Steps of inflammation : pathology lectures FMGE & NEET PG

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Steps of inflammation: pathology lectures FMGE & NEET PG

Acute inflammation is the innate immune system's immediate response to any insult, including:
• Infections (bacterial or viral)
• Immune reactions (e.g. bee sting)
• Tissue necrosis (e.g. acute MI, trauma, burns, radiation)

Acute inflammation lasts for minutes to days, and is mediated most prominently by neutrophils, as well as eosinophils and antibodies. Eosinophils are the predominant inflammatory cells in allergic reactions and parasitic infestations.

The cardinal signs of inflammation are:
• Rubor (redness)
• Dolor (pain)
• Calor (heat)
• Tumor (swelling)
• Functio laesa (loss of function)
These five characteristics are evident locally in a tissue following injury, and are often accompanied by fever, a systemic sign of inflammation.

Rubor and calor (redness and heat, respectively) are caused by vasodilation and increased blood flow in a tissue, which occurs via relaxation of smooth muscle in arterioles. Important mediators of this process include histamine, prostaglandins, and bradykinin.

Dolor is pain due to increased pressure exerted by the accumulation of interstitial fluid, as well as due to sensitization of sensory nerve endings by two key mediators, importantly bradykinin and PGE2.

Tumor is swelling due to extravasation of fluid from postcapillary venules into the interstitium, which results in the formation of an exudate. Causes of this process include:
• Histamine release, which causes contraction of endothelial cell
• Direct damage to endothelial cells

Functio laesa is loss of function.

Fever is an increased body temperature that is often present in a patient with acute inflammation. It is mediated by pyrogens (such as bacterial lipopolysaccharide [LPS]), which induce macrophages to secrete cytokines such as IL-1, IL-6, and TNF-alpha to act as "endogenous pyrogens." Together, these cytokines increase cyclooxygenase activity in the perivascular cells of the hypothalamus, causing release of PGE2, which raises the body temperature "set point."

In addition to leukocytes (especially neutrophils), which undergo extravasation and phagocytosis to respond to tissue injury, the vasculature also plays an extensive role in acute inflammation. Sequential events in the vasculature include
• Vasoconstriction of arterioles (reflex neurogenic)
• Vasodilation of arterioles (via histamine, NO, prostaglandins)
• Increased permeability of venules (via histamine and other mediators)
• Fluid exudation and tissue swelling
• Reduced blood flow (via decreased vessel hydrostatic pressure)

Neutrophils are the most prominent cells during acute inflammation. They enter tissue via the leukocyte extravasation pathway and participate in phagocytosis, degranulation, and inflammatory mediator release.

Neutrophils have a short lifespan in the tissue, undergoing apoptosis within 24 hours of resolution of the tissue insult.

Following neutrophils (1-2 days later), macrophages manage the next step of the inflammatory process, which can be any of the following:
• Resolution and healing
• Continued acute inflammation
• Chronic inflammation
• Abscess formation

Resolution and healing is achieved when macrophages produce anti-inflammatory cytokines such as TGFβ and IL-10.

Continued acute inflammation results when macrophages release Interleukin (IL)-8 leading to recruitment of more neutrophils and more pus formation.

Abscess formation is characterized by fibrin-lined cavity filled with pus, which consists of neutrophils, macrophages, and liquefied cellular debris.

Macrophages may present antigen to activate lymphocytes (CD4+ helper T cells) and secrete IL-12, leading to chronic inflammation.

Acute-phase reactants are factors whose serum concentration significantly changes in response to inflammation.

In response to injury, macrophages and other inflammatory cells secrete interleukins IL-1, IL-6 and TNF-α and IFN-γ and the liver responds by significantly increasing or decreasing the production of acute-phase reactants.

The following acute phase reactants are elevated in the serum in response to inflammation:
• C-reactive protein
• Ferritin
• Fibrinogen
• Hepcidin
• Serum amyloid A

C-reactive protein enhances phagocytosis and is measured clinically as a sign of ongoing inflammation.
Ferritin binds and sequesters iron to inhibit microbial iron scavenging.
Fibrinogen promotes endothelial repair and parallels erythrocyte sedimentation rate.
Hepcidin inhibits release of storage iron from ferritin and is involved in anemia of chronic disease.

Persistent elevation of serum amyloid A can lead to amyloidosis.

The following acute-phase reactants are reduced in the serum in response to inflammation:
• Albumin
• Transferrin