NON-SPECIFIC HOST DEFENSE MECHANISMS

THESE ARE GENERAL MECHANISMS (CELLULAR FUNCTIONS AND BIOCHEMICAL PATHWAYS) WHICH BECOME ENGAGED AFTER ANY KIND OF INJURY AND PROTECT AGAINST ALL PATHOGENS IN GENERAL.

NON-SPECIFIC HOST DEFENSE MECHANISMS ARE DISTINCT FROM SPECIFIC HOST DEFENSE MECHANISMS, WHICH RELY UPON THE SPECIFIC RECOGNITION OF THE PATHOGEN BY LYMPHOCYTES. SPECIFIC IMMUNITY IS BASED UPON THE ANTIBODIES MADE BY B-CELLS AND UPON THE ACTIVITIES AND CYTOKINE SECRETIONS OF T-CELLS. B-CELLS AND T-CELLS HAVE RECEPTORS WHICH RECOGNIZE MOLECULES ON THE INVADING ORGANISMS. EACH B-CELL AND T-CELL HAS A UNIQUE RECEPTOR. THERE ARE MILLIONS OF SPECIFICITIES.

CELLS OF THE BLOOD - see pg. 410 Tortora

ERYTHROCYTES - RBC'S

LEUKCOCYTES - WBC'S - HANG OUT IN THE BLOOD AND LYMPH - see pg. 411, fig. 16.6 for description of LYMPHATIC SYSTEM

GRANULOCYTES -

NEUTROPHILS - (POLYMORPHONUCLEAR LEUKOCYTES, POLYS, PMN'S) THESE ARE ACTIVELY PHAGOCYTIC CELLS

BASOPHILES - (MAST CELLS) - ALLERGIES AND INFLAMMATION

EOSINOPHILES - ALLERGIES, ANTI-HELMINTH

MONOCYTES / MACROPHAGES - THESE ARE PHAGOCYTIC CELLS. VERY IMPORTANT IN ANTIGEN PRESENTATION. THESE CELLS HAVE DIFFERENT ACTIVATION STATES - ANGRY MACROPHAGES. MACROPHAGES IN DIFFERENT TISSUE COMPARTMENTS ARE GIVEN DIFFERENT NAMES: KUPFFER CELLS, MICROGLIAL CELLS, ALVEOLAR MACROPHAGES, SPLENIC MACROPHAGES, LANGERHANS CELLS

LYMPHOCYTES

T-CELLS -- THYMUS DERIVED; CD4+ = T-HELPER AND T-DELAYED HYPERSENSITIVITY; CD8+ = T-CYTOTOXIC AND T-SUPPRESSOR. T- CELLS HAVE T CELL RECEPTORS ON THEM

B-CELLS -- BONE MARROW DERIVED (BURSA DERIVED); THESE CELLS MAKE ANTIBODIES. IF THE CELL IS ACTIVELY MAKING AND SECRETING ANTIBODIES IT IS CALLED A PLASMA CELL. ANTIBODY ALSO SERVES AS A RECEPTOR ON THE SURFACE OF B-CELLS.

NK-CELLS -- NATURAL KILLER CELLS

THROMBOCYTES / PLATELETS ARE DERIVED FROM MEGAKARYOCYTES IN THE BONE MARROW. ACTIVE IN BLOOD CLOT FORMATION. ALSO CONTAIN MANY MEDIATORS OF INFLAMMATION.

TYPES OF NON-SPECIFIC MECHANISMS:

A.) MECHANICAL AAND PHYSICAL BARRIERS - READ ABOUT THE MUCOUS MEMBRANES, LACRIMAL APPARATUS AND TEARS, SALIVA, CILIARY ESCALATORS, URINE FLOW.

B.) CHEMICAL BARRIERS - READ ABOUT THE CHEMICAL BARRIERS ASSOCIATED WITH THE SKIN ( SEBUM, SWEAT ) AND THE MUCOUS MEMBRANES ( LYSOZYME) AND THE STOMACH ( ACIDITY OF THE GASTRIC JUICE )

C.) COMPLEX BIOLGICAL MECHANISMS AND REPONSES

(1.) PHAGOCYTOSIS AND PHAGOCYTIC CELLS -LOOK AT PICTURES ON Page 412 - 413 of Tortora

CHEMOTAXIS

ADHERENCE - (INCLUDING OPSONIZATION WITH ANTIBODY OR COMPLEMENT

INGESTION AND THE FORMATION OF THE PHAGOLYSOSOME

KILLING AND DIGESTION

ANTIGEN PRESENTATION - PIECES OF THE DIGESTED MATERIAL IS DISPLAYED ON THE SURFACE OF THE ANTIGEN PRESENTING CELL (APC). THE PIECES ARE STUCK ON TOP OF THE TRANSPLANTATION PROTEINS (MAJOR HISTOCOMPATIBILITY COMPLEX PROTEINS (MHC PROTEINS OR MHC ANTIGENS)). T-CELLS HAVE TO HAVE FOREIGN ANTIGENS PRESENTED IN THIS MANNER.

(2.) INFLAMMATION - see Tortora pages 414 - 416

A COMPLEX REACTION TRIGGERED BY ANY DAMAGE TO THE BODY. CAN BE PROVOKED BY INFECTIOUS AGENTS, PHYSICAL AGENTS, AND BY CERTAIN IMMUNE PATHWAYS.

SYMPTOMS INCLUDE: PAIN, REDNESS, SWELLING, HEAT AND LOSS OF FUNCTION.

PURPOSE IS TO DESTROY THE INVADER, LIMIT DAMAGE AND REPAIR THE DAMAGE.

THERE ARE A NUMBER OF BIOCHEMICAL MEDIATORS INCLUDING HISTAMINE, PROSTAGLANDINS, LEUKOTRIENES, COMPLEMENT AND KININ.

THESE PROMOTE VASODILATION AND INCREASED VASCULAR PERMEABILITY AS WELL AS PHAGOCYTE AND LYMPHOCYTE CHEMOTAXIS AND ACTIVATION.

EVENTUALLY CYTOKINES AND HORMONES STIMULATE TISSUE REGENERATION.

(3.) FEVER

ACTIVATED MACROPHAGES RELEASE INTERLEUKIN-1 (IL-1). THIS CYTOKINE RESETS THE HYPOTHALAMUS THERMOSTAT AND THE BODY TEMPERATURE INCREASES. HIGHER TEMPERATURE MAY INCREASE THE METABOLIC RATE OF WHITE CELLS AS WELL AS SLOW DOWN THE GROWTH OF SOME PATHOGENS. FEVER STIMULATES THE RELEASE OF TRANSFERIN AN IRON BINDING PROTEIN.

(4.) COMPLEMENT ACTIVATION - See pages 416 - 419 Tortora

ACTIVATED COMPLEMENT a.) DESTROYS CELLS, b.) STIMULATES INFLAMMATION, c.) STIMULATES CHEMOTAXIS AND PHAGOCYTOSIS.

COMPLEMENT IS ACTIVATED BY TWO DIFFERENT CASCADES:

THE CLASSICAL PATHWAY AND THE ALTERNATIVE PATHWAY

BOTH PATHWAYS ACTIVATE C3 TO FORM C3a (INFLAMMATORY MEDIATOR) AND C3b (OPSONIN AND ENZYME WHICH THEN ACTIVATES C5) - See the book on this.

C5 IS BROKEN DOWN BY C3b TO FORM C5a (INFLAMMATORY MEDIATOR AND LEUKOCYTE ATTRACTOR) AND C5b (ACTIVATES C6, C7, C8 AND C9 TO FORM THE MEMBRANE ATTACK COMPLEX WHICH FORMS THE TRANSMEMBRANE CHANNEL IN THE TARGET CELL AND LEADS TO CYTOLYSIS). THIS IS COMPLEMENT FIXATION.

(5.) INTERFERON