Cells involved in acute inflammation:

Leukocytes: -POLYMORPHONUCLEAR CELLS: neutrophils, eosinophils & basophils (BEN) -MONONUCLEAR CELLS: mast cells, monocytes (macrophages), & lymphocytes & plasma cells (MMLP) -OTHERS: platelets, endothelial cells and fibroblasts 1. POLYMORPHONUCLEAR CELLS: 1. 1. NEUTROPHILS:

-1st line of defense bacteriocidal -Produced: bone marrow mature for 2 weeks; released; stay in circulation for < 24h (irreversible migration into tissue); apoptosis after 1-2 days. -2 functional pools: -Marginated - apposed to blood vessel walls -Circulating - free in blood -Balance between pools altered by inflammation (> margination) & anti-inflammatory drugs (eg. corticosteroids inhibit margination) -Functions: -Part of innate immunity (dont need prior exposure to act) -Participate in: -phagocytosis -release of lytic enzymes & chemotaxins into ECM -have cytoplasmic granules containing enzymes (proteinases), antibacterial substances (myeloperoxidases) & receptors (for complement & adhesins) -granules fuse with phagocytosed particles = phagolysosomes 1. 2. EOSINOPHILS

-Allergic, parasitic & fungal inflammatory reactions -Produced: bone marrow; differentiation & maturation dependent on IL-3, IL-5 & GM-CSF -Found in environmental contact tissues eg. intestine, skin, lung & mucous membranes -Corticosteroids reduce numbers

-Functions: -Helminthocidal -Precipitation & assistance in hypersensitivity reactions (esp. Type 1) -Phagocytic activity (neutrophils & macrophages better) -Granules main components (anti-parasitic) = major basic protein (MBP) & eosinophil cationic protein (ECP) -Adhere to parasites & degranulate -MBP = mast cell histamine degranulation & neutralizes heparin -ECP = reacts & causes damage to neg. charged helminthes -Eosinophils attracted to areas of mast cell degranulation (mast-cell derived histamine stimulates fibroblasts & epithelial tissues to release eotaxin) helps regulate & neutralize mast cell released mediators 1.3. MAST CELLS & BASOPHILS

-Functionally closely related -Involved in inflammatory (induction of vascular permeability) & immunological (esp, allergic) reactions -Mast cells produced: bone marrow; released as undifferentiated cells; migrate to tissues (esp. perivascular areas of almost all tissues esp. in environmental contact areas); proliferation & differentiation occurs here -Basophils produced: bone marrow but remain in circulation -Functions: -Receptors for Fc portion of IgE -Re-exposure of antigen = degranulation of these cells & contents (heparin, histamine, proteinases & cytokines (interleukins, TNF-alpha, IFN- gamma)) -Principal sources for histamine (histamine = initiator for vascular permeability & smooth muscle contraction during acute inflammation) -Degranulation not ass. with cell death 1.4. MACROPHAGES

-Master minds -Phagocytic & bacteriocidal activity -Regulation of inflammatory reactions soon after arrival of neutrophils -Most derived from circulating monocytes (orig. bone marrow) -Monocytes activated & migrate to tissues become macrophages -Capable of cell division & may specialize

-Functions: -Antimicrobial & phagocytic -Recruitment of other leukocytes to tissue -Modulate/ regulate cellular activities in tissue -Removal of tissue debris -Induce systemic effects (acute phase reaction = systemic signs of fever, malaise etc.) -Formation of multinucleate giant cells reaction to indigestible/ poorly degradable foreign bodies, fungal infections & mycobacteria -Epithelioid macrophages (larger, angular with ovoid nucleus) formed in reaction to hard-to kill organisms -Dep. tissue type store inorganic non-antigenic substances eg. iron, silicates & carbon 1.5. LYMPHOCYTES & PLASMA CELLS

-Involved in immune reactions -Derived: primary organs eg. bone marrow & thymus, & migrate to secondary organs eg. spleen & lymph nodes -Lymphocytes leave the circulation at the site of inflammation (like neutrophils); recirculate to & from normal tissue through specialized endothelia (unlike neutrophils) -Functions: -Prominent in chronic phase of inflammation -However, certain antigens provoke an early lymphocyte reaction eg. Mycoplasma, Leptospira & viral infections. -B-lymphocytes antibody production -Antibodies serve as opsonins & interact with cellular phagocytic defense during inflammation. -T-lymphocytes (T-helper-1) source of lymphokines (IL-2, TNF-alpha & IFN-gamma) regulate inflammatory reaction. 1.6. PLATELETS

-Vascular damage platelets adhere to exposed subendothelial collagen that express von Willebrands factor (vWF) -Release various factors cause continuation & coagulation (expression of integrin adhesion receptors for binding fibrinogen & more platelets), recruitment of neutrophils (P-selectin receptor expression on platelet surface), healing (fibroblast growth factor) & inflammation (histamine).

1.7.

ENDOTHELIAL CELLS & FIBROBLASTS

-Leukocyte-endothelial interaction vital for leukocyte migration during inflammation -Involved during healing due to proliferative potential -Fibroblasts release critical inflammatory cytokines & produce most ECM proteins that are vital for leukocyte locomotion and activation.