Pathology Lab Topic: Chronic inflammation - labsstudies

Pathology Lab Topic: Chronic inflammation

Pathology Lab Topic: Chronic inflammation

Chronic inflammation

  • Chronic inflammation is Inflammation that occur of prolonged period (weeks to months to years) in which continuous swelling, tissue damage, and healing continue simultaneously.

Causes of chronic inflammation

  • Chronic inflammation can be caused by one of three ways:
  •  Chronic inflammation following with Acute inflammation.
  •  Frequent episodes of acute inflammation.
  •  Chronic inflammation starts from agents known to cause long-term inflammatory responses rather than Acute.
  • As shown, Acute inflammation can persist for a long time. This transition occurs when the immediate response cannot be resolved due to the persistence of the damaging agent or due to interference with the normal healing process.
  • For example, a duodenal peptic ulcer initially presents with acute inflammation followed by early resolution.
  • However, recurrent damage to duodenal epithelial wounds interrupts this process and leads to ulceration, that is Acute and Chronic inflammation.
  • Alternatively, certain types of injury (eg, viral infections) produce a response involving chronic inflammation from the start.

General components of Chronic inflammation

  • Mononuclear cell infiltration
  • Tissue damage or necrosis
  • Proliferative changes

 

Mononuclear cell infiltration

  • Chronic inflammatory lesions are infiltrated by nuclear inflammatory cells such as phagocytes and lymphoid cells.
  • Phagocytes are represented by circulating monocytes, tissue macrophages, epithelial cells, and sometimes large multinucleated cells.

 

Chronic inflammatory Cells and Mediator

  • Macrophages are tissue cells derived from circulating monocytes after migration from the blood. This is dominant cells of chronic inflammation.
  • Macrophages are generally widely distributed in many connective tissues and are also present in these organs such as:
  •  Liver (called Kupffer cells)
  •  Spleen and lymph nodes (called sinus histioocytes)
  •  Central nervous system (microglia)
  • Lungs (alveolar macrophages)
  • Together these cells form the so-called phagocytic mononuclear system, also known as the reticuloendothelial system.
  • In all tissues, microbes act as filters for cells, microbes, and skin cells, as well as guards against harmful stimuli by specific components of the changing immune system (T and B lymphocytes).
  • Macrophages may appear at sites of chronic inflammation from:
  •  Chemical elements and adhesion molecules for continuous macrophage infiltration
  •  Internal proliferation of macrophages.
  • Other chronic inflammatory cells include lymphocytes, plasma cells, eosinophils and mast cells.
  • In chronic inflammation, lymphocytes and eosinophils interact and release inflammatory mediators.
  • Lymphitis is collected to preserve any specific immune triggers (ie infection) as well as unprotected inflammation (eg due to infarction or tissue damage).
  • Both T and B lymphocytes use pairs of sticky molecules that bind to other leukocytes to migrate to the site of inflammation.
  • Lymphocytes and macrophages interact in two ways, and this interaction plays an important role in chronic inflammation.
  • Eosinophils are present in areas of inflammation near parasitic infections or as part of an IgE-mediated immune effect, often associated with allergies.
  • Their recruitment is driven by sticky molecules similar to those used by neutrophils, and by specific chemokines (eg, eosinophils) derived from leukocytes or epithelial cells.
  • Eosinophils contain a major protein, a very abundant cannabinoid protein, that is toxic to parasites but also causes necrosis of epithelial cells.
  • Mast cells are cells widely distributed in connective tissue throughout the body and may be involved in acute and chronic inflammatory responses.

 

Tissue damage or necrosis

  • Tissue damage and necrosis are the main features of many types of chronic inflammatory lesions.
  • This is caused by activated macrophages that produce various biologically active substances such as: protease, elastase, collagenase, lipase, estrogen; Cytokines (Interleukin [IL]-1, Interleukin [IL]-8, Tumor Necrosis Factor [TNF]), Nitric Oxide, Angiogenesis and Growth Factors.

Proliferative Changes

  • Due to necrosis, the proliferation of small blood vessels and fibroblasts is stimulated, leading to the formation of inflammatory granulation tissue, the end result of which is healing by:
  •  Fibrosis and collagen deposition occur.

Types of Chronic Inflammation

There are two types of chronic inflammation based on their historical features:

  • Nonspecific chronic inflammation
  •  It is characterized by penetration of nonspecific cells such as chronic osteomyelitis and lung abscesses.
  •  The category of this type of chronic inflammatory response is chronic inflammatory neoplasms where polymer infiltration and abscess formation are additional features, such as actinomycosis.
  • Chronic granulomatous inflammation
  •  Granulomatous inflammation is a different form of chronic inflammation.
  • It is characterized by the accumulation of activated macrophages with an epithelioid appearance.
  •  Granulomas occur in certain pathological conditions, and the diagnosis of granulomatous structures is important because they cause few (some life-threatening) conditions.
  •  Granulomas can form in a sequence of permanent T-cell responses to certain organisms such as Mycobacterium tuberculosis, Treponema pallidum, or fungi, where T-cell-derived cytokines are responsible for long-term activation of macrophages.
  •  Tuberculosis is an example of a granulomatous disease caused by infection and should always be excluded when diagnosing granulomas.
  •  Granulomas can also develop from airless foreign bodies, such as seams or debris, to form so-called foreign body cells.
  •  Formation of granulomas protects against causative agents and is therefore an important means of protection.
  •  However, granuloma formation does not always lead to elimination of the causative agent, it is often resistant to murder or destruction
  • Inflammation of the granuloma and subsequent inflammation may be a major cause of organ failure in some diseases, such as chest pain.

 Sequels of Chronic inflammation

Granulomatous inflammation

  •  Is defined as a unique structure of chronic tumors characterized by the accumulation of activated cartilage with an epithelioid appearance.

Granuloma

  •  It is defined as the formation of a small wound about 1 mm in diameter.
  • In particular, the concentration of modified macrophages called epithelioid cells and Surrounded by lymphoid cells.

 

The Epithelial cells are named because of their epithelial appearance.

  •  These are macrophages/recovered tissue cells, some are long, with smooth, slightly shaped and slightly shaped shapes. Nucleus, while the cell membranes of adjacent epithelial cells are tightly packed due to blurring the contours of the cells.
  •  Epithelial cells are weak phagocytic cells, and in addition to the presence of epithelial cells, granulomas may have large cells, necrosis, and fibrosis.

Factors that favor granuloma formation

  • Presence of non-digestive irritation that may be caused by microorganisms such as Mycobacterium tuberculosis, talc cells, etc.
  • Presence of cellular immunity to inflammation, thus suggesting a role for hypersensitivity in granulomatous inflammation.

Also read: Pathology Lab Topic: Inflammation

Examples of Granulomatous Inflammatory Diseases

  • Tuberculosis (pathogen – Mycobacterium tuberculosis)
  • Leprosy (pathogen – Mycobacterium leprae)
  • Syphilis (pathogen – Treponema pallidum)
  • Cat scratch disease (Gram-negative bacilli)
  • Sarcoidosis (of unknown etiology)
  • Crohn’s disease or inflammatory bowel disease (immune response to gut bacteria, individual antigens)
  • Cholera
  • Histoplasmosis
  • Cryptococcus
  • Foreign objects such as seams

Consequences of chronic inflammation

  • Erosive scar healing is responsible for some problems in the inflammatory response, such as: pyloric stenosis in peptic ulcer disease, vascular heart damage in rheumatoid arthritis, and stress in burns.
  • Chronic sinus discharge is often seen in chronic osteomyelitis.
  • Pathological fractures.

Effects of inflammation, acute and chronic processes

Fever

  • Presented as an increase in body temperature, usually 1° to 4°C, and is one of the most common manifestations of acute-phase reactions, especially when inflammation is caused by infection.
  • Fever is produced by substances called pyrogens, which work by stimulating the synthesis of prostaglandins (PGs) in the cells surrounding the hypothalamic arteries and blood vessels.
  • Bacterial products, such as lipopolysaccharides (LPS, called extrinsic pyrogens), stimulate the release of cytokines from leukocytes, such as IL-1 and TNF (known as endogenous pyrogens), which increase the cycle of converting AA to prostaglandins oxygenase levels.
  • In the hypothalamus, PGs, especially PGE2, stimulate the production of neurotransmitters, which play a key role in restoring body temperature.
  • Non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin, reduce fever by inhibiting cyclooxygenase, thereby inhibiting PG synthesis.
  • High levels of acute-phase plasma proteins, or plasma proteins, mostly attached to the liver, can increase in concentration up to 100-fold as part of an inflammatory stimulus response.
  •  The three most popular proteins are C-reactive protein (CRP)
  •  Fibrinogen
  •  Serum amyloid A protein (SAA).
  •  Hepatocyte synthesis of these molecules is regulated by cytokines, especially IL-6.
  •  Many acute phase proteins, such as CRP and SAA, attach to the cell walls of small cells and can act as opsonin’s and modification supplements, thereby promoting microbial elimination.
  •  Fibrinogen binds to red blood cells and causes them to form a roulette that comes out of a unit of gravity faster than a single red blood cell.
  •  This is the basis for measuring the erythrocyte sedimentation rate (ESR) as a simple measure of the systemic inflammatory response to any number of stimuli, including LPS.
  •  High levels of CRP serum are now used as an indicator of increased risk of myocardial infarction or stroke in patients with atherosclerotic arterial disease. Inflammation is thought to be associated with the development of atherosclerosis, and elevated CRP is a measure of inflammation
  • Leukocytosis is a common feature of an inflammatory response, mainly caused by bacterial infection.
  • White blood cell counts typically rise to 15,000 or 20,000/μL cells, but can sometimes reach extremely high levels, as high as 40,000 to 100,000/μL cells.
  • These extreme elevations are called leukemic effects because they are similar to the white blood cell counts found in leukemia.
  • Leukocytosis is initially caused by the rapid release of cells from the bone marrow after breast cancer (caused by cytokines, including TNF and IL-1) and is therefore associated with an increase in the number of immature neutrophils in the blood. left).
  • Chronic infection also stimulates collagen (CSF) production, which leads to an increase in bone marrow white blood cells, compensating for the loss of these cells in the inflammatory response.
  •  Many bacterial infections can cause an increase in the number of neutrophils in the blood, called neutropenia.
  •  Viral infections, such as infectious mononucleosis, measles, and measles in Germany, are associated with an increase in the number of lymphocytes (lymphocytosis).
  •  Bronchial asthma, hay fever, and parasite attacks all involve an increase in the total number of eosinophils, resulting in eosinophilia.
  •  Some infections (typhoid and other viral infections, rickettsia, and some protozoa) are associated with a dramatic reduction in the number of circulating white blood cells (leukopenia), possibly due to cytokines that cause lymphocyte separation in lymph nodes.
  • Other manifestations of acute phase reactions include:

o Elevated heart rate and blood pressure

o Decreased sweating, mainly due to reflow of blood from the skin to the walls of the deep arteries to reduce heat loss through the skin, and severity (tremor), chills (feeling cold as the hypothalamus regulates body temperature), anorexia, insomnia. and discomfort, possibly because of the effect of cytokines on brain cells.

  • Chronic inflammation is associated with a wasting disease called cachexia, which is the result of suppressing TNF appetite and stimulating fat storage.
  • In acute bacterial infections (sepsis), LPS-rich microorganisms in the blood or extra-arterial tissue stimulate the production of a large variety of cytokines, especially TNF, as well as IL-12 and IL-1.
  • As a result, circulating levels of these cytokines increase and the nature of the host response changes.
  • High levels of TNF can lead to coagulation (DIC), hypoglycemia and hypertension.

 

Systemic effects of chronic inflammation

Similar effects may occur in the chronic phase of the disease. The following are specific to the long-term phase.

  • Fever

o Always have a mild fever, usually with weight loss and weakness.

  • Anemia

o Chronic inflammation with varying degrees of anemia.

  • Leukocytosis

o Increased white blood cells (white blood cells)

  • Elevated Erythrocyte Sedimentation Rate (ESR) 

o ESR increases in all cases of chronic inflammation.

  • Amyloidosis

o Chronic cases of chronic inflammation can promote secondary systemic amyloidosis.

 

References

  • Kumar, A. et al (2004). Robbins Basic Pathology. WB: Saunders.
  • Spector, T.D. & Axford, J. S. (1999). Introduction to General Pathology. Edinburgh: Churchill Livingstone.
  • Walter, J.B., & Talbot, I. C. (1996). General Pathology. New York: Churchill Livingstone.

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