Innate and Acquired Immunity: A Comprehensive Overview

Innate (Natural) Resistance – Born With

                                                                                                                                                                                 Abnormalities of inflammation – “not enough” inflammation – defect in phagocytic functions (quantitative defect –

1st line – body’s physical barriers (immediate + nonspecific)                                                                                                                                                     leukopenia – deficiency in WBCs; neutropenia), qualitative defects (chemotactic defects – won’t respond normally,

Skin/glands – desquamation of skin – shedding of skin/bacteria; Stressors that can breach – lacerations, abrasions, punctures, etc                                        impaired functions – disease causes decreased ability to fight microbes), complement deficiencies (disorders 

Glands secrete sweat – attack cell walls of certain bacteria; makes skin acidic (pH 3-5) = inhospitable to most bacteria                                                          caused from a genetic defect, antibody deficiencies – extra susceptible to infections); “too much” inflammation – 

Membranes/glands of body openings – Eyes’ defense – tears, eyelashes, stressors that can breach (dry eye syndrome,                                                         goes into overdrive/chronic, examples – SIRS, sepsis septic shock (low BP) and chronic inflammation disorders;

Sjogren’s syndrome (autoimmune; dries up lubricating fluids); Respiratory system defenses – mucus + hair =  traps bacteria,                                              SIRS (systemic inflammatory response syndrome) – widespread inflammation in the entire body (not just local),

cilia, cough reflex, stressors that can breach (cigarette smoking, cough reflex suppression (head injury/stroke) ; GI system defenses –                                 causes impaired tissue function and organ damage, presents when 2+ S&S happens (unexplained change in

saliva contains protective enzymes, stomach (HCl destroys microbes), gag reflex (vomiting), bowels (defecation), stressors that can breach                       mental status, fever – > 100.4 F, increased HR and RR, abnormal WBC count); Sepsis – SIRS + infection; Septic 

(Sjogren’s, any changes to bowel flora); GU system defenses – flow of urine washes away microbes, vaginal secretions slightly acidic, stressors                 shock – sepsis (SIRS + infection) + low BP, extreme vasodilation = no arterial vessel “tone” – too relaxed – blood

(decreased urine flow – kidney stones/failure, changes in vaginal acidity – douching)                                                                                                             pools in periphery instead of normal – low BP volume reduces amount of O2 and decreases BP, S&S (SIRS S&S,

2nd line – inflammation (immediate + nonspecific)  NORMAL TEMP = 98.6 F                                                                                                                         low BP – ischemia to organs that can lead to renal/respiratory/heart failure or death); chronic inflammation 

Process of normal inflammation (vasodilation + increased capillary permeability) – swelling, heat, erythema (redness), and pain (SHEP);                            Therapeutics for inflammation – protected ice (cold numbs pain, vasoconstricts the blood vessels); Anti

defend against stressors, begin the healing process, acute + short-lived (2 weeks); Purpose of response – “clean up” area – begin clotting                        inflammatory meds (suppress the effects of prostaglandins – ex. steroids, NSAIDs), Prostaglandins (PGs) are 

process – healing; Steps – irritation/injury (stimulates “leakiness”), loss of cell membrane integrity and leakage of fluid, mast cell degranulation                 mediators (either protective or proinflammatory – stimulate further inflammation by increasing vascular

(local inflammatory mediators released – histamine, leukotrienes, prostaglandins (HLP)), HLP leads to vasodilation of capillaries (“leaked” plasma –            permeability + induce fever and pain), side effects (suppress protective prostaglandin effect + proinflam – 

neutrophils, clotting factors, fibrin; acute phase reactants – CRP, complement, circulating prostaglandins; S&S – capillary swelling/leakage – SHEP – pain);         ideal = specific + suppress proinflammatory only) 

Neutrophils and macrophages phagocytize the area – exudate (thick fluid) = serous (little microbes – clear gold) or serosanguinous (blood present) or 

purulent (pus – more microbes + WBC – whitish/yellowish); secrete chemotactic substances (biochemical mediators), T cell/CD4 lymphocytes. display 

remnants on cell membranes, clotting factors, platelets, and fibrin create healing, granulating tissue, local (lacerations/abrasions to skin);

Normal systemic inflammatory response – nonspecific (local turns into possible systemic), leukocytosis + more acute phase reactants (causes fever), S&S – fever 

(dilate blood vessels – too much vasodilation = low BP); lab tests – CBC = increased WBCs (leukocytes – mostly neutrophils – leukocytosis + neutrophilia)

Acquired (adaptive) immunity – 3rd line of defense 

Resist certain diseases bc of immunocytes (lymphocytes – B/T cells) involvement 

Delayed and specific