Inflamation
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Transcript of Inflamation
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objectives Overview
Historical aspect
Acute inflammation
Mediators of inflammation
Morphologic Patterns of Inflammation
Outcomes of Acute Inflammation
Chronic inflammation
Systemic effects on inflammation
Consequence of Defective Inflammation
Implication of inflammation in medical practice
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INFLAMMATION
Protective Mechanism
Tissue damage
Necrotic tissue
Foreign Invader
Plasma protein
leukocyte phagocytes
Types
Acute
chronic
BU
T
adly
ncontrolled
riggered
Inflammatory Response
TISSUE INJURY
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In 3000 BC Egyptian Papyrus
Celsus (Roman Writer)- 1st century AD- listed four cardinal signs
Rubor (Redness)
Tumor (Swelling)
Color (Heat)
Dolor (Pain)
In 19th century Rudolf Virchow
Functio Laesa
More Prominent in ACUTE INFLAMMATION
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JULIUS COHNHEIM (1839- 1884) provided
one of the first microscopic descriptions of
inflammation.
The Russian biologist ELLIE METCHNIKOFF
discovered the process of PHAGOCYTOSIS by
observing the ingestion of rose thorns by
amebocytes of starfish larvae (1882) & of bacteria by mammalian leukocytes (1884).
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SIR THOMAS LEWIS : established the concept that chemical substances, locally induced by injury, mediate the vascular changes of inflammation.(1924)
The reaction so elicited is known as TRIPLE RESPONSE or REDLINE RESPONSE consisting of following:
Redline: appears within a few seconds following stroking & results from local vasodilation of capillaries & venules.
Flare: is the bright reddish appearance or flush surrounding the redline & results from vasodilation of adjacent arterioles.
Wheal: is the swelling or edema of the surrounding skin occurring due to transudation of fluid into the extravascular spaces.
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‘Inflammation is a localized protective response elicited by injury or destruction of tissues which serves to destroy , dilute or wall off both the injurious agent and injured tissue .’
Medical dictionary of pathology
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characteristic Rapid Host Response
Alterations in vascular calibre
Increase blood flow
Structural changes in microvasculature
Plasma protein & Leukocyte leave circulation
Emigration
Leukocyte
To accumulate in injurious foci
normal
inflamed
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• Bacterial, viral, fungal, parasitic
• ischemia, trauma, chemical injury• release uric acid, ATP, DNA-binding protein• Hypoxia – HIF-1α – VEGF – permeability –inflammation
hyper sensitivity reactionAuto-immune diseaseImmune mediated inflammatory disease
INFLAMATION
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Connective tissue cellsMast cells
Macrophages
Fibroblasts
Connective tissue matrix Elastic fibers
Collagen fibers
Proteoglycans
Vessels Soluble proteinsNeutrophils Complement Eosinophils CoagulationPlatelets Kinin system MonocytesLymphocytes
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Changes in vascular flow and caliber
Vasodialation
Induce by – histamine, NO
Increase blood flow– heat & redness
increase RBC concentration
Vascular congestion of small vessels – localized redness
Increased vascular permeability
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Hallmark of acute inflammation
Accomplished by the following steps Contraction of endothelial cells –
increase interendothelial space
Mediated by – histamine, bradykinin, substance-p
Endothelial injury – cell necrosis and detachment
Sometimes neutrophils that adhere to endotheliam – may injure endothelium – thus amplify the tissue reaction
Increased transport of fluid and protein – transcytosis
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•
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Lymph flow is increased
Drains edema fluid that accumulate at extra vascular space
Lymph channels proliferate to control the edema
Painfull enlargement of draining lymph node – LYMPHADENITIS
Secondarily infected lymphatics –LYMPHANGITIS
TELLTALE sign red streak near wound indicative of infection involvement of lymphatics
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Reaction of LEUKOCYTES in inflammation
Inflammation causes migration of
leukocytes from vessels to site of injury.
This recruitment accomplish by the
following steps
In the lumen – margination, rolling, adhesion
Migration across endothelium
Migration toward the site of injury by
chemotaxis
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Blood flow reduces at early stage of inflammation
Redistribution of leukocyte along the endothelium
Leukocyte – adhere – detach – bind = Rolling
Mediated by
Cytokines
TNF, IL-1, Chemokines
Selectin
L-selectin
E-selectin
P-selectin
Responsible for rolling
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Progressively rolling action slows down
Bind firmly with endothelium
Mediated by – Integrins
TNF & IL-1 induce expression of Integrins
Chemokine activate rolling leukocyte
Cytokine induced integrin binds with leukocyte to produce firm adhesion to the endothelium
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Leukocyte Migration through Endothelium
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Leukocyte moves by extending a pseudopod
Network of filaments in the interior of pseudopods
Locomotion involves rapid assembly of actin monomers into linear polymers at pseudopodledging edge
Cross-linking of filaments
Disassembling of filaments away from the ledging edge
These events are controlled by Calcium ions and Phosphoionositol on actinregulating proteins -filamin, calmodulin.
These components interact with actinand myosin in pseudopod to produce contraction
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Release of soluble mediators
Vasodilation
Increased blood flow
Extravasation of fluid (permeability)
Cellular influx (chemotaxis)
Elevated cellular metabolism
Heat (calor)
Redness (rubor)
Swelling (tumor)
Pain (dolor)
Physiological Symptoms Responses
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Mediators of inflammationMediators Principal sources Actions
CELL DERIVED
Histamine Mast cell, basophil, platelet
Vasodilation , increased vascular permiability, endothelial activation
Serotonin Platelets Vasodilation , increased permeability
Prosta glandin Mast cell, leukocyte Vasodilation, pain, fever
Leukotrienes Mast cell, leukocyte Chemotaxis, leukocyte adhesion & activation
Platelet- activating factor Leukocyte, mast cell Degranulation, Oxidative burst
Reactive Oxygen Species Leukocyte Microbicidal, Tissue damage
Nitric Oxide Endothelium, Macrophages
Vascular smooth muscle relaxation
Cytokine ( TNF, IL-1)Chemokines
Macrophage, mast cellleukocyte
Local endothelial activationChemotaxis, leukocyte activation
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Mediator Principal source Functions
PLASMA PROTEINDERIVED
Complement Products(C5a, C3a, C4a)
Plasma (produced in liver)Leukocyte chemotaxis and activation, vasodialation
Increased permeability, smooth muscle contraction
Endothelial activation, leukocyte recruitment
Kinins Plasma (produced in liver)
Protease activated during coagulation
Plasma (produced in liver)
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Platelet Activating Factor
Also synthesize other mediators like Eicosonoids by leukocytes and other cells
Causes Vasoconstriction and Bronchoconstriction
Regulated by Acetyl hydrolases
PAF mediates its effects via single G-protein coupled receptor
Bioactive phospholipid derived mediator
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Coagulation & Kininsystems
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Complement system
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Systemic effects of acute inflammation
Fever
Leucocytosis (15-20,000)Bacterial infection- NeutrophiliaViral infection -LymphocytosisParasitic infection- Eosinophilia
Hypotension
Increased ESR and C-reactive protein
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Classification of Inflammation
BASED ON EXUDATE Suppurative (purulent) inflammation Serousinflammation Catarrhal inflammation (inflammation of mucous membranes) Fibrinous inflammation: fibrinogen -fibrin Pseudomembranous inflammation: surface necrosis
Necrotizing inflammation
Hemorrhagic inflammation
Ulcerative inflammation
BASED ON HISTOLOGICAL FEATURE
BASED ON CAUSATIVE AGENT
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Based on EXUDATE
Suppurative (purulent) inflammation: pus
Localized proliferation of pus-forming organisms, such as Staphylococcus aureus(e.g., skin abscess).
S. aureus contains coagulase. which cleaves fibrinogen into fibrin and traps bacteria and neutrophils
Pyogenic bacteria, eg, staphylococci, streptococci, gram–negative bacilli, anaerobes.
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Serous inflammation: (effusion)
Thin, watery exudate
Insufficient amount of fibrinogen to produce fibrin
Example -blister in second-degree burns, viral pleuritis
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EXUDATE TRANSUDATE
Caused by inflammation
High protein content
Specific gravity high
Generally associated with infection
caused by disturbances
of hydrostatic or colloid osmotic pressure
Less protein content
Specific gravity less
Generally associated with thermal or chemical injury
Rivalta’s test:: is a very simple, inexpensive method that does not require special laboratory equipment and can be easily performed in private practice. This test was originally developed by the Italian researcher Rivalta around 1900 and was used to differentiate transudates and exudates in human patients.
A test tube is filled with distilled water and acetic acid is added. To this mixture one drop of the effusion to be tested is added. If the drop dissipates, the test is negative, indicating a transudate. If the drop precipitates, the test is positive, indicating an exudate
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Catarrhal inflammation (inflammation of mucous membranes)
Marked secretion of mucus.
Infections, eg, common cold (rhinovirus); allergy (e.g. hay fever)
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Fibrinous inflammation: fibrinogen -fibrin Due to increased vessel permeability. with deposition of
a fibrin-rich exudate Often occurs on the serosal lining o f the pericardium,
peritoneum, or pleura
Danger of adhesions
Example: fibrinous pericarditis
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Pseudomembranous inflammation:
surface necrosis Bacterial toxins damage mucosal lining, producing a
membrane composed of necrotic tissue
Example ― pseudomembranes associated with Corynebacteriumdiphtheriaeproduces a toxin causing pseudomembrane formation in the pharynx
and trachea.
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Necrotizing inflammation:
Marked tissue necrosis
Highly virulent organisms (bacterial, viral, fungal)
Eg, plague (Yersinia pestis), anthrax (Bacillus anthracis),
mucormycosis, maxillofacial gangrene (noma).
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Hemorrhagic inflammation:
Destruction of blood vessel walls resulting in leakage of a
large number of red blood cells resulting in the red
coloration of inflammatory exudate.
Example ― Epidemic hemorrhagic fever, Leptospirosis and
Plague
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Ulcerative inflammation:
Necrosis on or near the surface leads to loss of tissue and
creation of a local defect (ulcer)
Example ― Ulcerative gingivitis
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Nonspecific:
Produce non-specific histologic picture
Specific:
Produce a specific histologic picture that is peculiar to that type of infection e.g. TB.
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Aseptic(sterile)
chemical substances, radiation
Septic
(caused by living organisms)
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Is the persistence of inflammation with attempts
of repair resulting from persistence of theinjurious agent.
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Persisting infection or prolonged exposure to irritants (intracellular surviving of agents -TB)
Repeated acute inflammations (otitis, rhinitis)
Primary chronic inflammation -low virulence, sterile inflammations (silicosis)
Autoimmune reactions (rheumatoid arthritis, glomerulonephritis, multiple sclerosis)
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Mechanism...... Defective acute inflammatory response
Poor blood supply Poor general nutrition Abnormal neutrophil function Anti-inflammatory drugs, especially corticosteroids
Agent is resistant to phagocytosis and/or intracellular destruction Intracellular infectious agents, e.g. tuberculosis, salmonellosis, brucellosis, viral
infections
Foreign-body reactions
The provoking agent is a body constituent as in: Auto-immune diseases, e.g. diffuse lymphocytic thyroiditis (Hashimoto’s
disease), auto-immune atrophic gastritis, adrenal atrophy, etc.
Reactions to altered self-antigens, e.g. contact dermatitis to rubber, nickel, etc
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Continuing some features of acute inflammation Polymorph infiltration
Fibrinous exudation
Increased vascularity
Features of healing-repair and/or regeneration
Infiltration by chronic inflammatory cells Lymphocytes
Plasma cells
Macrophages
Eosinophils
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Granulomatous inflammation
A distinct pattern of chronic inflammation characterized by formation of granulation tissue.
It is a protective response to chronic infection or foreign material, preventing dissemination and restricting inflammation.
Some autoimmune diseases such as rheumatoid arthritis and Crohn’s disease are also associated with granulomas
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? Granuloma.......
A granuloma is a localized mass of granulation tissue with aggregationsof chronic inflammatory cells
The granuloma consists of a kernel of infected macrophagessurrounded by foamy macrophages and a ring of lymphocytes and afibrous cuff.
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Causes of granuloma...... Bacteria:
Tuberculosis, Leprosy, Syphilis, Actinomycosis
Parasites: Schistosomiasis
Fungi: Histoplasmosis, Blastomycosis
Foreign bodyGranulomas Endogenous
keratin, necrotic bone or adipose tissue uric acid crystals
Exogenous wood, silica, asbestos, silicone
Unknown cause such as sarcoidosis
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Ascitis / Hydroperitonium Accumulation of fluid in peritoneal cavity Classification
G-I – mild G-II – detectable with flank bulging & shifting dullness G-III – directly vbissible
Cause Transudative
Cirrhosis Heart failure kwashiokor
Exudative Cancer ( primary / Metastatic) Tuberculosis Pancreatitis serositis
Treatment Pharmacological
Diuretics – aldosteron / spironolactone / furosemide
Non-pharmacological Fluid tapping
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Inflammation of pleural layer Inflamed layer rub together to
cause pain Symptom
Dry cough, fever, shortness of breath, rapid pulse
Collection of fluid in pleural space
Cause Auto-immune disease – SLE/ RA Pneumonia, Tuberculosis Pulmonary Embolism
Management Putting Chest Drain
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Inflammatory reaction is greater in diabetic status
Conversely local inflammation causes intensification of diabetes
According to Russel in 1966 Cellular dehydration
Loss of alkali reserve
Vessels lumen get obliterated
Thickening of capillaries - Role in inflammation acts as a barrier to leukocytic emigration into site (Brayton et al 1970)
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Role of surgical drain After surgery, have to put one or two drains, called a Jackson-Pratt
(JP) drain, placed near the incision.
This device collects fluid, under suction, from your surgical area.
The drain promotes healing and recovery, and reduces the chance of infection.
The drain will be in place until the drainage slows enough for your body to reabsorb fluid on its own.
The tube may be removed once a single tube output is less than 30cc (1 oz.) in 24 hours.
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NSAIDs: Drug Effects Analgesic (mild to moderate)
Anti-gout
Anti-inflammatory
Antipyretic
Relief of vascular headaches
Platelet inhibition (ASA)
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Role in inflammation
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NSAIDs Adverse Effects Platelet Dysfunction
Gastritis and peptic ulceration with bleeding (inhibition of PG + other effects)
Acute Renal Failure in susceptible
Sodium+ water retention and edema
Analgesic nephropathy
Prolongation of gestation and inhibition of labor.
Hypersenstivity (not immunologic but due to PG inhibition)
GIT bleeding and perforation
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Role of seratiopeptidase Serratiopeptidase is an enzyme isolated from a non-pathogenic bacteria called
enterobacteria Serratia E15
Serratiopeptidase has powerful anti-inflammatory properties and is particularly useful for post-traumatic swelling, fibrocystic breast disease and bronchitis. It is able to digest dead tissue, blood clots, cysts, and arterial plaques. Clinical studies have shown it to be effective at reducing swelling and edema and metabolizing scar tissue in the body.
A 2003 study found that 30mg of serratiopeptidase was effective at loosening and reducing mucous build-up in respiratory pathways. This was credited to its ability to reduce the neutrophil white blood cell numbers and to improve the viscoelasticity of the sputum in patients with chronic airway disease.
A 2006 study looked at the role serratiopeptidase has on improving immunity
studies have shown similar anti-inflammatory effects after oral surgery was performed
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Trypsin –chymotrypsin --- proteolytic enzyme
When an injury occurs, the body responds with an inflammatory cascade. Excessive inflammation can retard the healing process.
Proteolytic enzyme supplementation reduces inflammation by neutralizing bradykinins and pro-inflammatory eicosanoids to levels where the synthesis, repair and regeneration of injured tissues can begin.
Proteolytic enzymes do not completely inhibit all phases of the inflammatory cascade to a point where the body is unable to trigger the normal healing process.
Low-dose chymotrypsin treatment inhibits neutrophil migration into sites of inflammation in vivo: Effects on Mac-1 and MEL-14 adhesion protein expression and function
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Chemical Make-Up Hydrocortisone or cortisol is the primary agent
Glucocorticoid, which is naturally secreted by body is derivative
Currently, many AI steroids are available more powerful than cortisol, but have the same chemical structure as glucocorticoid
Long term use will inhibit body’s glucocorticoid activity and the body’s ability to produce this substance naturally
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How it Works
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Time Action Profile
Drug Onset Peak Duration Half Life
Cortisone PO rapid 2 hrs 1.25-1.5
dys
8-12 hrs
Cortisone IM slow 20-48
hrs
1.25-1.5
dys
Prednisolone
PO
UK 1-2 hrs 1.25-1.5
dys
18-36
hrs
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Adverse effect of corticosteroids Receive long-term, high-dose steroid
Hypertension, heart failure
Osteoporosis, DM, impaired wound healing, metal depression and psychosis
Peptic ulcer, Cataract, glaucoma, growth suppression, hypocalcemia, PTH increased
Cushing syndrome
Secondary adrenal insufficiency
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interferon-γ (IFN-γ) constitutes a positive factor triggering or promoting the inflammatory response
Systemic interferons, fulfil a down-regulating role, as evidenced by the observation that
exogenously administered IFN-α, -β, and -γ inhibit local inflammation.
type I interferons (IFNs), IFN-α and IFN-β, are cytokines that have antiviral, antiproliferative, and
immunomodulatory activities
Type I IFNs, through their ability to induce the immunosuppressive cytokine interleukin-10 (IL-10),
mediate the inhibition of pro-inflammatory gene products.
In addition, type I IFNs induce other immunosuppressive mediators such as suppressor of cytokine
signaling–1 (SOCS-1) and tristetrapolin (TTP), which act by divergent mechanisms to restore
homeostasis to the immune system.
Furthermore, type I IFNs mediate anti-inflammatory and protective effects in a variety of autoimmune
disease
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Dimethyl Sulfoxide (DMSO)Drug of question - used with
animals and to clean floors
Highly effective in the reduction of edema
Clinical trials inconclusive or were stopped (changes in eyes)
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DMSO FDA approved 50% solution for TX of cystitis
Canada approved 70% solution for TX of Scleroderma
Vets approved 90% solution for TX of edema
Public gets 99% industrial solution approved for degreasing
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conclusion Humans owe to inflammation & repair their ability to
contain injuries & heal defects. Without inflammation, infections would go unnoticed, would never heal, & injured organs might remain permanent festering sores. However inflammation & repair may be potentially harmful
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refferences Basics of Pathology, Robins & Cotrans
Pharmacological basis of theraputic, Goodman-Gillman
Essentials of medical pharmacology, KD Tripathi
Oxford hand book of clinical medicine, 8th edition
Reducing Inflammation with Proteolytic Enzymes, Part One: Absorption and Sources ;By G. Douglas Andersen, DC, DACBSP, CCN
Dynamic Chiropractic – July 12, 1999, Vol. 17, Issue 15 Reducing Inflammation with Proteolytic Enzymes, Part One: Absorption and Sources;By G. Douglas Andersen, DC, DACBSP, CCN
Cellular Immunology, vol.132 issue 1, jan.1991
http://www.naturalnews.com/033498_SerratioPeptidase_inflammation.html
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