Jump to content

Photo

Immune Response


This topic has been archived. This means that you cannot reply to this topic.
46 replies to this topic

#21 SweetJade1980

SweetJade1980

    Senior Member

  • Veteran Members
  • Posts & Likes
    Posts: 2,109
    Likes: 19
About Me
  • Joined: 19-October 02

Posted 29 May 2008 - 08:44 PM

Another study:


QUOTE
Hautarzt. 2008 May 18. [Epub ahead of print] Links
[Acne : Current pathophysiologic considerations.][Article in German]


Degitz K, Ochsendorf F.
Dermatologische Gemeinschaftspraxis, Pasinger Bahnhofsplatz1, 81241, München, Deutschland, Klaus.Degitz@lrz.uni-muenchen.de.

Seborrhea, follicular hyperkeratosis, propionibacteria, and inflammatory reactions are the most important factors leading to acne. The combination of increased sebum producation and follicular hyperkeratosis facilitates an increased growth of Propionibacterium acnes. Its metabolic products lead to follicular inflammation and, in extreme cases, even to perifollicular abscesses. Sebum production is influenced by androgens, so that abnormalities in androgen levels can produce seborrhea and acne. Follicular hyperkeratosis may be triggered by a relative deficiency in linoleic acid, peroxides from sebum components, and especially by inflammatory mediators such as interleukin-1. Bacterial metabolic products such as lipases, proteases, or chemotactic factors lead to the perifollicular inflammation. This inflammation is not only a response to other pathogenetic factors, but also a cause of acne. An initial mild perifollicular infammation can induce comedogenesis via a variety of mediators. The influence of dietary factors on the initiation and course of acne has recently received increased recognition. A connection has been postulated between acne and a high nutrients with glycemic index, as well as with milk products. http://www.ncbi.nlm....Pubmed_RVDocSum


#22 farmerjack

farmerjack

    New Member

  • Members
  • Posts & Likes
    Posts: 17
    Likes: 0
About Me
  • Joined: 30-December 06

Posted 30 May 2008 - 07:05 PM

QUOTE (sim @ Apr 28 2008, 04:38 PM) <{POST_SNAPBACK}>
Hi people.

this has been bothering me for a while. i have a degree in microbiology but i still don't understand why this happens. when bacteria such as p. acne grows in a blocked follicle it causes a spot.

the bodies immune system will quickly detect these microbes and begin to attacked using white cells on many types (mainly macrophages) this causes inflamtion dues to chemicles released by the white cells. as time goes by puss occurs signalling death of the bacteria then healing and repair phase.

once we have been exposed once shouldn't our immune system destroy any p .acnes in the follicle before a spot forms? this would be true for any microbe that invades our body. antibodies would still linger in the body, macrophages would be more effective against the bacteria and memory cells would be made. so why are we still prone to them?


Here's your answer. Macrophages produce non-specific immune response. Meaning they don't have the role of identifying and producing antibodies against P.acne or any other pathogen. eusa_naughty.gif That's done by B cells and T cells and its called specific immune response. eusa_dance.gif But unfortunately B cells and T cells don't play a role here (as far as we know).

#23 john1234

john1234

    Member

  • Veteran Members
  • Posts & Likes
    Posts: 948
    Likes: 3
About Me
  • Joined: 17-July 06

Achievements

     

Posted 31 May 2008 - 08:27 PM

QUOTE (farmerjack @ May 30 2008, 07:05 PM) <{POST_SNAPBACK}>
QUOTE (sim @ Apr 28 2008, 04:38 PM) <{POST_SNAPBACK}>
Hi people.

this has been bothering me for a while. i have a degree in microbiology but i still don't understand why this happens. when bacteria such as p. acne grows in a blocked follicle it causes a spot.

the bodies immune system will quickly detect these microbes and begin to attacked using white cells on many types (mainly macrophages) this causes inflamtion dues to chemicles released by the white cells. as time goes by puss occurs signalling death of the bacteria then healing and repair phase.

once we have been exposed once shouldn't our immune system destroy any p .acnes in the follicle before a spot forms? this would be true for any microbe that invades our body. antibodies would still linger in the body, macrophages would be more effective against the bacteria and memory cells would be made. so why are we still prone to them?


Here's your answer. Macrophages produce non-specific immune response. Meaning they don't have the role of identifying and producing antibodies against P.acne or any other pathogen. eusa_naughty.gif That's done by B cells and T cells and its called specific immune response. eusa_dance.gif But unfortunately B cells and T cells don't play a role here (as far as we know).


That's actually not true. T cells are extensively involved in acne and thus the proliferation/induction of macraphages. That's why acne's considered a DTH response...

#24 farmerjack

farmerjack

    New Member

  • Members
  • Posts & Likes
    Posts: 17
    Likes: 0
About Me
  • Joined: 30-December 06

Posted 01 June 2008 - 10:24 AM

QUOTE (john1234 @ May 31 2008, 10:27 PM) <{POST_SNAPBACK}>
QUOTE (farmerjack @ May 30 2008, 07:05 PM) <{POST_SNAPBACK}>
QUOTE (sim @ Apr 28 2008, 04:38 PM) <{POST_SNAPBACK}>
Hi people.

this has been bothering me for a while. i have a degree in microbiology but i still don't understand why this happens. when bacteria such as p. acne grows in a blocked follicle it causes a spot.

the bodies immune system will quickly detect these microbes and begin to attacked using white cells on many types (mainly macrophages) this causes inflamtion dues to chemicles released by the white cells. as time goes by puss occurs signalling death of the bacteria then healing and repair phase.

once we have been exposed once shouldn't our immune system destroy any p .acnes in the follicle before a spot forms? this would be true for any microbe that invades our body. antibodies would still linger in the body, macrophages would be more effective against the bacteria and memory cells would be made. so why are we still prone to them?


Here's your answer. Macrophages produce non-specific immune response. Meaning they don't have the role of identifying and producing antibodies against P.acne or any other pathogen. eusa_naughty.gif That's done by B cells and T cells and its called specific immune response. eusa_dance.gif But unfortunately B cells and T cells don't play a role here (as far as we know).


That's actually not true. T cells are extensively involved in acne and thus the proliferation/induction of macraphages. That's why acne's considered a DTH response...


Then I take it back. What's the specific role of T cells in P.acne response and where can I read the related literature/studies?

#25 SweetJade1980

SweetJade1980

    Senior Member

  • Veteran Members
  • Posts & Likes
    Posts: 2,109
    Likes: 19
About Me
  • Joined: 19-October 02

Posted 01 June 2008 - 10:47 AM

QUOTE (farmerjack @ Jun 1 2008, 10:24 AM) <{POST_SNAPBACK}>
Then I take it back. What's the specific role of T cells in P.acne response and where can I read the related literature/studies?



Confused. Do you want to know how the body responds to p.acnes or how p. acnes contributes to the development of acne...since p. acnes does not cause acne?

#26 SweetJade1980

SweetJade1980

    Senior Member

  • Veteran Members
  • Posts & Likes
    Posts: 2,109
    Likes: 19
About Me
  • Joined: 19-October 02

Posted 01 June 2008 - 11:32 AM

This might help:


QUOTE
Rev Med Chir Soc Med Nat Iasi. 2004 Apr-Jun;108(2):319-24.

[Immunohistochemical evidence of chronic inflammation in acne vulgaris][Article in Romanian]


Brănişteanu D, Cianga C, Cianga P, Petrescu Z, Carasevici E.
Universitatea de Medicină şi Farmacie Gr.T. Popa Iaşi, Facultatea de Medicină, Clinica Dermatologică.

The etiology and pathogenesis of acne vulgaris are not yet completely understood. Therefore we have investigated 5 patients with different clinical forms of disease, including the rare form of acne fulminans. Taking into consideration the four factors that are currently incriminated in the development of acne, sebaceous hypersecretion, hyperkeratosis of the pilosebaceous infundibulum, bacterial colonisation and perifollicular inflammation, we have focused our study on a set of cells involved in the chronic inflammatory process. We have evidenced by immunohistochemistry methods, using appropriate monoclonal antibodies, the presence of T lymphocytes and macrophages, while the B cells could be evidenced only in the severe forms. We were also interested to investigate the occurrence of new capillary formation, as an accompanying phenomenon of the inflammatory process. The presence and histological distribution of these cells highly supports the hypothesis that the mechanisms underlying the development of acne vulgaris belong to the Delayed Type Hypersensitivity.
http://www.ncbi.nlm....Pubmed_RVDocSum


More info:
http://www.acne.org/...es-t199729.html

#27 AutonomousOne1980

AutonomousOne1980

    Senior Member

  • Veteran Members
  • Posts & Likes
    Posts: 3,076
    Likes: 51
About Me
  • Joined: 30-June 06

Posted 01 June 2008 - 09:15 PM

here is something that could add to this thread, what do you guys think??

http://www.physorg.c...s112424870.html

http://www.attitudef....com/immune.htm

#28 farmerjack

farmerjack

    New Member

  • Members
  • Posts & Likes
    Posts: 17
    Likes: 0
About Me
  • Joined: 30-December 06

Posted 04 June 2008 - 09:51 AM

After reading the study, I'm confused at the original post. The study does say that B cells do not respond in normal acne cases, only during severe acne. We also know that B cells are responsible for producing antibodies. So why should one expect that antibodies would be produced against P.acne in normal acne cases?



#29 SweetJade1980

SweetJade1980

    Senior Member

  • Veteran Members
  • Posts & Likes
    Posts: 2,109
    Likes: 19
About Me
  • Joined: 19-October 02

Posted 04 June 2008 - 07:33 PM

QUOTE (farmerjack @ Jun 4 2008, 08:51 AM) <{POST_SNAPBACK}>
After reading the study, I'm confused at the original post. The study does say that B cells do not respond in normal acne cases, only during severe acne. We also know that B cells are responsible for producing antibodies. So why should one expect that antibodies would be produced against P.acne in normal acne cases?



OK...you're confusing me confused.gif

What I don't get is why we need a vaccine against p. acnes when we already produce antibodies against p. acnes (plenty of studies shows this)......and p. acnes doesn't CAUSE acne.

I guess...in severe cases....like nodulocystic acne, p. acnes is trapped and builds up within this particular pore. This is further irritating, thus the antibodies come out....too simplistic?

However...antibodies can also be present due to other antigenic triggers such as pore clogging ingredients, irritating skin care ingredients, herbs, foods, etc.

#30 john1234

john1234

    Member

  • Veteran Members
  • Posts & Likes
    Posts: 948
    Likes: 3
About Me
  • Joined: 17-July 06

Achievements

     

Posted 04 June 2008 - 07:47 PM

I sort of get what he means. You can have both memory B-cells and memory T-cells. When we talk about acne as a DTH, we are speaking of a T-cell mediated response. Basically, you have a feedback loop in which T cells activate macrophages upon exposure to the antigen. Macrophages can then activate the T cells. This chronic activation will lead to inflammation, because lots of inflammatory mediators are released. So when the OP wrote about developing "antibodies," he wasn't completely correct--only the most severe cases have antibodies involved....

#31 sim

sim

    Junior Member

  • Veteran Members
  • Posts & Likes
    Posts: 73
    Likes: 0
About Me
  • Joined: 15-July 07

Posted 08 August 2008 - 05:14 PM

double post

#32 sim

sim

    Junior Member

  • Veteran Members
  • Posts & Likes
    Posts: 73
    Likes: 0
About Me
  • Joined: 15-July 07

Posted 08 August 2008 - 05:26 PM

hey hey hey,

been reading the literature sweetjade posted which is informtive and has cleared some of my misconceptions.

my immunology is a bit sketchy its been a while since i've used it. macrophages are always first at a site of infection not always the first for immune response but contributes to the immune response but causing a chain reaction ultimatly if needed, B cells for antibdies and memory cells.

when a spot forms the number of p. acne in the follicle is abnormal, this causes waste products to accumulate in the follicle. i suspect the first stages of the immune response occures but its this response that causes acne.

if i understand correctly inflammation occures, the site becomes red and heavily dilated because of the body redirecting resources to fight the infection. the body does not know if this invasion is by a simple organism or something more serious one. during the next couple of days, the bacteria dies probably through phagocytosis in relation to john1234's comment, it most probably be a t-cell mediated response, antibodies i don't believe assists much, possibly neutralizing toxins produced or improving phagocytosis (or in cystic or severe acne where the bacteria has grown beyound the follicle and erupted in the hypodermis and getting close to the blood supply thus causing a harsher response?). anyway; ultimatly puss forms at the site due to bacteria destruction and bacteria replication; samaging surrounding cells. at the end of the infection all the bacteria would have been killed and the body begins the repair stage.

p. acne is part of the natural human flora. we have many other organisms. they are hamless and helps the body but when they appear in unsual places or when their number get to high, the body will defend itself causing adverse physiological and biological reactions.

#33 gda_11

gda_11

    Member

  • Veteran Members
  • Posts & Likes
    Posts: 417
    Likes: 2
About Me
  • Joined: 16-March 09

Posted 26 June 2009 - 05:07 PM

QUOTE (sim @ Apr 28 2008, 06:08 PM) <{POST_SNAPBACK}>
Hi people.

this has been bothering me for a while. i have a degree in microbiology but i still don't understand why this happens. when bacteria such as p. acne grows in a blocked follicle it causes a spot.

the bodies immune system will quickly detect these microbes and begin to attacked using white cells on many types (mainly macrophages) this causes inflamtion dues to chemicles released by the white cells. as time goes by puss occurs signalling death of the bacteria then healing and repair phase.

once we have been exposed once shouldn't our immune system destroy any p .acnes in the follicle before a spot forms? this would be true for any microbe that invades our body. antibodies would still linger in the body, macrophages would be more effective against the bacteria and memory cells would be made. so why are we still prone to them?



Because your body doesn't see the p. acne as an actual threat, hence is why it doesn't get eaten by the macrophages. The acne bacteria are normal, and everyone has it. It's not foreign to our body. This is just a rough guess, I might be way off but that's my 2 cents.

#34 Packerfan785

Packerfan785

    Veteran Member

  • Veteran Members
  • Posts & Likes
    Posts: 1,128
    Likes: 2
About Me
  • Joined: 03-June 08

Posted 10 September 2009 - 01:08 AM

So let me get this straight, hormones and other factors onset a inflammatory response, but we are not exactly sure how?

Could someone put this all into perspective for me. I get that the bacteria does not play a part and that something is causing the body to inflict an inflammatory response, I just don't get why or where the hormones come in.

#35 theComfyCat

theComfyCat

    Member

  • Veteran Members
  • Posts & Likes
    Posts: 322
    Likes: 0
About Me
  • Joined: 31-July 09

Posted 01 October 2009 - 03:43 PM

QUOTE (Packerfan785 @ Sep 10 2009, 12:08 AM) <{POST_SNAPBACK}>
So let me get this straight, hormones and other factors onset a inflammatory response, but we are not exactly sure how?

Could someone put this all into perspective for me. I get that the bacteria does not play a part and that something is causing the body to inflict an inflammatory response, I just don't get why or where the hormones come in.


Well, to start off, there are several factors involved in acne formation: hyperkeratinization, sebum (over)production, presence/activity of P. acnes bacteria, and inflammation. Hyperkeratinization is abnormal shedding of skin cells within the follicles, which creates plugs... these "plugged follicles" are called microcomedones... if there is some drainage (of sebum and the other contents), it will become an open comedo, or blackhead. If there is no drainage, it will become a closed comedo, or whitehead, which can become an inflamed lesion, such as a pustule or cyst. So, microcomedones are the precursors to all acne lesions.

The big question, is what causes these factors in the first place, namely, what triggers the formation of microcomedones? The info found earlier in this post is about research involved with the answer to this question. I’ll just sum it all up for you, which will hopefully help you put it into perspective.

Basically, it appears that in most cases, hereditary differences in our skin’s innate immune system make us more likely to produce an immune response to certain internal or external stimuli. The immune response changes the cycle of the sebaceous follicle, increasing the proliferation of skin cells within the follicle… and because of the other substances within the follicles (e.g. keratin, sebum), plugs form (microcomedones), and normal drainage can no longer occur.

The stimuli discussed as the probable triggers of this initial immune response are a combination of androgens, certain hormone receptors, certain regulatory neuropeptides/ cytokines, deficiency in certain anti-oxidants, and certain environmental factors (specifically, stress response or topical stress, diets containing pro-inflammatory substances, and smoking).

A further immune response can result due to chemical changes which occur to the obstructed comedo as it progresses, which is where P. acnes can be involved. At this point, pustules or other inflamed lesions are formed.

Edited by theComfyCat, 01 October 2009 - 03:47 PM.


#36 heehee3

heehee3

    Junior Member

  • Veteran Members
  • Posts & Likes
    Posts: 67
    Likes: 0
About Me
  • Joined: 04-December 09

Posted 04 December 2009 - 08:38 PM

yeah the acne bacteria DOES NOT cause acne. because everyone whether u hav acne or not have the p.acne bacteria. whats causes acne is not just the skin but something deep down internally

#37 agileox

agileox

    New Member

  • Members
  • Posts & Likes
    Posts: 24
    Likes: 0
About Me
  • Joined: 25-March 09

Posted 15 June 2011 - 12:44 PM

QUOTE (theComfyCat @ Oct 1 2009, 04:43 PM) <{POST_SNAPBACK}>
QUOTE (Packerfan785 @ Sep 10 2009, 12:08 AM) <{POST_SNAPBACK}>
So let me get this straight, hormones and other factors onset a inflammatory response, but we are not exactly sure how?

Could someone put this all into perspective for me. I get that the bacteria does not play a part and that something is causing the body to inflict an inflammatory response, I just don't get why or where the hormones come in.


Well, to start off, there are several factors involved in acne formation: hyperkeratinization, sebum (over)production, presence/activity of P. acnes bacteria, and inflammation. Hyperkeratinization is abnormal shedding of skin cells within the follicles, which creates plugs... these "plugged follicles" are called microcomedones... if there is some drainage (of sebum and the other contents), it will become an open comedo, or blackhead. If there is no drainage, it will become a closed comedo, or whitehead, which can become an inflamed lesion, such as a pustule or cyst. So, microcomedones are the precursors to all acne lesions.

The big question, is what causes these factors in the first place, namely, what triggers the formation of microcomedones? The info found earlier in this post is about research involved with the answer to this question. I’ll just sum it all up for you, which will hopefully help you put it into perspective.

Basically, it appears that in most cases, hereditary differences in our skin’s innate immune system make us more likely to produce an immune response to certain internal or external stimuli. The immune response changes the cycle of the sebaceous follicle, increasing the proliferation of skin cells within the follicle… and because of the other substances within the follicles (e.g. keratin, sebum), plugs form (microcomedones), and normal drainage can no longer occur.

The stimuli discussed as the probable triggers of this initial immune response are a combination of androgens, certain hormone receptors, certain regulatory neuropeptides/ cytokines, deficiency in certain anti-oxidants, and certain environmental factors (specifically, stress response or topical stress, diets containing pro-inflammatory substances, and smoking).

A further immune response can result due to chemical changes which occur to the obstructed comedo as it progresses, which is where P. acnes can be involved. At this point, pustules or other inflamed lesions are formed.


I think most Unified Acne theories could be shoehorned rationally under a framework approximating this description. Even databased's very unconventional melatonin maintenance regimen which heavily relies on tending to pineal melatonin levels through controlled stimulation of the ganglion would seem to be explained under such a framework.

I would wonder though, do people who suffer visible to no acne, are they simply less responsive to stimuli or is it that their autoimmune response is dampened so as to not upset the normal balance and processes of the sebaceous gland?

#38 Guest_davidtheskinking_*

Guest_davidtheskinking_*
  • Guests
  • Posts & Likes

Posted 08 July 2011 - 08:00 PM

There are a lot of factors that come into play.

Unfortunately most people's immune system and immune response isn't as strong and effective as it should be. This is why it is important to get nutrition that feeds your immune system.

Also, many people don't have enough good bacteria to balance out the bad bacteria in their body so this balance is crucial and most people don't get real alive probiotics in their diet anymore.

Also, when you feed the bad bacteria with your diet this helps it grow out of control.

So simply making a few changes can help a lot.

Hope this helps,


David

#39 Guest_Timehealsall_*

Guest_Timehealsall_*
  • Guests
  • Posts & Likes

Posted 08 October 2011 - 01:15 AM

There are a lot of factors that come into play.

Unfortunately most people's immune system and immune response isn't as strong and effective as it should be. This is why it is important to get nutrition that feeds your immune system.

Also, many people don't have enough good bacteria to balance out the bad bacteria in their body so this balance is crucial and most people don't get real alive probiotics in their diet anymore.

Also, when you feed the bad bacteria with your diet this helps it grow out of control.

So simply making a few changes can help a lot.

Hope this helps,


David

which changes?

this thread is very confusing. would be awesome if someone could type out a step by step way to get rid of acne using all these methods mentioned (i.e. elimination diet)

#40 alternativista

alternativista

    Senior Member

  • Veteran Members
  • Posts & Likes
    Posts: 11,542
    Likes: 1,107
About Me
  • Joined: 13-February 07

Posted 06 January 2012 - 10:35 AM

this thread is very confusing. would be awesome if someone could type out a step by step way to get rid of acne using all these methods mentioned (i.e. elimination diet)


Chronic inflammation is at the root of acne formation as well as most health conditions. It has many causes but diet and lifestyle habits are major. What you want is a nutrient dense, blood sugar stabilizing, anti-inflammatory diet that doesn't include anything you have an intolerance for. And you need to sleep well, keep as natural as possible circadian rhythm, manage stress and be physically active but in ways that do not cause inflammation. Avoid or manage stress. Don't irritate your skin topically.


Keep all meals, drinks and snacks low to moderate glycemic load. It's the impact of the meal that matters, not each and every food. Never drink or snack on sugar without plenty of fiber and fat to lower the glycemic impact.

Eat real, whole nutrient dense food. Limit/avoid sugar, grains-especially gluten grains and refined grain products, hydrogenated/trans fats (margarine, crisco, most fried foods, corn & veggie oil). This means avoiding most commercially prepared foods.

Also limit dairy, especially unfermented and especially from cows. Milk contains hormones meant to make tons of things happen in a rapidly growing infant's body. This causes bad things in our no longer rapidly growing post-adolescent bodies.

The most anti-inflammatory foods are plant foods and fish. Have lots of veggies, fruit, herbs, teas, spices, fish, etc. Try to have only products from pastured animals as much as possible. You want to reduce your intake of omega 6 fats and increase omega 3 and monounsaturated fats. High omega 3 fish like wild salmon, sardines, herring. Farmed trout and certain other fish is also ok depending on where it's from, but avoid farmed salmon. It just isn't a good fish for farming. Avocados, olive oil and products from pastured animals and fish are sources of healthy fats that result in healthy sebum that works.

The most inflammatory foods/meals are anything that spikes your blood sugar/insulin, anything you have an intolerance for, trans fats and high omega 6 sources like grains, grain oils, and products from grain fed animals.

Follow an elimination diet to determine any intolerances you may have. Either follow a very hypoallergenic diet for a couple months, then methodically add foods back in, or methodically eliminate foods starting with the most commonly problematic ones such as grains, nuts, peanuts, soy, eggs, citrus, shellfish, dairy, etc. Perfectly healthy foods could be causing your breakouts.

Try completely avoiding gluten grains and dairy for at least a month. And even if you notice no improvement, they should not be a big part of your diet. Dairy always affects acne for a number of reasons and gluten isn't good for anyone, causing serious harm for some people, and is usually part of some high glycemic food anyway.

Avoid harsh cleansers and topicals. Soap is alkaline. Even tap water is mildly alkaline. Washing with them strips away the acidic layer on the surface of your skin that protects your from microbes. It's restored with sebum and sweat, but in the meantime, your skin is vulnerable.

And then maybe you need to pay extra attention with supplements, foods and habits to address any issue you might have such as gut permeability and other digestion issues, poor liver, thyroid or adrenal function.

More info on all of the above: http://www.acne.org/...ar-skin-health/

Various environmental pollutants are also factors in inflammation. Perfumes, cosmetics, detergents, Auto exhaust, mercury, all kinds of crap in our water. Maybe be even all the EM waves we now have bouncing around.

Edited by alternativista, 12 January 2012 - 12:36 PM.