Inflammatory Response and Immune Cells Quiz

Inflammatory Response: Cells, Chemical Mediators, and Healing Process

Basophils produce heparin and histamine, but are not phagocytic and have limited amoeboid movement.
Lymphocytes include B-lymphocytes and T-lymphocytes, are not phagocytic, and are numerous in viral diseases and toxic conditions.
Plasma cells produce antibodies, undergo mitosis, and have limited amoeboid movement.
Macrophages have strong phagocytic activity for bacteria and protozoa, and may secrete enzymes and neutralizing substances.
Giant cells are large multinucleated cells, not found in peripheral blood, and include foreign body, Langhans, and Touton types.
Chemotaxis is the directional movement of inflammatory cells in response to chemotactic factors, such as bacteria, dead tissue, and lymphokine.
Chemical mediators of inflammation, including histamine, serotonin, SRS-A, and cationic proteins, induce vascular changes.
Phagocytosis involves the engulfing and digestion of foreign matter by phagocytes, including neutrophils, monocytes, and epithelial cells.
Steps of phagocytosis include recognition and attachment, engulfment, and killing or degradation.
Exudates consist of fluid and leukocytes that move from circulation to the site of injury, providing beneficial functions such as dilution of toxic substances, mechanical washing of irritants, and bringing phagocytic cells and antibodies to the area.
Fibrin in exudates entraps and protects the irritant, seals the lymphatic lumen, aids in healing and repair, and stimulates fibroblast proliferation.
The final phase of the inflammatory response is healing, which includes regeneration and fibrosis, with regeneration replacing lost cells and tissues with the same type, while fibrosis involves healing by connective tissue of different origin.

Overview of Inflammation: Types, Manifestations, and Fates

Acute inflammation is characterized by leukocytosis, fever, and general symptoms such as fatigue and appetite loss.
Inflammation can be classified based on duration, exudate content, sequalae, degenerative changes, extent distribution, and position in organs.
Chronic inflammation can be destructive and fibrotic, with varied neutrophil and mononuclear cell count, and can lead to chronic organ insufficiency.
Granulomatous inflammation is a distinctive pattern of chronic inflammation characterized by activated macrophages and the formation of granulomas.
Granulomas are tiny lesions composed predominantly of epithelioid and lymphoid cells, and can be caused by bacterial, fungal, parasitic, or inorganic agents.
Two types of granulomas can be seen: foreign body granulomas and immune granulomas.
The fate of acute inflammation can be the dissolution of exudates or the development of secondary post-infectious disorders.
The fate of chronic inflammation can be fibrosis, cirrhosis, regeneration, or the development of chronic inflammation.
Serous inflammation is characterized by mild degeneration, congestion, and finely granular eosinophilic material, and is seen in affections of serous membranes.
Catarrhal inflammation is characterized by mucin as the predominant constituent of the exudates, and occurs in organs with mucous-secreting cells as a result of infection or foreign bodies.
Fibrinous inflammation is characterized by the presence of fibrin and can be pseudomembranous or diphtheretic.
Supportive inflammation is characterized by the presence of pus and can manifest as microabscesses, abscesses, pustules, furuncles, cellulitis, or empyema.

Healing and Repair: Factors Affecting Regeneration and Repair Process

Healing and repair is the replacement of damaged tissues by healthy ones, which is considered the final phase of the inflammatory response.
The process includes two major components: regeneration and repair (fibrosis).
Regeneration is the replacement of lost cells and tissues with cells of the same type, while repair is the more common type of healing as a result of lost cells being replaced by connective tissue of different origin, leaving scar tissues.
Factors affecting the regeneration/repair process include the type of damaged cells, the role of growth factors and inhibitory factors, extracellular matrix (ECM) synthesis, cell matrix interaction, and angiogenesis.
Labile cells are continuously dividing cells with a short G0 phase, and they heal by regeneration. Examples include surface epithelia of various tracts and haematopoietic cells.
Stable cells are quiescent cells in G0 of the cell cycle, and they are replaced by regeneration or fibrosis depending on the extent and severity of injury and surrounding framework. Examples include parenchymal cells of organs, such as the liver, kidney, and mesenchymal cells like smooth muscle cells, fibroblasts, vascular endothelium, bone and cartilage cells.
Permanent cells have no ability for multiplication and cannot be replaced by regeneration, but they can be replaced by repair (fibrosis). Examples include nerve cells, cardiac muscle cells, skeletal muscle cells, and cells of the lens of the eye.
Stem cells may be embryonic or adult and are characterized by unique properties such as the ability to divide and renew themselves for a long period. They may replicate many times, and they are used in replacing damaged tissues.
Growth factors are proteins that stimulate cellular proliferation, migration, differentiation, contractility, and the synthesis of specialized proteins such as collagen in fibroblasts. They also stimulate the function of growth control genes (proto-oncogenes).
Cytokines and growth factors have different sources and functions, such as epidermal growth factor (EGF) being mitogenic for keratinocytes and fibroblasts, transforming growth factor β (TGF-β) being chemotactic for PMNs, macrophages, lymphocytes, fibroblasts, and smooth muscle cells, and vascular endothelial cell growth factor (VEGF) increasing vascular permeability and being mitogenic for endothelial cells.
Platelet-derived growth factor (PDGF) is chemotactic for and activating PMNs, macrophages, and fibroblasts. It is mitogenic for fibroblasts, endothelial cells, and smooth muscle cells and stimulates the production of MMPs, fibronectin, and HA. It also stimulates angiogenesis and wound remodeling and regulates integrin expression.
Understanding the factors affecting the regeneration/repair process is crucial in promoting healing and preventing complications.