ct proper components

8/6/2019 Ct Proper Components

http://slidepdf.com/reader/full/ct-proper-components 1/55

Department of Natural SciencesUniversity of St. La Salle



� They have fewer cells that are set apart due to anabundance of intercellular substance or ground

substance which contains fibers.

� The different contents of intercellular substance,

CT cells and fibers account for the difference inappearance of the various CT.

� Except in a few CT types (mucous and cartilage),

there are blood vessels, lymphatics and nerves

found in the ground substance.

� The physical properties of CT allow it to bind, fillspaces, and to separate functional units of other

tissues and organs, allowing maintenance and

coordination of all body functions.

GENERAL CHARACTERISTICS



All CT celltypes are

derived from

cells of

embryonic

mesenchyme

originating

from theembryonic

mesoderm.



In any type of CT, there are 3 basic elements

to consider.

CT types and subtypes are classified

according to the amount, types, and

proportions of these 3 components:

1.Ground substance- forms the extracellularmatrix together with tissue fluid (bound

water of solvation) and protein fibers; maybe

fluid, gelatinous or solid

2.Fibers- maybe white or collagenous, yellowor elastic, reticular or argyrophyl

3.CT cells- of several types, mobile wandering

or relatively fixed elements



� This abundant intercellular substance vary in

consistency from a thin fluid to a hard,

calcareous substance.

� The formed elements of CT are embedded in

this matrix of amorphous, colorless,

transparent material with the properties of a

viscous solution or thin gel.

� It is the medium through which all nutrients

and waste products must pass in transit between the blood and parenchymal cells of

the organs.

� It consists mostly of tissue fluids, salts and 2

classes of glycoconjugates:

GROUND SUBSTANCE



1.PROTEOGLYCANS-

composed of a core protein

to which glycosamino-

glycans (GAGs) are

attached. GAGs are straight-

chain polymers of repeating

sugar heterodimers made up

of hexosamine and uronic

acid.

2.Five major classes of GAGs exist in CT: hyaluronic acid

(does not form proteoglycans, and determines the

structural and physiological characteristics of ground

substance), chondroitin sulfate, dermatan sulfate, keratan

sulfate, and heparan sulfate.

� Lysosomal enzyme deficiencies for degradation of GAGs

lead to their accumulation, resulting to several human

disorders e.g., Hurler syndrome, Hunter syndrome,

Morquio syndrome



ECM of mouse endometrium after

fixation in the presence of Safranin O. A network of

proteoglycans fills the intercellularspaces. Some proteoglycan

filaments are in close contact withthe cell surface (arrows).

Schematic diagram of cell-surface

proteoglycan. The core proteinspans the plasma membrane

through the cytoplasmic domain.The proteoglycans possess 3

heparan sulfate chains andsometimes chondroitin sulfate.



2.GLYCOPROTEINS- globular proteins to which

shorter, branched oligosaccharide chains are

covalently bound.� These so-called adhesion

glycoproteins mediate

attachment of cells to their

matrix, influence the state

of differentiation of cells,

and organization of their

cytoskeleton.

� Examples: Fibronectin- long flexible molecule with

cell-binding, collagen-binding, GAG-binding, andcytoskeleton-binding domains along their length;

cell surface receptors are called integrins; plasma

fibronectin synthesized by liver and endothelial cells

binds to fibrin during blood clotting reactions



Laminin- binds to membranes of epithelial and muscle

cells, to type-IV collagen, and heparan sulfate;

significant in the assembly of the basal lamina,influencing the form and function of epithelial cells

Thrombospondin- activated platelet-product; binds to

fibrinogen, plasmalogen and its activator; a participant

in blood clotting; function is poorly understood

Chondronectin- a component of cartilage matrix that mediates attachment of chondrocytes to their matrix

Fibrillin- a nonsulfated glycoprotein speculated to be

essential for normal development. It is often associated

with elastic fibers or with epithelial basal laminae

Marfan syndrome is due to a defective fibrillin geneon chromosome 15, characterized by excessively

long arms and legs and progressive dilatation and

fatal rupture of the ascending aorta (Pres. Abraham

Lincoln).



A: The structure of fibronectin.

Fibronectin is a dimer bound by

S³S groups, formed by serially

disposed coiled sites, that bind to

type I collagen, heparan sulfate,

other proteoglycans, and cell

membrane receptors.

B: The structure of laminin,which is formed by 3 intertwined

polypeptides in the shape of a

cross. There are sites on the

molecule with a high affinity for

cell membrane receptors andtype IV collagen and heparan

sulfate, which are components of

basal laminae. Laminin thus

promotes adhesion of cells to

basal laminae.



Transverse section of

mouse endometrium.Immunocytochemical

staining shows the

distribution of fibronectin in

the endometrial stroma.

Transverse section of tongue.

Immunocytochemical stainingshows the distribution of

laminin basement

membranes in epithelial layer,

capillary blood vessels, nerve

fibers, and striated muscle.



� GAGs in CT are highly sulfated which attracts water of

hydration. If fluid is injected into CT, it remains localized,

walled off by a viscous ground substance.� This property acts as barrier to the spread of bacteria that

gains access to the tissues.

� Some bacteria secrete hyaluronidase (Staphylo/ Strepto/

Pneumococci), and collagenase (Clostridium perfringens)

that breakdown matrix components.� EDEMA is a condition characterized by accumulation of

excess tissue fluid.

� The water in tissue fluid is forced out by hydrostatic

pressure from the arterial end.

� Loss of fluid to the tissues increases the colloid osmoticpressure, and draws most of the fluid back into the blood.

� Excess fluids remaining in tissues is normally drained

away by lymphatic capillaries, so that there is no net

change in the amount of blood or tissue fluid.



Edema accompanies pathological conditions that

cause:

Increased hydrostatic pressure in capillaries byobstructing venous blood flow (e.g. congestive

heart failure)

Decreased colloid osmotic pressure in the blood

caused by lack of blood proteins (e.g. starvation)

Increased hydrostatic pressure in the tissuecaused by blockage of lymphatic drainage by

parasites or tumor cells

Increased colloid osmotic pressure in the tissue

caused by excessive accumulation of GAGs in

the matrix.

Hypothyroidism resulting

from this condition is

referred to as myxedema.



1.COLLAGEN FIBERS

� Principal producers are fibroblasts; epithelial and smoothmuscle cells also secrete their own type-IV collagen.

� Most numerous CT matrix, running in all directions in a

wavy course; dull and opaque in appearance.

� Fibers bundled together branch and anastomose;

individual fibers do not branch.� With the EM, unit fibrils of collagen show periodic cross

striations every 67 nm of their length.

CONNECTIVE TISSUE FIBERS



Unit fibrils are made up of 3 polypeptide chains

(E-chains) held together by hydrogen bonds.



� Collagen occurring in

bundles, or as individual

fibrils, exhibit acidophilic

properties in H & E

stained sections.

� In sections stained with

Massons·s trichome, they

stain green, blue with

Mallory·s trichome stain.� Thin fibers (type III) stain

darkly with silver stains,

but thicker bundles do

not.

� Collagen that do not form

fibers (type IV) cannot be

distinguished from the

surrounding ground

substance except by

immunohistochemistry.



1.INTRACELLULAR ² free polysomes reading collagen mRNA

attach to the rER, and protocollagen or precollagen-chainsare deposited in the cisternae. Each chain has about 250

amino acids; every 3rd amino acid is glycine.

� The signal peptide is clipped off. Proline and lysine residues

within the chains are then hydroxylated in the ER to form

hydroxyproline and hydroxylysine (unusual amino acidspresent in large amounts in collagen).

� Core sugars (galactose and glucose) attach to the

hydroxylysine residues in the ER.

� Each chain is synthesized with an extra length of peptides

known as registration peptides, which ensure that the

appropriate chains assemble in their correct position in the

resulting triple helical molecule called procollagen.

� Further glycosylation may occur in the Golgi complex, where

procollagen is packaged for secretion. Golgi vesicles release

procollagen into the extracellular space by exocytosis.

Synthesis and Assembly of Collagen



2.EXTRACELLULAR- in the extra

cellular space, the enzyme

procollagen peptidase cleavesthe registration peptides from

procollagen, converting it to

tropocollagen. Catalyzed by

lysyl oxidase, these become

aligned in staggered fashion to form collagen fibers, possibly

under the control of adjacent

fiber-producing cells.

� The turnover of collagen is

slowest in tendons, fastest inloose CT. Macrophages and neutrophils break down old

collagen, and replaced by fibroblasts.

� As humans age, extracellular collagen becomes

increasingly cross-linked, & turn-over slows down in CT.



COLLAGEN TYPES- fibril-forming (I,II,III,V,XI), fibril-

associated (IX, XII), network-forming (IV), anchoring

(VII):

� Type I- most abundant and widespread, forms large

fibers and fiber bundles. It is found in tendons,

ligaments, bone, dermis, organ capsules, and loose CT.

� Type II- form only very thin fibers; found in embryonic

notochord; in adults, only in the nucleus pulposus of the

intervertebral disk, vitreous body of the eye, and in the

hyaline and elastic cartilage matrix.

� Type III- similar to type I, but is more heavily glycosylated

and stain with silver.

� Often found in association with type I, these reticular

variety forms networks of thin fibrils that are

abundant in loose CT, in soft and compliant organs

such as the walls of blood vessels, in the stroma of

spleen, kidney and uterus, and compose the reticular

laminae underlying epithelial basal laminae.



Collagen types I, II, and III are called interstitial

collagens which form microscopically visible

fibers.

� Type IV- does not form fibers or fibrils; major

collagen type found in basal laminae.

� Type V- present in external lamina of muscle

fibers, epithelial basal lamina, blood vessels andin small amounts elsewhere

� Type VI- present where types I and III are found;

kidney, uterus, cornea.

� Type VII- largest of the collagen family; formanchoring fibrils of epithelial basal lamina,

serving to stabilize and firmly anchor the

epithelium to the dermis.



� Type VIII- secretory product of endothelial cells;

a major component of Descemet·s membrane,

the corneal epithelium basal lamina.� Type IX- found mainly in cartilage; maintains the

3-D arrangement of type II fibrils by serving as

coupler in their sites of intersection

� Type X- found in the matrix surrounding

hypertrophic chondrocytes of degenerating

growth plate cartilage in sites of future bone

formation.

� Type XI (cartilage) and XII (tendon fibroblasts)-

very poorly understood types

Weight for weight, collagen tensile strength

is greater than that of steel.



� Chemical Characteristics- easily stained byordinary dyes; yield gelatin when boiled; dissolve

easily in boiling dilute acids and alkali; easily

digested by artificial gastric juice; resistant to

solutions of alkaline pancreatic juice.� Cortisol (hydrocortisone) produced by adrenal

glands under the influence of ACTH inhibits CT

fiber synthesis and retards local inflammatory

and immune responses by CT cells.� Cortisol reduces local heat, redness and

tenderness, but delay and impair wound

healing.

Histophysiology of Collagen



� Because collagen synthesis depends on the expression of

several genes and on several post-translation events,

many human diseases are associated with faulty collagensynthesis. Examples:

� Progressive systemic sclerosis- excessive

accumulation of collagen (fibrosis) in almost all organs;

� Keloid- local swelling caused by abnormal amounts of

collagen that form in scars of skin;� Ehlers-Danlos type IV- aortic/ intestinal rupture due to

faulty transcription of collagen type III;

� Ehlers-Danlos type VII- increased articular motility due

to decreased procollagen peptidase activity;

� Scurvy- ulceration of gums, hemorrhages due to lackof Vit. C, a cofactor for proline hydroxylase;

� Osteogenesis imperfecta- spontaneous fractures &

cardiac insufficiency due to mutation in collagen type I



Section of a muscular artery stained with picro-sirius andobserved with polarization optics. The upper tunica media

(muscular layer) contains reticular fibers consisting mainly of

collagen type III. The lower layer (tunica adventitia) contains

thick fibers and bundles of collagen type I. Deficiencies of

collagen type III may result in rupture of the arterial wall



2. YELLOW or ELASTIC FIBERS

� Form gentle curves or spirals at their free ends

when released from tension� Do not form bundles; individual fibers branch and

anastomose to form networks

� They can be stretched to 150% of their length

without breaking, but lose their resiliency withadvancing age.

� Appears yellowish, highly refractile, homogenous

and are not made up of fibrillar subunits that are

visible with the light microscope.� Composed of 2 elements: microfibrils, aggregated

in bundles which are embedded in abundant and

amorphous elastin.



Each fibril is made up of still smaller fibrils united by

a small amount of ground substance. These smaller

´microfibrilsµ have periodic cross bandings.

Ground substance stains with PAS due to its protein-

polysaccharide content: mucopolysaccharides,

hyalurinate, chondroitin sulfates.

Chemical characteristics:Stains poorly with standard ionic dyes since it

contains a few charged amino acids; as such it

requires the special Verhoeff·s (Weigerts· resorcin

fuschin) stain or Halmi·s aldehyde-fuchsin method.

It does not yield gelatin on boilingDoes not easily dissolve in boiling dilute acids and

alkali; and easily digested by pancreatic juice which

contains elastase.



In this side by side comparison of fibrous and elastic tendons cut in

cross-section, the relative sizes of fibers is compared. Notice how

large and robust the collagen fibers are compared to the smaller

elastic types. Nuclei of fibroblasts visible along the edges of fibers

are a good indicator these are tendons in cross-section.



1.Intracellular- microfibrillar proteins containing

mostly hydrophilic amino acids, and proelastin(contains large amounts of the hydrophobic amino

acids glycine, proline and valine, thus accounting for

elastin·s insolubility) are synthesized on rER and

secreted separately.

2.Extracellular- proelastin molecules polymerizeextracellularly to form elastin chains.

� Lysyl oxidases then catalyze the conversion of

certain lysine residues of elastin to aldehydes, 3

of which condense with a 4th unaltered lysine

residue to form desmosine and isodesmosine.

� These very rare amino acids found in elastin

cross-link individual chains, which then associate

with numerous microfibrils to form a branching

and anastomosing network of elastic fibers.

Synthesis and Assembly of Elastin:



Skin dermis, selectively stained for elastic fibers. Dark

elastic fibers are interspersed with pale red collagen

fibers. The elastic fibers are responsible for skin·selasticity . Elastin molecules are joined by covalent

bonds to generate an extensive cross-linked network.

Because each elastin molecule in the network can

expand and contract like a random coil, the entire

network can stretch and recoil like a rubber band.



A: Rat mesentery showing

nonanastomosing bundles

of collagen fibers, whilethe elastic fibers appear as

thin, dark anastomosing

fibers. Collagen and elastic

fibers provide structure

and elasticity, respectively,to the mesentery.

B: The same preparation

observed with polarizing

microscopy. Collagen

bundles of variousthicknesses are observed.

In the superimposed

regions, the bundles of

collagen are a dark color.



3.ARGYROPHYL or RETICULAR FIBERS

� Fibers are not branched, and are not so wavy as the

collagenous fibers when released from tension.� They are chemically identical to collagen, hence

these fibers are considered as precursors of type I

and III collagen; however, they are thinner and form

delicate networks instead of thick bundles

� Chemical characteristics- show affinity to silver(black) stains, hence argyrophyl; do not yield gelatin

on boiling; not easily dissolved by dilute acids and

alkali; not so easily digested by gastric juice; not so

resistant to solutions of alkaline pancreatic juice.

� Distribution- abundant in regions around blood

vessels, muscle fibers, fat cells, basement membrane

of epithelia, endoneurium, lymphoid organs and red

bone marrow.



Section of an adrenal cortex, silver stained to show reticular

fibers. This is a thick section made to emphasize the networks

formed by these fibers, which consist of collagen type III. Nuclei

are black, and cytoplasm is unstained.



1. FIXED CELLS

a. Mesenchymal cells- these cells have multipledevelopmental potentialities, differentiating along

several different lines to produce many different kinds

of CT cells, smooth muscle cells, blood cells.

� They disappear when component cells undergo

differentiation.� Embryonic mesenchyme

consists of a loose network

of stellate mesenchymal

cells and abundant

intercellular fluid.� Undifferentiated mesen-

chymal cells remain in adult

CT as reserve cells called adventitial cells, which are

difficult to distinguish from some fibroblasts.

CONNECTIVE TISSUE CELLS



b.Fibroblasts (fibrocytes or

desmocytes)

� Flattened cells with a finelygranular cytoplasm and a

vesicular nucleus.

� Young fibroblasts are stellate

cells with long cytoplasmic

processes and a large, ovoid,pale-staining nucleus with

nucleoli and sparse chromatin.

� They have long, slender mitochondria extending into

the processes, presence of ER and well-developedGolgi complex, a sign of active protein synthesis.

� Cytoplasm appears acidophilic but becomes slightly

basophilic when actively synthesizing ground

substance



� The smaller, mature type ( fibrocytes) are less active,

spindle-shaped with a dark, elongate nucleus and

fewer cytoplasmic organelles.� They can revert to the fibroblast stage and participate

in tissue repair.

� Differentiated cells ordinarily do not give rise to other

CT cell types. They are suspected to become adiposeor bone-forming cells, but it is debatable whether it is

actually the fibroblasts or their undifferentiated

mesenchymal progenitors that undergo these

transformations.

� In other locations, fibroblasts can take on different shapes and acquire additional functions (e.g.,

intestinal villi, interstitial cells of renal papillae,

periniurium of peripheral nerves)



Fibroblasts actively engaged in synthesis (left) are richer in

mitochondria, lipid droplets, Golgi complex, and rER than

are quiescent fibroblasts or fibrocytes (right).



c.Reticular Cells

� These make us a functionally

diverse yet morphologicallysimilar group. They produce

the reticular fibers that form

the netlike stroma of hema-

poietic & lymphoid tissues.

� They can phagocytoseantigenic materials and

cellular debris. Others collect antigens on their

surfaces and help activate immunocompetent cells.

� They are typically stellate with long, cytoplasmic

surfaces, with a central, pale, irregularly rounded

nucleus and a prominent nucleolus. The number of

mitochondria, rER and Golgi complex is variable; less

developed organelles maybe stem cells of various

blood types.



d.Fat or Adipose Cells

� These conspicuous cells are a normal component of

areolar tissue occurring singly or in clumps alongsmall blood vessels. If they accumulate in large

numbers, the tissue is transformed into adipose tissue.

� These are fixed cells containing fat globules in the

cytoplasm. They accumulate so much lipid that the

nucleus is flattened and displaced to one side, thecytoplasm so thinned that it appears as a narrow rim

around the edge of the single large lipid droplet giving

the cell the characteristic signet ring appearance.

� Individual cells are surrounded by a fine network of

reticular or argyrophil fibers.

� The biggest CT cell while all the others are small and

thus are difficult to demonstrate in ordinary slide

preparation.



� In fresh or formalin-fixed tissue,

the fat droplet can be stained

with osmic acid, but in most histological preparations, the

lipid has been extracted, leaving

only the plasma membrane.

� Fat cells are fully differentiated

and incapable of mitotic division.� The fat cells of the brown fat tissue prominent in

hibernating animals do not contain one big fat globule

but usually several small fat droplets with some

brownish pigment granules.

� In starvation and malnutrition, the fat content of the

fat cells disappears; the cytoplasm becomes more

abundant, serous in character with very tiny fat

droplets. These cells are termed serous fat cells.



2.FREE, MOBILE or WANDERING CELLS:

a.Macrophages (phagocytes, clasmatocytes,

histiocytes, resting wandering cells or rhagiocrinecells)

� These are large, irregularly shaped cells in loose CT

with vacuoles and abundant cytoplasm, abundant

lysosomes, well-developed Golgi complex, and

protruding pseudopods.� They are infrequent in CT

where blood vessels are few;

being abundant in richly

vascular areas; life spanis about 2 months.

� Maybe either fixed (resident)

or resting, attached to fibers

or free in the ground substance.



� Fixed macrophages are inactive and

immobile; they are elongated or

stellate shaped.� The fixed variety becomes the

rounded and motile free (elicited)

macrophages when mobilized at the

site in response to a stimulus; the

latter become activatedmacrophages when presented with

phagocytic and antigen-processing

activity.

� These phagocytes help maintain the

integrity of CT by removing foreignsubstances and cellular debris, and

participate in the immune response

by presenting phagocytosed antigens

to lymphocytes and plasma cells.



Section of rat

skin showing

multinuclear

giant cells

surrounded

by

macrophages

� They may form closely packed masses forming

epithelioid cells. In chronic infection, they may fuse to

form multinucleated foreign body giant cells around foreign objects that are too large or resistant to be

engulfed and destroyed.

� The cell enlarges during phagocytosis, the Golgi net

becomes prominent and the lysosomes discharge

enzymes into the vacuoles.



� The MONONUCLEAR PHAGOCYTE SYSTEM (formerly the

reticulo-endothelial system) is a group of widely

dispersed cells types that are related by theirmorphology, phagocytic functions and a common origin.

The phagocytic cells in all of the tissues and organs are

derived from precursors in the bone marrow, thru blood

monocytes.

� They all take up vital dyes, react positively for peroxidase,esterase and other lysosomal enzymes, and all have

surface receptors for IgG and complement.

� This system is composed of free or fixed macrophages of

CT (histiocyte), liver (stellate cells of Kupffer), pulmonary

alveoli, lymph node, spleen, bone marrow, serous cavity(pleural and peritoneal macrophages aggregated in small

patches known as ´milky spotsµ), bone (osteoclasts),

nervous system (microglia of the CNS), skin (histiocyte),

synovia (type A cell), tissue macrophages



b.Mast Cells- large, round or ovoid cells

resembling the basophils of the blood, with pale-

staining nuclei and large basophilic granulesobscuring the nuclei.



b.These granules are easily soluble in water and

seldom seen in the specimen. The granules contain

pharmacologically active substances such as:

� Heparin- anticoagulant and antiagglutinant

� Histamine- together with leukotrienes and the

eosinophilic chemotactic factor (ECF-A), its

release is responsible for the allergic response to

some foreign proteins or anaphylaxis. Histaminerelease during massive degranulation of mast

cells of anaphylaxis results to increased capillary

permeability with leakage of plasma into tissues,

dramatic fall in blood pressure, unconsciousness,

and even death.� Serotonin- a vasoconstrictor that increases the

permeability of capillaries and venules, having a

marked effect upon blood pressure.



Mast-cell secretion. 1: IgE molecules are bound to the surface receptors.

2: After a 2nd exposure to an antigen (e.g, bee venom), IgE molecules

bound to surface receptors are cross-linked by the antigen. This

activates adenylate cyclase & results in the phosphorylation of certain

proteins. 3: At the same time, Ca+2 enters the cell. 4: These events lead

to intracellular fusion of specific granules & exocytosis of their contents.5: In addition, phospholipases act on membrane phospholipids to

produce leukotrienes. The process of extrusion does not damage thecell, which remains viable and synthesizes new granules. ECF-A,

eosinophil chemotactic factor of anaphylaxis.



c.Plasma Cells� Spherical cells with an eccentric

´clock-faceµ nucleus resulting from

a large, central nucleolus & severallarge heterochromatin clumps

regularly spaced inside the nuclear

envelope.

� EM show the presence of an

extensive ER associated withribosomes or RNP granules which

are involved in the synthesis of

antibodies. The secreted proteins

do not aggregate into secretory

granules.� The cytoplasm has well developed Golgi complex and

centrioles, finely granular and intensely basophilic.

� They possess a slight amoeboid motility and are not

actively phagocytic.



� This cell type arise by further differentiation

of B lymphocytes

� Has a very important function in resistance todisease and is now known to be the principal

producer of antibodies, the immune globulins

of the blood that participate in the body·s

humoral defenses against bacterial infection.� These cells are abundant in the mucous

membrane of GI tract.

� When they disintegrate, their cytoplasmic

inclusions (believed to be products of defective antibody synthesis) are set free and

become acidophilic in staining, termed the

Russell granules or bodies.



Portion of a chronically inflamed intestinal villus. The plasma cells

are characterized by their size and abundant basophilic

cytoplasm (rER). A large Golgi complex (arrows) is where the

terminal glycosylation of the antibodies (glycoproteins) occurs.



d. Leukocytes- wandering cell types that originate in the bone

marrow and are carried to CT by the blood and lymph.

� Lymphocytes ² production of immunocompetent cells;

may originate in CT and remain there. However, they mayenter the circulation at any time.

� Eosinophil- abundant in lactating breast and of the

respiratory and alimentary tracts. They accumulate in

the blood and in the tissues in certain allergic, parasitic

infections and sub-acute inflammatory conditions. Theycontain a slight amount of histamine.

� Basophil- contain the anticoagulant heparin, which

prevents blood from clotting too quickly; the vasodilator

histamine; found in sites of exoparasite infection; and

where allergic reactions are occurring

� Neutrophil- generally escapes into CT from capillaries

only in regions of inflammation.

� Monocytes- are rarely seen; are considered as

phagocytes because they may become amoeboid and

show inclusions that stain supravitally with neutral red.



Section of an inflamed intestinal lamina propria. Inflammation

was caused by nematode parasitism. Aggregated eosinophils

and plasma cells function mainly in the connective tissue by

modulating the inflammatory process.

ct proper components

Documents