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    Inflammation

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    ramsiya
    This document defines inflammation and describes the key events in acute inflammation. It discusses how acute inflammation is characterized by redness, swelling, heat, pain, and loss of function. The main events are vascular changes like vasodilation and increased permeability, and cellular changes like leukocyte exudation, phagocytosis, and chemotaxis. Leukocytes marginate, roll, adhere and migrate through the endothelium toward the site of injury or infection, where they phagocytose pathogens and cell debris using opsonins, granules and reactive oxygen species.

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    Inflammation

    Uploaded by

    ramsiya
    21 views44 pages
    This document defines inflammation and describes the key events in acute inflammation. It discusses how acute inflammation is characterized by redness, swelling, heat, pain, and loss of function. The main events are vascular changes like vasodilation and increased permeability, and cellular changes like leukocyte exudation, phagocytosis, and chemotaxis. Leukocytes marginate, roll, adhere and migrate through the endothelium toward the site of injury or infection, where they phagocytose pathogens and cell debris using opsonins, granules and reactive oxygen species.

    Original Title

    1. Inflammation

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    This document defines inflammation and describes the key events in acute inflammation. It discusses how acute inflammation is characterized by redness, swelling, heat, pain, and loss of function. The main events are vascular changes like vasodilation and increased permeability, and cellular changes like leukocyte exudation, phagocytosis, and chemotaxis. Leukocytes marginate, roll, adhere and migrate through the endothelium toward the site of injury or infection, where they phagocytose pathogens and cell debris using opsonins, granules and reactive oxygen species.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    21 views44 pages

    Inflammation

    Uploaded by

    ramsiya
    This document defines inflammation and describes the key events in acute inflammation. It discusses how acute inflammation is characterized by redness, swelling, heat, pain, and loss of function. The main events are vascular changes like vasodilation and increased permeability, and cellular changes like leukocyte exudation, phagocytosis, and chemotaxis. Leukocytes marginate, roll, adhere and migrate through the endothelium toward the site of injury or infection, where they phagocytose pathogens and cell debris using opsonins, granules and reactive oxygen species.

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    of 44

    INFLAMMATION

    Dr Aravind P
    Associate professor
    Dept of Pathology
    A.J. Institute of Medical sciences
    INFLAMMATION

    Defn:
     Local response of living mammalian tissues to
    injury due to any agent.
    Signs of inflammation
     Rubor (Redness)
     Tumor (Swelling)
     Callor (Heat)
     Dollar (Pain)
     Functeo leasa (Loss of function)
    Types of inflammation

     Acute inflammation

     Chronic inflammation
    Acute inflammation

     Rapid host response that serves to deliver


    leukocytes and plasma proteins, such as
    antibodies, to sites of infection or tissue
    injury.
    Stimuli for acute inflammation
     Infections (bacterial, viral, fungal, parasitic)
     Tissue necrosis from any cause, including
    ischemia trauma, physical and chemical
    injury
     Foreign bodies (splinters, dirt, sutures)
     Immune reactions (hypersensitivity
    reactions)
    Events in acute inflammation

     Vascular events
     Cellular events
    Vascular events
    1. Changes in Vascular Flow and Caliber
    2. Altered vascular permeability
    1. Changes in Vascular Flow
    and Caliber
     Vasodilation, sometimes it follows a
    transient constriction of arterioles,
    lasting a few seconds.
     Vasodilation first involves the arterioles
    and then leads to opening of new capillary
    beds in the area.
     The result is increased blood flow, which is
    the cause of heat and redness (erythema).
    1. Changes in Vascular Flow
    and Caliber
     Vasodilation is followed by increased
    permeability of the microvasculature.
     The loss of fluid and increased vessel
    diameter will slow the blood flow resulting
    stasis
     Blood leukocytes, principally neutrophils,
    accumulate along the vascular
    endothelium.
    2. Increased Vascular Permeability
    (Vascular Leakage)
     A hallmark of acute inflammation is
    increased vascular permeability leading to
    the escape of a protein-rich exudate into
    the extravascular tissue, causing edema.
    Mechanisms responsible for increased vascular
    permeability

     Contraction of endothelial cells


    resulting in increased interendothelial
    spaces is elicited by histamine and other
    chemical mediators
     Endothelial injury,
    resulting in endothelial cell necrosis and
    detachment.
     Transcytosis
    Increased transport of fluids and proteins,
    through the endothelial cell.
    The major local manifestations
    of acute inflammation
    (1) Vascular dilation and increased blood
    flow (causing erythema and warmth)
    (2) Extravasation and extravascular
    deposition of plasma fluid and proteins
    (edema)
    (3) Leukocyte emigration and accumulation
    in the site of injury.
    The major local manifestations of acute
    inflammation
    Cellular events
    A. Exudation of leucocytes
    B.Phagocytosis
    A. Exudation of leucocytes

    1. Cellular margination
    2. Pavementing
    3. Rolling
    4. Adhesion,Emigration and
    chemotaxis
    1. Exudation of leucocytes
     Margination : white cells assume a peripheral
    position along the endothelial surface.
     Rolling : Individual and then rows of leukocytes
    adhere transiently to the endothelium.
     Pavementing : Endothelium lined by white cells.
     Adhesion : The cells adhere firmly to
    endothelial cells mediated by adhesion
    molecules.
    Adhesion molecules
     The initial rolling interactions are mediated
    by a family of proteins called selectins.
    There are three types of selectins:
     one expressed on leukocytes (L-selectin),
     one on endothelium (E-selectin),
     one in platelets and on endothelium (P-
    selectin).
    Adhesion molecules
    Firm adhesion is mediated by a family of
    heterodimeric leukocyte surface proteins
    called integrins.
     Vascular cell adhesion molecule 1
    (VCAM-1)
     Intercellular adhesion molecule-1
    (ICAM-1).
    Endothelial-Leukocyte Adhesion Molecules

     Endothelial Molecule /Leukocyte Molecule / Role


     P-selectin / Sialyl-Lewis X–modified proteins /Rolling
     E-selectin / Sialyl-Lewis X–modified proteins /Rolling
    and adhesion
     GlyCam-1, CD34 / L-selectin / Rolling
     ICAM-1 / CD11/CD18 (β2) integrins / Adhesion,
    arrest, transmigration
     VCAM-1 / VLA-4 (β1) integrin / Adhesion
    2. Transmigration
     Migration of the leukocytes through the
    endothelium.
     Chemokines stimulate the cells to migrate
    through interendothelial spaces towards the site
    of injury.
     Adhesion molecules PECAM-1 (platelet
    endothelial cell adhesion molecule) present in
    the intercellular junctions between endothelial
    cells are involved in the migration of leukocytes.
     Leukocytes pierce the basement membrane by
    secreting collagenases, and enter the
    extravascular tissue.
    3. Chemotaxis
     Locomotion oriented along a chemical gradient.
     Exogenous and endogenous substances act as
    chemoattractants.
     Exogenous agents are bacterial products,
     Endogenous chemoattractants
     (1) cytokines, (e.g., IL-8);
     (2) components of the complement system,
    particularly C5a
     (3) arachidonic acid (AA) metabolites, mainly
    leukotriene B4 (LTB4).
    Chemotaxis
     The leukocyte moves by extending
    filopodia that pull the back of the cell in the
    direction of extension.
    MULTISTEP PROCESS OF LEUCOCYTE
    MIGRATION
    4. Phagocytosis
     Three sequential steps :
    (1) Recognition and attachment of the
    particle to be ingested by the leukocyte
    (2) Engulfment
    (3) Killing or degradation of the ingested
    material.
    1. Recognition and attachment
     Receptors on phagocytic cells recognise
    components of of microbes
     Toll like receptors
     G protein coupled receptors
     Mannose receptors, scavenger receptors,
    and
     receptors for various opsonins all function
    to bind and ingest microbes.
    Opsonins
     Microbes are coated or opsonized by
    specific proteins (opsonins) for which the
    phagocytes express receptors.
    The major opsonins
     IgG antibodies
     C3b breakdown product of complement
     Certain plasma lectins.
    2. Engulfment.
     Extensions of the cytoplasm pseudopods flow
    around it
     Plasma membrane pinches off to form a vesicle
    phagosome that encloses the particle.
     The phagosome then fuses with a lysosomal
    granule, resulting in phagolysosome.
     During this process the phagocyte may also
    release granule contents into the extracellular
    space.
    Free Radical injury
     Unstable chemical compounds with single
    unpaired electrons in their outer orbit
     Usually rapidly destroyed
     Types f Free radicals
    ROS- O, H2o2,oh-
    NO,ONOO,NO3,NO3-
    Chemicals and drugs
    Free radical injury occurs in
     Phagocytosis
     Chemical carciogenesis
     Radiation injury
     REDOX reactions
     Cellular aging
    Pathologic effects of
    Free radicals
     Lipid peroxidation and membrane damage
     Modification of proteins causing abnormal
    enzyme activity or misfolding of proteins
     Damage to DNA and Mutations
     H2O2 is converted to OH- which is a
    powerful destructive agent
    Reactive oxygen species
     Azurophilic granules of neutrophils contain the
    enzyme myeloperoxidase (MPO), which, in the
    presence of a halide such as Cl-, converts H2O2
    to hypochlorite (OCl•).
     (OCl•) destroys microbes by halogenation or by
    oxidation of proteins and lipids
     The H2O2-MPO-halide system is the most
    efficient bactericidal system of neutrophils.
     H2O2 is also converted to hydroxyl radical
    (•OH), another powerful destructive agent.
    NO
     NO reacts with superoxide ( o- ) to
    generate the highly reactive free radical
    peroxynitrite (ONOO•).
     These oxygen- and nitrogen-derived free
    radicals attack and damage the lipids,
    proteins, and nucleic acids of microbes.
    Microbial killing by the action substances in
    leukocyte granules.

     Neutrophil granules contain many enzymes (elastase),


    defensins, cationic arginine-rich granule peptides,
     Cathelicidins, antimicrobial proteins found in neutrophils
    and other cells
     Lysozyme, found in the glycopeptide coat of all bacteria
     Lactoferrin, an iron-binding protein is cytotoxic to many
    parasites;
     Bactericidal/permeability increasing protein, important in
    defense against some gram-negative bacteria
    THANK YOU

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