To promote the migration of leukocytes from peripheral blood to the damaged or infected tissue.
Rolling.
Tethering.
Rolling.
Both Gram-positive and Gram-negative bacteria are trapped by NETs.
Endothelial contraction.
http://www.nobelprize.org
Activation.
It converts arginine to citrulline.
Exudate is drained by lymphatic vessels.
S. aureus, S. typhimurium, and S. flexneri.
COX-1 and COX-2 inhibitors, such as NSAIDs (e.g., Aspirin, Ibuprofen, Indomethacin), function by blocking the cyclooxygenase enzymes COX-1 and COX-2. This inhibition reduces the production of prostaglandins, thereby decreasing inflammation, pain, and fever.
Eosinophils release toxic proteins such as major basic protein, eosinophil cationic protein, and eosinophil peroxidase, which are effective against parasites.
Basophils represent about 0.5% to 1% of circulating white blood cells.
It is released by eosinophils and is toxic to parasites.
Selectins bind to mucin-like ligands.
E-selectin (CD62E) is expressed by endothelial cells.
4 - 10 hours
Net flow out.
P-selectins are adhesion molecules expressed on activated endothelial cells and platelets.
TNF-α (Tumor Necrosis Factor-alpha) and IFN-γ (Interferon-gamma).
VCAM-1 (Vascular Cell Adhesion Molecule-1) and MadCAM-1 (Mucosal Addressin Cell Adhesion Molecule-1) are adhesion molecules on the endothelium that bind to integrins on leukocytes.
It has anti-cancer effects.
RGD motifs (Arginine-Glycine-Aspartic Acid) link the extracellular matrix (ECM) to the cell cytoskeleton (via vinculin and actin) at focal adhesion points.
Integrins modulate cell proliferation, differentiation, and motility.
Leukocyte migration involves rolling, adhesion, and transmigration through the endothelium to reach the site of inflammation.
Polymorphonuclear leukocytes, commonly known as neutrophils.
NET formation, which stands for Neutrophil Extracellular Traps.
Polymorphonuclear leukocytes (PMNL), specifically neutrophils.
30 mm Hg.
The primary function of NETs is the capture and killing of extracellular bacteria.
Activation.
NETs trap and kill pathogens by releasing a web-like structure composed of DNA, histones, and antimicrobial proteins.
Arachidonic acid derivatives, such as prostaglandins and leukotrienes, are key mediators in the inflammatory response. They are involved in vasodilation, increased vascular permeability, chemotaxis, and pain.
Integrins are subdivided into 4 groups according to their β chains that couple with different α chains.
Occurs early, has protein content less than 3 g/L, and leukocytes are absent.
Arrest.
The essential components of NETs are DNA, chromatin, and serine proteases.
NETs act as a physical barrier by containing and preventing the spread of bacteria.
Arrest.
Elie Metchnikoff (1845 - 1916).
Occurs late, has protein content greater than 3 g/L, and leukocytes are present.
Tethering.
Activation.
Leukocyte migration is a multistep process.
Resolution refers to the complete return to normal structure and function, while restoration of normal vascular permeability involves the re-establishment of the normal barrier function of blood vessels.
Loose interaction.
Histamine, Bradykinin, Leukotrienes, leading to RhO GTPases activation.
Tethering.
Edema is the first cellular event in acute inflammation, characterized by the accumulation of fluid in tissues.
Activation.
Selectins are sugar-binding mammalian lectins.
Neutrophil Extracellular Traps.
The receptor for phosphatidylserine on apoptotic bodies is known as the 'Eat-me' signal.
Fluid excess.
NETs concentrate different antibacterial enzymes, which helps in preventing tissue damage.
By trapping and killing pathogens, thus preventing their spread and aiding in the resolution of infection.
Neutrophils, eosinophils, and basophils.
CCL3/Eotaxin.
To promote the migration of leukocytes from peripheral blood to the damaged or infected tissue.
Converts arginine to citrulline.
Neutrophil Extracellular Traps.
Glucocorticoids, which can be hormones or drugs, suppress inflammation by inhibiting the synthesis of arachidonic acid derivatives. They reduce the production of pro-inflammatory cytokines and other mediators, thereby decreasing the inflammatory response.
They are phagocytes and act as 'kamikaze' single-shot killers due to their oxidative burst.
Polymorphonuclear leukocytes (PMNL), including neutrophils, eosinophils, and basophils.
Arterioles, capillaries, post-capillary venules.
Protein arginine deiminase 4.
Neutrophils.
NADPH oxidase.
DNA, histones, and antimicrobial proteins.
Myeloperoxidase.
The text does not provide specific details on the effect of IL-8 in the context of NETs.
Immediate, sustained, and prolonged leakage.
The Ig superfamily of receptors.
Vasodilation leads to slower blood flow.
Basophils are responsible for inflammatory reactions during immune response and in the formation of acute and chronic allergic diseases, including anaphylaxis, asthma, atopic dermatitis, and hay fever.
70%
Tethering.
Protein arginine deiminase 4.
Neutrophil Extracellular Traps (NETs).
Arrest.
The transfer of an electron to O2 to form Superoxide Anion (O2-).
Glucocorticoids are hormones and drugs that have potent anti-inflammatory effects. They inhibit the synthesis of arachidonic acid derivatives by blocking the enzyme phospholipase A2, thereby reducing inflammation.
Pro-inflammatory cytokines such as TNF-α, IL-1β, IFN-γ, among others.
PMNLs have a multi-lobulated nucleus, while mononuclear phagocytes (such as monocyte-macrophages) have a single, unsegmented nucleus.
CCR3.
Transmigration.
Diapedesis allows leukocytes to move from the bloodstream into tissues where they can combat infection or injury.
Endothelial cells express adhesion molecules that capture leukocytes and facilitate their migration through the vessel wall.
eNOS (endothelium) and nNOS (neural tissue).
Chemical signals such as cytokines and chemokines released at sites of inflammation or injury.
iNOS (inducible NO synthase).
Arachidonic acid derivatives, such as prostaglandins and leukotrienes, play a crucial role in mediating and regulating the inflammatory response. They are involved in vasodilation, increased vascular permeability, chemotaxis, and pain.
Vasodilation.
C5a, PAF (Platelet-Activating Factor), LTB4 (Leukotriene B4), and formyl peptides from bacteria.
VCAM-1 (Vascular Cell Adhesion Molecule-1) binds to integrins on leukocytes, facilitating their firm adhesion to the endothelium.
Hemodynamic changes, such as increased blood flow and vascular permeability, help deliver immune cells and proteins to the site of injury or infection.
Fluid accumulation in the interstitial space.
It increases to 50 mm Hg.
Arachidonic acid derivatives, such as prostaglandins and leukotrienes, are key mediators in acute inflammation. They are involved in the regulation of various inflammatory responses, including vasodilation, increased vascular permeability, chemotaxis, and pain.
Neutrophils transition from circulating in the bloodstream to actively participating in the inflamed tissue, where they help combat infection and facilitate the inflammatory response.
Rolling.
Neutrophil Extracellular Traps.
Macrophages undergo apoptosis and are phagocytosed by other macrophages.
IgE-mediated response leading to the activation of eosinophils.
Eosinophils.
Macrophages arrive after neutrophils, typically within 24 to 48 hours, and play a role in phagocytosing debris and pathogens, as well as orchestrating the resolution of inflammation.
PSGL-1 (P-selectin glycoprotein ligand-1) is a glycoprotein that binds to selectins on the endothelium, facilitating leukocyte tethering and rolling.
Ca2+ (calcium ions).
Peroxynitrite.
Diapedesis is crucial for the immune response as it enables leukocytes to reach and eliminate pathogens or damaged cells in tissues.
Cyclooxygenase (COX) and lipoxygenase (LOX) enzymes are responsible for converting arachidonic acid into prostaglandins and leukotrienes, respectively.
Chemokines are signaling proteins that direct the movement of leukocytes towards sites of inflammation.
Integrins, such as α4β7 and α4β1, are involved in the firm adhesion of leukocytes to the endothelium and their subsequent transmigration into tissues.
Thromboxanes function in the inflammatory process by promoting platelet aggregation and vasoconstriction.
Lipoxygenase (LOX) enzymes are significant because they convert arachidonic acid into leukotrienes, which are key mediators of inflammation, particularly in allergic and asthmatic responses.
Secondary granules contain Lactoferrin and Cathelicidins.
BPI (Bactericidal-Permeability Increasing protein) is involved in killing bacteria by increasing their membrane permeability.
Cathepsin-G is a serine protease that contributes to the degradation of bacterial proteins.
Elie Metchnikoff, 1845 - 1916.
The transition from circulating neutrophils to their active role in the inflamed tissue.
Extracellular bactericidal activity is greatly reduced after incubation with DNase, which dissociates NETs.
Extracellular bacterial killing by neutrophils is reduced by the addition of antibodies against histones.
Polymorphonuclear leukocytes (PMNL).
Neutrophils are the first cells to arrive at the site of acute inflammation, typically within minutes to hours.
The hypothesis suggests that segmentation ensures the natural order of chromosomes is conserved despite the high amount of reactive oxygen species produced by Neutrophils, which cause covalent breaks and rearrangements of DNA.
Tethering of leukocytes to the endothelium.
Basophils produce histamine, serotonin, and heparin, which prevents blood clotting.
PNAd, MadCAM-1, VCAM-1.
Basophils stain by basic dyes.
Selectins such as L-Selectin, E-Selectin, and P-Selectin.
Mucins form gels that bind to pathogens and act as lubricants and chemical barriers.
PSGL-1 (P-selectin glycoprotein ligand-1) is involved in the tethering and rolling of leukocytes on the endothelium during the initial steps of leukocyte migration.
The primary products of the lipoxygenase pathway are leukotrienes and lipoxins.
7TMR (Seven-Transmembrane Receptors) are involved in the detection of chemotactic signals.
Chronic Granulomatous Disease (CGD) is characterized by defective oxidative burst.
Mutations in genes encoding integrins or selectins, which are crucial for leukocyte adhesion, are often involved.
LAD is diagnosed through genetic testing and flow cytometry to assess the expression of adhesion molecules on leukocytes.
Pinocytosis.
Eosinophils are a type of white blood cell involved in the immune response, particularly in combating parasitic infections and in allergic reactions.
Detection of myeloperoxidase is used for quantifying the presence of neutrophils.
Rolling.
Basophils are the largest type of granulocyte.
Leukocyte margination is the process of leukocytes approaching and interacting with the endothelium.
50%.
Leukocytes, including neutrophils and other white blood cells.
1 - 2 days
α4β7 and α4β1.
Integrins on leukocytes and ICAM-1 and VCAM-1 on endothelial cells are involved in the firm adhesion process.
Net flow in.
Selectins bind to glycoproteins and glycolipids during the tethering process.
Through its vasodilatory effects.
Leukotrienes play a role in acute inflammation by promoting chemotaxis, increasing vascular permeability, and contributing to bronchoconstriction.
The consequence is a reduced ability to kill ingested pathogens, leading to recurrent infections.
Thromboxanes are involved in promoting platelet aggregation and vasoconstriction during the inflammatory process.
Mutations in genes encoding components of the NADPH oxidase complex are often involved.
Leukocytes are activated by chemokines and other signaling molecules such as C5a, PAF, LTB4, and formyl peptides from bacteria.
Lipoxygenase (LOX) enzymes convert arachidonic acid into leukotrienes, which are involved in chemotaxis, increased vascular permeability, and bronchoconstriction.
Hydrogen peroxide (H2O2) by spontaneous conversion.
Neutrophils.
Neutrophils play a crucial role in acute inflammation by phagocytosing pathogens, releasing enzymes, and producing reactive oxygen species to kill microbes.
Eosinophils release cytokines and chemokines that attract and activate other immune cells, such as T cells and macrophages, thereby amplifying the inflammatory response.
The large fragments of DNA are trapped within the segments, allowing granulocytes to function normally and remain active in the immune response.
L-Selectin.
E-selectins are adhesion molecules expressed on activated endothelial cells.
Tethering, rolling, activation, and adhesion.
Mucins are a family of high molecular weight, heavily glycosylated proteins produced by epithelial tissues, mostly at mucosal surfaces.
Chemokines activate leukocytes, increasing the affinity of integrins for their ligands on endothelial cells, thus promoting firm adhesion.
Integrins such as α4β7 and α4β1.
Vasodilation.
Prostaglandins contribute to inflammation by causing vasodilation, increasing vascular permeability, and sensitizing nerve endings to pain.
Endothelial cells regulate vascular permeability and leukocyte extravasation, facilitating the movement of immune cells to the site of inflammation.
Key cell players include neutrophils, macrophages, mast cells, and endothelial cells, each contributing to different stages and aspects of the inflammatory response.
Arachidonic acid derivatives are synthesized from arachidonic acid, which is released from cell membrane phospholipids by the action of phospholipase A2. The arachidonic acid is then metabolized by cyclooxygenase (COX) and lipoxygenase (LOX) pathways to produce prostaglandins, thromboxanes, and leukotrienes.
Leukotriene D4 (LTD4) is most associated with bronchoconstriction in asthma.
Prostaglandins play a role in vasodilation, increasing vascular permeability, and sensitizing nerve endings to pain. They also contribute to the fever response.
The key enzymes involved in the metabolism of arachidonic acid are cyclooxygenase (COX) and lipoxygenase (LOX). COX enzymes produce prostaglandins and thromboxanes, while LOX enzymes produce leukotrienes.
Hypoxia, toxins, burns, chemicals, etc.
Eosinophils release mediators such as histamine and leukotrienes that contribute to the symptoms of allergic reactions, including tissue swelling and bronchoconstriction.
Through contact-dependent activation causing endothelial cell contraction.
Delayed response.
It connects to the cytoskeleton.
32 mm Hg.
It was once thought that mast cells were basophils that migrated from blood into their resident tissues, but they are now known to be different types of cells.
In the post-capillary venules.
L-selectin (CD62L) is expressed by leukocytes.
S-nitrosylation of proteins.
Monocytes.
By inhibiting platelet adhesion and aggregation, and leukocyte-endothelium interaction.
E-selectins and P-selectins are involved in the rolling of leukocytes on the endothelium during the leukocyte migration process.
Prostaglandins contribute to the inflammatory response by causing vasodilation, increasing vascular permeability, and sensitizing nerve endings to pain.
Chemotactic receptors detect chemotactic factors and guide leukocytes towards the site of inflammation.
Acute inflammation is resolved through the removal of the initial trigger, clearance of inflammatory cells and mediators, and tissue repair and regeneration.
Tethering is the initial weak interaction between leukocytes and the endothelium, mediated by selectins and their ligands.
Prostaglandins contribute to the inflammatory response by causing vasodilation, increasing vascular permeability, and sensitizing nerve endings to pain.
ICAM-1 and ICAM-2 (Intercellular Adhesion Molecules) are expressed on endothelial cells and bind to integrins on leukocytes, aiding in firm adhesion and transmigration.
Corticosteroids inhibit the enzyme phospholipase A2, which prevents the release of arachidonic acid from cell membrane phospholipids. This reduces the production of all arachidonic acid derivatives, including prostaglandins, thromboxanes, and leukotrienes, thereby reducing inflammation.
Junctional retraction.
Eosinophils release granules containing enzymes and toxic proteins that can kill parasites and modulate inflammatory responses. They also release cytokines and chemokines that influence other immune cells.
PMNLs, or polymorphonuclear leukocytes, include Neutrophils, Eosinophils, and Basophils. They are grouped together because of their multi-lobulated nucleus.
1. Intracellular domain connected to the cytoskeleton, 2. Transmembrane (TM) domain, 3. Extracellular domain for homo- or heterophilic interactions.
Macrophages help resolve acute inflammation by clearing dead cells and debris, secreting anti-inflammatory cytokines, and promoting tissue repair.
Allergies.
Eosinophils.
Endothelial cells line the blood vessels and regulate the passage of leukocytes through the vascular barrier.
Leukocytes adhere to the endothelium through interactions between adhesion molecules on their surface and those on endothelial cells.
PSGL-1 is a glycoprotein that binds to E-selectins and P-selectins.
Cyclooxygenase (COX) enzymes convert arachidonic acid into prostaglandins, while lipoxygenase (LOX) enzymes convert it into leukotrienes.
The primary defect is the inability of leukocytes, particularly neutrophils, to produce reactive oxygen species (ROS) necessary for killing pathogens.
The initial trigger for acute inflammation is typically tissue injury or infection, which activates the innate immune response.
CGD is diagnosed using tests like the nitroblue tetrazolium (NBT) test or dihydrorhodamine (DHR) flow cytometry to assess the oxidative burst capability of neutrophils.
Primary granules include Myeloperoxidase, BPI (Bactericidal-Permeability Increasing protein), Defensins, Elastase, and Cathepsin-G.
Myeloperoxidase.
L-selectin is expressed on leukocytes and binds to ligands on the endothelium to mediate rolling.
Prostaglandins play a role in vasodilation, increasing vascular permeability, and sensitizing nerve endings to pain. They also contribute to fever by acting on the hypothalamus.
COX-1 is constitutively expressed and involved in maintaining normal physiological functions, such as protecting the gastric mucosa. COX-2 is inducible and primarily involved in the inflammatory response, producing prostaglandins that mediate inflammation and pain.
During arrest, leukocytes firmly adhere to the endothelium via integrins and adhesion molecules, preparing for transmigration.
Post-capillary venules and pulmonary vessels.
Arrest.
Basophils.
Neutrophils, the most abundant leukocytes in circulation.
The May-Grunwald Giemsa staining method, which uses Eosin and Methylene Blue, is used for PMNLs.
2.5 - 7.5 x 10^9/L
Very short, lasting only seconds.
Bacterial peptides (f-Met-Leu-Phe), C5a (a fragment of the complement system), and chemokines (particularly Interleukin-8).
May-Grunwald Giemsa (Eosin + Methylene Blue)
High lipid reactivity.
Nitric Oxide (NO).
The main types are prostaglandins, thromboxanes, and leukotrienes.
It leads to impaired immune response as leukocytes cannot effectively reach and accumulate at sites of infection or inflammation.
Leukotrienes are primarily involved in bronchoconstriction during inflammation.
Leukocyte Adhesion Deficiency (LAD) is a disease characterized by defective leukocyte adhesion.
NSAIDs inhibit the cyclooxygenase (COX) enzymes, thereby reducing the production of prostaglandins and thromboxanes, which helps to alleviate inflammation and pain.
Nitric oxide acts as a vasodilator, increasing blood flow to the inflamed area and also has antimicrobial properties.
Defensins are antimicrobial peptides that disrupt the integrity of bacterial cell membranes.
Integrins are activated by chemokines and other signaling molecules such as C5a, PAF, and LTB4.
During rolling, leukocytes transiently adhere to the endothelium via selectins, allowing them to slow down and roll along the vessel wall.
E-selectins and P-selectins are expressed on endothelial cells and mediate the initial tethering and rolling of leukocytes.
MadCAM-1 (Mucosal Addressin Cell Adhesion Molecule-1) is an endothelial adhesion molecule that binds to integrins like α4β7, aiding in leukocyte migration to mucosal tissues.
NSAIDs inhibit the cyclooxygenase (COX) enzymes, reducing the production of prostaglandins and thromboxanes. This leads to decreased inflammation, pain, and fever.
The lipoxygenase (LOX) pathway is significant in inflammation because it produces leukotrienes, which are potent mediators of chemotaxis, vascular permeability, and bronchoconstriction.
The process is called diapedesis, also known as transmigration.
Glycoproteins and glycolipids.
Endothelial cells regulate the passage of materials and the transit of white blood cells into and out of the bloodstream.
E-selectins and P-selectins.
Selectins mediate the initial tethering and rolling of leukocytes on the endothelial surface.
Chemotaxis, which is the directional movement towards a chemotactic factor.
Cell Adhesion Molecules.
PSGL-1 (P-Selectin Glycoprotein Ligand-1) binds to selectins on the endothelium to mediate rolling.
Endothelial cell junctions loosen to allow leukocytes to transmigrate from the bloodstream to the site of inflammation.
L-selectin is involved in the rolling of leukocytes on the endothelium, facilitating their migration to sites of inflammation.
Leukotrienes play a role in acute inflammation by promoting chemotaxis, increasing vascular permeability, and causing bronchoconstriction.
Leukotrienes are primarily involved in bronchoconstriction during inflammation.
The α4β7 integrin is a homing receptor for T lymphocytes in the Gut-Associated Lymphoid Tissue (GALT).
The two main types of edema are transudate, which is low in protein, and exudate, which is high in protein and cellular content.
Prostaglandins are known for their role in causing pain and fever during inflammation.
Tertiary granules include Cathepsins and Gelatinase.
Cyclooxygenase (COX) and lipoxygenase (LOX) enzymes are responsible for converting arachidonic acid into prostaglandins and leukotrienes, respectively.
The enzymes involved in the metabolism of arachidonic acid are cyclooxygenase (COX) and lipoxygenase (LOX). COX enzymes produce prostaglandins and thromboxanes, while LOX enzymes produce leukotrienes.
Formyl peptides are bacterial products that act as chemoattractants, guiding leukocytes to sites of infection.
It facilitates homo- or heterophilic interactions.
Arachidonic acid derivatives, such as prostaglandins and leukotrienes, play a crucial role in mediating various aspects of acute inflammation, including vasodilation, increased vascular permeability, chemotaxis, and pain.
These diseases are characterized by the inability of leukocytes to properly adhere to endothelial cells, which impairs their migration to sites of infection or injury.
Parasites, worms, bacteria, and viruses.
Integrin-mediated signaling involves the MAPK and PKC pathways.
Neutrophils release several anti-bacterial enzymes stored in cytoplasmic granules.
Elastase is a protease that breaks down proteins, including those in bacterial cell walls.
Arachidonic acid derivatives, such as prostaglandins and leukotrienes, play a crucial role in mediating various aspects of acute inflammation, including vasodilation, increased vascular permeability, chemotaxis, and pain.
α4β7 and α4β1 are integrins on leukocytes that bind to endothelial adhesion molecules like VCAM-1 and MadCAM-1, facilitating firm adhesion and transmigration.
Leukotrienes are involved in chemotaxis, attracting leukocytes to the site of inflammation, and increasing vascular permeability. They also contribute to bronchoconstriction in conditions like asthma.
Chemokines are signaling molecules that activate leukocytes and direct their migration towards sites of inflammation.
Thromboxanes are involved in promoting platelet aggregation and vasoconstriction, which are important in the formation of blood clots and controlling bleeding during inflammation.
12 mm Hg.
P-selectin (CD62P) is expressed by endothelial cells and platelets.
Selectins are adhesion molecules on endothelial cells that mediate the initial capture and rolling of leukocytes on the vessel wall.
Selectins bind to sialic acid residues covalently bound to mucinic glycoproteins.
Inflammatory cytokines such as TNF and IL-1 trigger the expression of adhesion molecules on endothelial cells.
Leukocyte migration is a multistep process involving tethering, rolling, adhesion, and transmigration.
Endothelial cells retract and increase their permeability, allowing leukocytes to pass through the vessel wall.
The primary products of the cyclooxygenase pathway are prostaglandins and thromboxanes.
MadCAM-1 (Mucosal Addressin Cell Adhesion Molecule-1) is involved in the homing of T lymphocytes to the Gut-Associated Lymphoid Tissue (GALT).
Lipoxins differ from other arachidonic acid derivatives as they are involved in the resolution phase of inflammation, promoting the cessation of inflammatory responses and aiding in tissue repair.
The release of arachidonic acid from cell membranes during inflammation is triggered by the activation of phospholipase A2 (PLA2) enzymes.
Neutrophils are the first responders, arriving at the site of inflammation within minutes to hours to phagocytose pathogens and debris.
Gelatinase breaks down gelatin and collagen, aiding in tissue remodeling and bacterial degradation.
The main types of arachidonic acid derivatives involved in inflammation are prostaglandins, thromboxanes, and leukotrienes.
Leukotrienes play a role in acute inflammation by promoting chemotaxis, increasing vascular permeability, and contributing to bronchoconstriction.
Thromboxanes promote platelet aggregation and vasoconstriction, which are important in the formation of blood clots and controlling bleeding during inflammation.
Thromboxanes are significant in the inflammatory process as they promote platelet aggregation and vasoconstriction, which are important for hemostasis and the initial response to tissue injury.
7TMR (Seven-Transmembrane Receptors) are involved in leukocyte activation and migration by responding to chemokines and other signaling molecules.
Arachidonic acid derivatives, such as prostaglandins and leukotrienes, mediate various aspects of inflammation including vasodilation, increased vascular permeability, and leukocyte recruitment.
Cathelicidins are antimicrobial peptides found in the secondary granules of neutrophils.
Arachidonic acid derivatives, such as prostaglandins and leukotrienes, play crucial roles in mediating and regulating the inflammatory response. They are involved in vasodilation, increased vascular permeability, chemotaxis, and pain.
PNAd (Peripheral Node Addressin) is a ligand for L-selectin that facilitates the homing of leukocytes to peripheral lymph nodes.
Arachidonic acid derivatives, such as prostaglandins and leukotrienes, play crucial roles in mediating and regulating the inflammatory response. They are involved in vasodilation, increased vascular permeability, chemotaxis, and pain.
Leukotrienes are involved in chemotaxis, attracting leukocytes to the site of inflammation, and increasing vascular permeability. They also contribute to bronchoconstriction in conditions like asthma.
Lactoferrin binds iron, which is essential for bacterial growth, thereby inhibiting bacterial proliferation.
The main types of arachidonic acid derivatives involved in inflammation are prostaglandins, thromboxanes, and leukotrienes.
NSAIDs inhibit the cyclooxygenase (COX) enzymes, thereby reducing the production of prostaglandins and thromboxanes, which helps to alleviate inflammation, pain, and fever.
VCAM-1 (Vascular Cell Adhesion Molecule-1) is an endothelial adhesion molecule that binds to integrins like α4β1, facilitating firm adhesion and transmigration of leukocytes.
Arachidonic acid derivatives are synthesized from arachidonic acid, which is released from cell membrane phospholipids by the action of phospholipase A2. The arachidonic acid is then metabolized by cyclooxygenase (COX) and lipoxygenase (LOX) pathways to produce prostaglandins, thromboxanes, and leukotrienes.
NSAIDs inhibit the cyclooxygenase (COX) enzymes, which are responsible for converting arachidonic acid into prostaglandins and thromboxanes. This reduces inflammation, pain, and fever.
Cathepsins are proteases that degrade proteins, aiding in the breakdown of bacterial components.
PSGL-1 (P-selectin glycoprotein ligand-1) is a ligand for selectins that mediates the initial tethering and rolling of leukocytes on the endothelium.
The main types of arachidonic acid derivatives involved in inflammation are prostaglandins, thromboxanes, and leukotrienes.
Peroxidase staining is used to identify the presence of myeloperoxidase in neutrophils, indicating their bactericidal activity.
Glycoproteins and glycolipids on the leukocyte surface interact with selectins on the endothelium to mediate tethering and rolling.
Prostaglandin E2 (PGE2) is primarily responsible for pain and fever during inflammation.
Lipoxygenase (LOX) enzymes metabolize arachidonic acid to produce leukotrienes, which are involved in chemotaxis, increasing vascular permeability, and bronchoconstriction.
