Life And Death Of A Macrophage Cell (Macrophage)

My name is Macrophage the macrophage.

I was named Macrophage by my friends who feel there is no other name for me.

Some of them even wanted to call me Super Phage or Big Eater.

We are white blood cells within tissues produced by the division of monocytes.

Our cells are large about 21 micrometers in diameter, still one-fifth of an ovum.

The human ovum measures approximately 100 micrometers in diameter and is the biggest cell.

We often have an elongated irregular shape that reflects our amoeboid wandering nature.

There may be many of us in one region but we are not contiguous.

We display our inclusions only as a result of substantial phagocytic activity.

The Monocytes and we are phagocytes acting in both:
1. Non-specific defenses (innate immunity)

2. Specific defense mechanisms (adaptive immunity) of humans.

Our role is to:
1. Phagocytose (engulf and then digest) cellular debris and pathogens either as stationary or as mobile cells

2. Stimulate lymphocytes and other immune cells to respond to the pathogen.

We move by action of amoeboid movement.

When a white blood cell enters the damaged tissue through the endothelium of a blood vessel (a process known as the leukocyte extravasations), it undergoes a series of changes to become a one of us macrophages

Monocytes are attracted to a damaged site by chemical substances through chemotaxis triggered by a range of stimuli including damaged cells, pathogens and cytokines released by us already at the site.

At some sites such as the testis, we have been shown to populate the organ through proliferation.

Unlike short-lived neutrophils, we survive longer in the body up to a maximum of several months.

An important role of us the macrophages is the removal of necrotic cellular debris in the lungs.

Removing dead cell material is important in chronic inflammation as the early stages of inflammation are dominated by neutrophil granulocytes which are ingested by us if they come of age.

The removal of necrotic tissue is handled by our fixed macrophage cells which will stay at strategic locations such as the lungs, liver, neural tissue, bone, spleen and connective tissue ingesting foreign materials such as pathogens recruiting more of us if needed.

When I ingest a pathogen, the pathogen becomes trapped in a phagosome which then fuses with a lysosome.

Within the phagolysosome, enzymes and toxic peroxides digest the pathogen.

However some bacteria such as Mycobacterium tuberculosis have become resistant to these methods of digestion.

We can digest more than 100 bacteria before we finally die due to our own digestive compounds, usually after a period of several months.

A Little Information on the Macrophage

Macrophages (big eater) are cells produced by the changes of monocytes in tissues.

Human macrophages are about 21 micrometers (0.00083in) in diameter.

Parts of a Macrophage:

1. Pathogens
2. Phagosome
3. Lysosomes
4. Waste material
5. Cytoplasm
6. Cell membrane

Life cycle of a macrophage:

When a monocyte enters the outside damaged tissue through the endothelium of a blood vessel, a process known as the leukocyte extravasation, it undergoes a series of changes to become a macrophage.

Monocytes are attracted to a damaged site by chemical substances through chemotaxis triggered by a range of stimuli including damaged cells, pathogens and cytokines released by macrophages already at the site.

At some sites such as the testis macrophages have been shown to populate the organ through proliferation.

Unlike short-lived neutrophils, macrophages survive longer in the body up to a maximum of several months.

TABLE OF CONTENT

Chapter 1 Story of Macrophage

Chapter 2 Life Cycle of Macrophage

Chapter 3 Formation of a Macrophage

Chapter 4 Death of a Macrophage

Chapter 5 Tuberculosis

1120957606
Life And Death Of A Macrophage Cell (Macrophage)

My name is Macrophage the macrophage.

I was named Macrophage by my friends who feel there is no other name for me.

Some of them even wanted to call me Super Phage or Big Eater.

We are white blood cells within tissues produced by the division of monocytes.

Our cells are large about 21 micrometers in diameter, still one-fifth of an ovum.

The human ovum measures approximately 100 micrometers in diameter and is the biggest cell.

We often have an elongated irregular shape that reflects our amoeboid wandering nature.

There may be many of us in one region but we are not contiguous.

We display our inclusions only as a result of substantial phagocytic activity.

The Monocytes and we are phagocytes acting in both:
1. Non-specific defenses (innate immunity)

2. Specific defense mechanisms (adaptive immunity) of humans.

Our role is to:
1. Phagocytose (engulf and then digest) cellular debris and pathogens either as stationary or as mobile cells

2. Stimulate lymphocytes and other immune cells to respond to the pathogen.

We move by action of amoeboid movement.

When a white blood cell enters the damaged tissue through the endothelium of a blood vessel (a process known as the leukocyte extravasations), it undergoes a series of changes to become a one of us macrophages

Monocytes are attracted to a damaged site by chemical substances through chemotaxis triggered by a range of stimuli including damaged cells, pathogens and cytokines released by us already at the site.

At some sites such as the testis, we have been shown to populate the organ through proliferation.

Unlike short-lived neutrophils, we survive longer in the body up to a maximum of several months.

An important role of us the macrophages is the removal of necrotic cellular debris in the lungs.

Removing dead cell material is important in chronic inflammation as the early stages of inflammation are dominated by neutrophil granulocytes which are ingested by us if they come of age.

The removal of necrotic tissue is handled by our fixed macrophage cells which will stay at strategic locations such as the lungs, liver, neural tissue, bone, spleen and connective tissue ingesting foreign materials such as pathogens recruiting more of us if needed.

When I ingest a pathogen, the pathogen becomes trapped in a phagosome which then fuses with a lysosome.

Within the phagolysosome, enzymes and toxic peroxides digest the pathogen.

However some bacteria such as Mycobacterium tuberculosis have become resistant to these methods of digestion.

We can digest more than 100 bacteria before we finally die due to our own digestive compounds, usually after a period of several months.

A Little Information on the Macrophage

Macrophages (big eater) are cells produced by the changes of monocytes in tissues.

Human macrophages are about 21 micrometers (0.00083in) in diameter.

Parts of a Macrophage:

1. Pathogens
2. Phagosome
3. Lysosomes
4. Waste material
5. Cytoplasm
6. Cell membrane

Life cycle of a macrophage:

When a monocyte enters the outside damaged tissue through the endothelium of a blood vessel, a process known as the leukocyte extravasation, it undergoes a series of changes to become a macrophage.

Monocytes are attracted to a damaged site by chemical substances through chemotaxis triggered by a range of stimuli including damaged cells, pathogens and cytokines released by macrophages already at the site.

At some sites such as the testis macrophages have been shown to populate the organ through proliferation.

Unlike short-lived neutrophils, macrophages survive longer in the body up to a maximum of several months.

TABLE OF CONTENT

Chapter 1 Story of Macrophage

Chapter 2 Life Cycle of Macrophage

Chapter 3 Formation of a Macrophage

Chapter 4 Death of a Macrophage

Chapter 5 Tuberculosis

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Life And Death Of A Macrophage Cell (Macrophage)

Life And Death Of A Macrophage Cell (Macrophage)

by Kenneth Kee
Life And Death Of A Macrophage Cell (Macrophage)

Life And Death Of A Macrophage Cell (Macrophage)

by Kenneth Kee

eBook

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Overview

My name is Macrophage the macrophage.

I was named Macrophage by my friends who feel there is no other name for me.

Some of them even wanted to call me Super Phage or Big Eater.

We are white blood cells within tissues produced by the division of monocytes.

Our cells are large about 21 micrometers in diameter, still one-fifth of an ovum.

The human ovum measures approximately 100 micrometers in diameter and is the biggest cell.

We often have an elongated irregular shape that reflects our amoeboid wandering nature.

There may be many of us in one region but we are not contiguous.

We display our inclusions only as a result of substantial phagocytic activity.

The Monocytes and we are phagocytes acting in both:
1. Non-specific defenses (innate immunity)

2. Specific defense mechanisms (adaptive immunity) of humans.

Our role is to:
1. Phagocytose (engulf and then digest) cellular debris and pathogens either as stationary or as mobile cells

2. Stimulate lymphocytes and other immune cells to respond to the pathogen.

We move by action of amoeboid movement.

When a white blood cell enters the damaged tissue through the endothelium of a blood vessel (a process known as the leukocyte extravasations), it undergoes a series of changes to become a one of us macrophages

Monocytes are attracted to a damaged site by chemical substances through chemotaxis triggered by a range of stimuli including damaged cells, pathogens and cytokines released by us already at the site.

At some sites such as the testis, we have been shown to populate the organ through proliferation.

Unlike short-lived neutrophils, we survive longer in the body up to a maximum of several months.

An important role of us the macrophages is the removal of necrotic cellular debris in the lungs.

Removing dead cell material is important in chronic inflammation as the early stages of inflammation are dominated by neutrophil granulocytes which are ingested by us if they come of age.

The removal of necrotic tissue is handled by our fixed macrophage cells which will stay at strategic locations such as the lungs, liver, neural tissue, bone, spleen and connective tissue ingesting foreign materials such as pathogens recruiting more of us if needed.

When I ingest a pathogen, the pathogen becomes trapped in a phagosome which then fuses with a lysosome.

Within the phagolysosome, enzymes and toxic peroxides digest the pathogen.

However some bacteria such as Mycobacterium tuberculosis have become resistant to these methods of digestion.

We can digest more than 100 bacteria before we finally die due to our own digestive compounds, usually after a period of several months.

A Little Information on the Macrophage

Macrophages (big eater) are cells produced by the changes of monocytes in tissues.

Human macrophages are about 21 micrometers (0.00083in) in diameter.

Parts of a Macrophage:

1. Pathogens
2. Phagosome
3. Lysosomes
4. Waste material
5. Cytoplasm
6. Cell membrane

Life cycle of a macrophage:

When a monocyte enters the outside damaged tissue through the endothelium of a blood vessel, a process known as the leukocyte extravasation, it undergoes a series of changes to become a macrophage.

Monocytes are attracted to a damaged site by chemical substances through chemotaxis triggered by a range of stimuli including damaged cells, pathogens and cytokines released by macrophages already at the site.

At some sites such as the testis macrophages have been shown to populate the organ through proliferation.

Unlike short-lived neutrophils, macrophages survive longer in the body up to a maximum of several months.

TABLE OF CONTENT

Chapter 1 Story of Macrophage

Chapter 2 Life Cycle of Macrophage

Chapter 3 Formation of a Macrophage

Chapter 4 Death of a Macrophage

Chapter 5 Tuberculosis


Product Details

BN ID: 2940046472837
Publisher: Kenneth Kee
Publication date: 12/17/2014
Sold by: Smashwords
Format: eBook
File size: 115 KB

About the Author

Medical doctor since 1972.

Started Kee Clinic in 1974 at 15 Holland Dr #03-102, relocated to 36 Holland Dr #01-10 in 2009.

Did my M.Sc (Health Management ) in 1991 and Ph.D (Healthcare Administration) in 1993.

Dr Kenneth Kee is still working as a family doctor at the age of 74

However he has reduced his consultation hours to 3 hours in the morning and 2 hours in
the afternoon.

He first started writing free blogs on medical disorders seen in the clinic in 2007 on http://kennethkee.blogspot.com.

His purpose in writing these simple guides was for the health education of his patients which is also his dissertation for his Ph.D (Healthcare Administration). He then wrote an autobiography account of his journey as a medical student to family doctor on his other blog http://afamilydoctorstale.blogspot.com

This autobiography account “A Family Doctor’s Tale” was combined with his early “A Simple Guide to Medical Disorders” into a new Wordpress Blog “A Family Doctor’s Tale” on http://ken-med.com.

From which many free articles from the blog was taken and put together into 1000 eBooks.

He apologized for typos and spelling mistakes in his earlier books.

He will endeavor to improve the writing in futures.

Some people have complained that the simple guides are too simple.
For their information they are made simple in order to educate the patients.
The later books go into more details of medical disorders.

He has published 1000 eBooks on various subjects on health, 1 autobiography of his medical journey, another on the autobiography of a Cancer survivor, 2 children stories and one how to study for his nephew and grand-daughter.

The purpose of these simple guides is to educate patient on health disorders and not meant as textbooks.

He does not do any night duty since 2000 ever since Dr Tan had his second stroke.

His clinic is now relocated to the Buona Vista Community Centre.

The 2 units of his original clinic are being demolished to make way for a new Shopping Mall.

He is now doing some blogging and internet surfing (bulletin boards since the 1980's) starting
with the Apple computer and going to PC.

The entire PC is upgraded by himself from XT to the present Pentium duo core.

The present Intel i7 CPU is out of reach at the moment because the CPU is still expensive.

He is also into DIY changing his own toilet cistern and other electric appliance.

His hunger for knowledge has not abated and he is a lifelong learner.

The children have all grown up and there are 2 grandchildren who are even more technically advanced than the grandfather where mobile phones are concerned.

This book is taken from some of the many articles in his blog (now with 740 posts) A Family Doctor’s Tale.

Dr Kee is the author of:

"A Family Doctor's Tale"

"Life Lessons Learned From The Study And Practice Of Medicine"

"Case Notes From A Family Doctor"

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