries and the opening of capillary beds. It can result in veins becoming congested from the increased amount of passing blood. This is what causes the redness and swelling we see in inflamed areas on our bodies.

Alongside hyperaemia, vascular permeability is also increased. This means that more molecules and cells are allowed to pass in and out of vessel walls in order to access neighbouring tissues. Therefore, not only do vessels dilate (hyperaemia) but also become more permeable (vascular permeability).

Any excess interstitial fluids end up in the lymphatic vessels and travel to lymph nodes before entering systemic circulation.

The fluid/vascular phase encompasses three types of cascades. A cascade is a chain of reactions yielding pro-inflammatory products. The cascades are:

Clotting (coagulation) cascade

Complement cascade

Kinin cascade

Several types of exudates can be released from the fluid/vascular phase:

Serous – watery

Haemorrhagic – bloody

Catarrhal – mucoid

Fibrinous – has fibrin

Pseudomembranous – fibrino-necrotic

The fluid/vascular phase then leads into the cellular phase as inflammatory cells start to engorge the damaged site…

CELLULAR PHASE

The cellular phase of acute inflammation is, as the name suggests, characterised by the arrival of inflammatory cells, known as leucocytes (white blood cells).

These leucocytes are able to pass through blood vessel walls and reach damaged tissues due to increased vascular permeability (see fluid/vascular phase) and chemotaxins (attractive chemical stimulus) released by the localised site of damage.

The leucocytes involved in the acute inflammatory response are:

Neutrophils

Nucleus: multilobulated (non-lobulated in younger neutrophils; like bands)

Cytoplasm: neutral-staining (granules stain faintly)

Eosinophils

Nucleus: lobulated but less so than neutrophils

Cytoplasm: has eosinophilic granules

Basophils

Nucleus: bilobed, often covered up by cytoplasmic granules

Cytoplasm: has basophilic granules

Macrophages/monocytes

Nucleus: large round cell with round, ovoidal nuclei (kidney-shaped nuclei in monocytes)

Cytoplasm: abundant, vacuolated

Macrophages are in tissues; monocytes are the inactive form and circulate blood

Plasma cells

Nucleus: has heterochromatin in clockface arrangement

Cytoplasm: abundant, basophilic

Lymphocytes e.g. Natural killer cells

Nucleus: NK cell has large, dense, round nucleus

Cytoplasm: NK cell has minimal cytoplasm

The other lymphocytes are T cells and B cells but these are not part of the innate immune system, thus not involved in inflammation.

The leucocytes can be split into two groups – granulocytes and mononuclear cells:

Granulocytes: neutrophils, eosinophils, and basophils

These are polymorphonuclear (nucleus is lobulated) and granulated, meaning there are granules in the cytoplasm (even neutrophils which have weakly staining granules). These granules are important because they contain enzymes that are released during degranulation to help these cells in digesting phagocytosed pathogens and microbes.

Mononuclear: macrophages/monocytes, plasma cells, lymphocytes e.g. natural killer cells

These have round nuclei and do not contain granules in their cytoplasm.

The cellular phase of acute inflammation is also the entryway into adaptive immunity.

Summary

Inflammation is a defence response of the body’s innate immune system and occurs in response to tissue damage. It has acute and chronic active stages. Acute inflammation involves a fluid/vascular phase and a cellular phase.

The fluid/vascular phase of peracute inflammation serves to dilute and localise the pathogen or site of damaged tissue. It also causes swelling resulting in connective tissue to pull apart. Fibrin clots are also formed during this phase. Hyperaemia and increased vascular permeability are also key features of the fluid/vascular phase.

The cellular phase of acute inflammation serves to draw inflammatory cells (leucocytes) to the localised site of tissue damage. The granulocytes also phagocytose pathogens. The cellular phase leads into adaptive immunity.

Hope that helps! See you in my next article Xx

Sources:

Higgins, D 2019, AVBS2001 Introduction to Veterinary Pathogenesis, lecture: Acute Inflammation and the innate response (non-adaptive/no memory), lecture Powerpoint slides, Faculty of Veterinary Science (The University of Sydney)

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