INFLAMMATION BY-ASHA NAYAK Class –M.sc . 4‘ Sem.(zoology) Year-2020
Contents Introduction cause of inflammation Lymphocytes Recirculation Cell adhesion molecules Neutrophill extravasations Lymphocytes extravasations Chemokines -key mediators of inflammation Other mediators of inflammation The inflammatory process Chronic inflammatory disease Anti-inflammatory agent's Conclusion References
Introduction . inflammation is defined as the local response of living tissues to injury due to any agent. .Body defense reaction - eliminate or limit the spread of injurious agents. This complex response is characterized by- Swelling (tumor) Redness( rubor ) Heat( calor ) Pain(dolor) by A.C.celcias Functionaries ( loss of function)by R.virchaw
Cause of inflammation 1.Infective agents like bacteria, viruses and their toxins , fungi, parasites . 2.Immunological agents like cell- mediated and antigen antibody reactions 3 physical agents li ke heat ,cold, radiation, mechanical trauma. 4.chemical agents like organic and inorganic poisons. 5 Inert materials S u ch as foreign bodies
Lymphocyte Recirculation Lymphocytes continully moving through the blood and lymph to the various lymphoid organs. Lymphocytes (45%)carried from blood (30min)directly to spleen(5hr.). 42% of lymphocytes exit from blood into various peripheral lymph nodes (12hr). 10% of lymphocytes migrate to tertiary extra lymphoid tissue by crossing between endothelial cells . Import them during inflammatory response. Only about one in 10 ⁵ lymphocytes recognize a particular antigen.
Cell-Adhesion Molecules Vascular endothelium serve as" gate-keeper". The cell must adhere and pass between the endothelial cells lining the wall of blood vessels ( extravasation ). It express leukocyte specific cell adhasion molecules( CAMs ). Recirculating lymphocytes, granulocytes and monocytes bear receptors to CAMs on v.e. CAMs have for family:- selectins , mucins, integrins ,ICAMS
Neutrophil Extravasation Various cytokinesis and inflammatory mediators act on local blood vessels. For steps of extravasation:- *Rolling mediated by selecting *Activation by chemoattractant stimulus *Arrest and adhasion mediated by integrins binding to lg- family * Transendothelial migration
Lymphocytes extravasation Similar to neutrophil extravasation and has same four stages - contact and rolling , activation, arrest and adhasion and finally transendothelial migration High endothelial venules are sites of lymphocytes extravasation Some region(exception spleen )of v.e.is composed by specialize d plump, cuboidal shape cells this rigion called HEVs 85% of bound cell found adhering to HEVs this account for only1-2%of total frozen section Many as1.4×10⁴ lymphocytes extravasate every sec . through HEVs into single lymph node.
* Neutrophil homing is directed by receptor profiles and signals * Naive lymphocytes recirculate to secondary lymphoid tissue * Effector and memory lymphocytes adopt different trafficking patterns * Adhasion -molecule interaction play critical roles in extravasation
Chemokines - key mediator of inflammation A superfamily of small polypeptides (90-130aa residue). Major regulator of leukocyte traffic( adhasion , chemotaxis , activation). Involve in inflammation, homeostatic /developmental processes "housekeeping". Induced in response to infection - assembly of leukocyte at site of infection >50 chemokines , possess 4 conserved cysteine residues (c-c subgroup ,c-x-c subgroup) >15 chemokines receptors (cc receptors,c -x-c receptors is of high affinity ( Ka>10⁹) and High specificity .
Other mediators of inflammation The kinin system is activated by tissue injury The clotting system yields fibrin -generated mediators of inflammation The fibrinolytic system holds plasmin generated mediators of inflammation The complement system produces anaphylatoxins Some lipids act as inflammatory mediators Some cytokines are important inflammatory mediators
The inflammatory process Neutrophils play an early and important role in inflammation localised inflammatory response:- it begins when tissue and endothelial damage age induces formation of plasma enzyme mediators that lead to vasodilation and increased vascular permeability Systemic acute - phase response:- Roles of IFN-gama,and TNF-alpha in chronic inflammation
Chronic inflammatory disease A chronic inflammatory response may accompany:- allergies Autoimmune disease microbial infections transplant and burns. Drug - based therapies employing corticosteroids and a variety of nonsteroidal anti-inflammatory drugs (NSAIDs) are the most commonly used medications for pain and inflammation .
Anti-inflammatory agents Antibody therapies reduce leukocyte extravasation - to block the activity of various adhasion molecules (anti-ICAM-1+anti-LFA-1) Corticosteroids are powerful anti-inflammatory drugs NSAIDs Combat Pain and Inflammation