Talk:Inflammation

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edit·history·watch·refresh Stock post message.svg To-do list for Inflammation:

  • Information on leukocyte involvement (extravasation, chemotaxis, activation, phagocytosis, extracellular release of products)
  • Food poisoning. (mould organisms)
  • Haemodynamics of inflammation
    • Diagram of vascular changes
  • Disorders of inflammation
  • Termination of inflammation
  • Morphologic patterns of inflammation (serous, fibrinous, purulent, ulceritive, granulomatous)
  • Involvement of lymphatic system
  • More references needed
  • Inflammation and allergy

AntoniusD (talk) 00:17, 16 August 2010 (UTC)The comment that "The correct Latin for loss of function however would be "Laesus Functionis" is incorrect and should be deleted. Functio is a nominative singular feminine noun (3rd declension). Laesa is a past participle (from "laedere") qualifying it and has a passive sense: i.e. "damaged (or impaired) function:. Looks like a "correction" made from a dictionary by someone who does not know Latin very well, if at all.AntoniusD (talk) 00:17, 16 August 2010 (UTC)


Exercise and Inflammation[edit]

I think this section is far too extensive for this article. Other specific, much more classical, examples of inflammation are not discussed here. I think it should be moved to another article, such as Muscle or Exercise. Ehudzel (talk) 15:30, 6 May 2011 (UTC)

General Concerns and Suggestions[edit]

This article needs to be reworked in a lot of different ways including conceptually. The basic problem is that there is no principled distinction between older/classic regional inflammatory concepts ,which this piece presents reasonably well, and newer and equally important concepts about chronic or systemic inflammation, particularly the destructive disinhibition of inflammation in aging (barely mentioned as an afterthought in relationship to diabetes towards the end of the article). Specifically, one might consult the work of E Sikora, B Aggerwal, S Bengmark, and the classic paper on this by Franceschi C, Bonafe M, Valensin S, Olivieri F, De Luca M, Ottaviani E, De Benedictis G: Inflamm-aging. An evolutionary perspective on immunosenescence. Ann N Y Acad Sci 2000, 908:244-254. This work suggests that aging itself may be both a consequence as well as a driver for progressive auto-inflammatory damage. These concepts have to be seen as having a huge influence on how we understand aging itself and how we might protect ourselves from the accelerated aging associated with the Western lifestyle and diet, which are strongly pro-inflammatory in a number of ways. It's a shame that despite previous and explicit suggestions about this, the author has chosen to ignore this entire realm of literature completely. for this reason I am spelling out my differences with this whole approach more explicitly in this extended comment.

First of all, the evidence is now virtually overwhelming that every disease of aging (Alzheimer's disease, cancer, heart disease, diabetes, arthritis, etc. etc.) is associated with long-term damage done by our own immune systems. For example, there is now solid evidence that the transition from mild cognitive impairment to dementia in patients with Alzheimer's disease is associated with up regulation of various cytokine systems, although it is not so clear what is driving this. There is also enormous evidence that cancer is associated with long-term inflammatory damage to various cell populations, and that upregulation of inflammatory pathways particularly the transcription factor nuclear factor kappa b, is critical to cancer pathogenesis. Heart disease is clearly associated with inflammatory processes on the arterial wall (in the context of oxidized lipids) enabling plaque formation. Diabetes particularly type II diabetes also has a close relationship with this pro-inflammatory transcription factor being upregulated.

I don't think that any reasonable treatment of inflammation can fail to emphasize all these basic linkages and still claim to be remotely comprehensive. Additionally, any treatment of the subject would have to at least link to a page on cytokines, which appear to come in both anti-and pro-inflammatory forms. The treatment here also fails to emphasize the relationship between stress and inflammation, between sleep deprivation and inflammation, and between depression and inflammation, as there is increasing evidence that depression is in part mediated by elevated cytokines. Additionally, treatment fails to mention numerous diseases that may involve dysregulation of inflammatory pathways and cytokines including particularly IBS, fibromyalgia, and chronic fatigue syndrome. There is also no principled discussion of anti-inflammatory drugs or anti-inflammatory foods, and there is more and more evidence that omega-3 supplementation is valuable because it reduces systemic inflammation (the omega-3 pathway competes with the omega six pathway for the same enzymes, and the omega six pathway promotes prostaglandins and other pro-inflammatory molecules.) Clearly there are a lot of things that could be improved here, but I would start with an emphasis on how the immune system cuts both ways, it clearly is essential for our survival, but its chronic overactivity may contribute hugely to diseases of aging and even to aging itself. This potentially makes the topic a lot richer and a lot more interesting.

Indeed it looks like one of the critical ways to prevent many of the diseases of aging is to keep the innate immune system under control by ensuring a good nights sleep, regular exercise, and an anti-inflammatory diet (decent amounts of fruits and vegetables and a good amount of omega-3, with not too much omega 6, or processed carbohydrates). DFWatt Harvard Medical School. —Preceding unsigned comment added by 67.110.143.19 (talk) 18:41, 24 April 2008 (UTC)

The role of the nervous system in inflammation isn't mentioned. Chronic inflammation has been experimental shown to be mediated by the nervous system in A.D. Speransky's Basis for the Theeory of Medicine 1943. This is obviously the reason that stress and other nervous systems ailments have an effect as well as reason stress reducing changes in life style can have positive effects. Inflammation can be a local vascular response, a more distributed nervous response or typically combination often with complex interactions between the two. Charleskenyon (talk) 18:49, 18 July 2010 (UTC)

Fifth cardinal sign[edit]

In the textbook Pathophysiology: Concepts of altered health states (7th edition) by Porth it says that the 5th cardinal sign "loss of function" was added by Galen in the 2nd century AD, not in the 19th century by Ahmed Abou Samra. Google searches containing one name and the term "loss of function" or the latin "functio laesa" seem to indicate that porth was correct. It also says that Celsus termed the first four signs in the 1st century AD if that helps anyone at all.58.170.163.218 (talk) 12:21, 9 April 2008 (UTC) Systemic inflammation and overeating

Hyperglycemia induces IL-6 production from endothelial cells and macrophages.[35] Meals high in saturated fat, as well as meals high in calories irrespective of macronutrient composition, have also been associated with increases in inflammatory markers.[36][37] While the inflammatory responses are acute and arise in response to overeating, the response may become chronic if the overeating is chronic. [edit] Outcomes

Scars present on the skin, evidence of fibrosis and healing of a wound

The outcome in a particular circumstance will be determined by the tissue in which the injury has occurred and the injurious agent that is causing it. Here are the possible outcomes to inflammation:[4 prepared by: ismaaciil c/qaadir cali (xaafid yare) — Preceding unsigned comment added by 193.220.51.224 (talk) 10:32, 18 July 2011 (UTC)

Systemic inflammation[edit]

The bit about systemic inflammation is intrigueing, twood be nice to have a page on it! Wblakesx 19:11, 18 March 2007 (UTC)wblakesx

Advertisment[edit]

I removed a bit of advertising text that seems to have been maliciously inserted. The text was "See www.softecare.com for information on anti-inflammation Soft-E-Lotion" Jwinget 18:37, 5 September 2006 (UTC)

Anti-inflammatory foods[edit]

I am interested to know what people think about the idea of Anti-Inflammatory foods. It seems to be a topic that is coming up more and more (see: Hello Anti-inflammatory foods, List of Anti-inflammatory foods). Is there a good scientific basis for this?

I was also curious about this. There doesn't seem to be any scientific basis for what the woman is saying in the referenced article. It's unfortunately that such an important subject like nutrition is flooded with all sorts of cult theories. DonPMitchell 19:53, 29 April 2007 (UTC)
Maybe it is flooded with all sorts of cult theories because the entire subject is given such short thrift in medical schools (and even less with the general public) thus most people, along with most conventional physicians, don't know hardly anything about it and just assume that it doesn't really make that much difference. Then, sometimes, when some people get ill, out of desperation, they "think outside the box" and try some of the "cult" methods and find that they seem to work, and the theories make sense (are rational), thus reject the orthodoxy and conventional wisdom that poo-poos all of it. Shanoman (talk) 23:00, 29 May 2009 (UTC)
Good Questions and Points. There is actually quite a bit of literature about anti-inflammatory foods. See for example virtually anything written by Aggarwal ( go to Medline and enter his name and you will get literally 100 pieces). In any case, the anti-inflammatory food business probably breaks down into three large topics (and there's probably more complexity to it than we currently understand). One large topic is the omega-3/omega-6 ratio, which as I mentioned above is a critical modulator of the inflammatory equation - this is where food technology has really screwed things up. For example, if you eat beef that has been fed corn, instead of its native grass diet, you completely alter the omega-3/omega six ratio and wipe out the omega-3 components virtually completely. However, bison or cows eating their native diet show a decent omega-3/omega six ratio. No one is exactly sure what this ratio should be, but the evidence argues that our ancestors had a ratio in their diets of between 1/2 to 1/4. The evidence is the current American diet is somewhere between 1/15 to 1/45. This is a hugely pro-inflammatory shift, given that the omega six fraction (which is restrained and competes with the omega-3 fraction for conversion enzymes) is the primary pathway into prostaglandins. This is why eating fish particularly fish high in omega-3 or taking fish oil supplements is really valuable (although people typically underdose this, and think that fish oil is the same as omega-3 when most fish oil preparations are roughly 30% of omega-3.) So that's one aspect of it.
The second aspect relates to phytochemicals (substances in plants - fruits and veggies) - that alter the inflammatory equation as well. Without going into too much detail, this is multifactorial, and there are lots of issues. But one interesting one is that almost all fruits and veggies in one way or another inhibit a transcription factor known as NF-kappa B. This is the transcription factor (and these control whole families of genes, like a conductor in front of the orchestra) most intimately linked to the upregulation of inflammation. Also, various polyphenols (simplistically labeled as antioxidants) found in virtually all fruits and veggies, affect classic inflammatory pathways like COX, LOX, and prostaglandins.
A third aspect is related to dietary fiber content. Fiber appears to down-regulate the inflammatory equation, perhaps because systemic controls on inflammation are intimately linked to the amount of GI inflammation, but this is not clear (at least to me). So eating lots of fiber is also anti-inflammatory.
The long and the short of it is that the Western lifestyle (poor sleep, sedentary lifestyle, poor omega3 intake, tons of omega 6 foods and processed food while not enough plants and protective phytochemicals, lots of stress and social isolation, is a one way ticket into inflammatory upregulation, with accelerated aging and vulnerability to the diseases of aging as a direct consequence. This brief summary doesn't do justice to the relationships between inflammation, oxidative stress, insulin resistance, and glycation of proteins (the primary biological factors involved in aging), but suffice it to say, the relationships are reciprocal. Reducing inflammation also reduces oxidative stress, and insulin resistance.

207.180.129.233 (talk) 14:00, 22 October 2009 (UTC)DFW Harvard Medical School

It would be good to have a section covering these kinds of concerns. Jeff Schweitzer does a good job of debunking a lot of the fad-diet marketing myths, but the majority discussion out in public comes from people trying to sell fad diets and quackery. --John Moser (talk) 00:20, 22 June 2016 (UTC)

Chronic inflammation merge[edit]

I would keep acute and chronic together, with specifics on chronic inflammatory disease issues in the relevent articles, give a chance for contrasting acute and Chronic in the same article. Steve Kd4ttc 14:46, 6 Jun 2004 (UTC)

question[edit]

WHICH CHEMICAL CAUSE INFLAMMATION?


Hope this will answer your question: NSAIDs are COX inhibitors that inhibit the enzyme cyclooxygenase from transforming arachidonic acid (a derivative of cell membrane phospholipids) to prostaglandins. The prostaglandin family contributes to an inflammatory response mainly by increasing vasodilatation and vascular permeability. If the formation of the different arachidonic acid metabolites in the prostaglandin family is inhibited, some of the cardinal signs of inflammation might be decreased. Use of COX inhibitors, such as aspirin, will also decrease the ability of platelets to adhese and form a primary clot (see hemostasis and coagulation for more info on the formation of a blood clot) This is because COX inhibitors inhibit the formation of thromboxane (TXA2) in platelets. When used excessively, most NSAIDs might predispose to gastric ulceration by inhibiting COX-1. Some of the prostaglandins produced in the cyclooxygenase pathway are essencial for the protection against acid induced damage of the gastric mucosa and by inhibiting COX-1, the production of these metabolites is decreased. Recently, selective COX-2 inhibitors have been developped, obliterating the harmful effects of the COX-1 inhibitors on the gastric mucosa. However recent studies have shown that these drugs might lead to acute coronary artery disease.

Yours Sincerely

Helge-André Flakk Norwegian Dentist

 —Preceding unsigned comment added by 194.54.110.98 (talk) 21:47, 24 April 2008 (UTC) 

extremely graphic images[edit]

So, here is the real issue: a lay reader is not going to be expecting this page to include depictions of the pathology anywhere near that graphic. I'm not sure why wikipedia doesn't have a standardized graphic-images warning, because this seems to be a textbook case where one would be important - at least for managing expectations and preparing oneself. Most viewers of this page will NOT be specialists. Many will be newly diagnosed with an inflammatory condition and looking for help. Clearly the images are important and should remain, but I found the images traumatic to view and would have been prepared for them with a simple warning.

it is very hard to watch them.. do something... GOER 11:52, 21 July 2007 (UTC)

If you find these pictures hard to digest then I am not sure why you are viewing a pathology site. These images go hand in hand with the pathological outcomes of inflammation. 09:02 20 August 2007. —The preceding unsigned comment was added by 203.34.164.71 (talk) 23:03:10, August 19, 2007 (UTC)

I agree with the reply, the pictures are part of the topic. In fact there are not enough disgusting pictures. It is a pity decent photographs are so hard to come by. FQ1513 (talk) 23:29, 22 December 2007 (UTC) discusting.. make you puke!!! —Preceding unsigned comment added by 67.140.211.227 (talk) 00:01, 9 January 2009 (UTC)

Need Help[edit]

I have started a new page called inflammatory diseases of unknown etiology and would like some help answering these questions: What are the inflammatory diseases of unknown etiology? How many of them are there? What are the most common inflammatory diseases of unknown etiology? What kind of inflammation is associated with inflammatory diseases of unknown etiology? And how many kinds of inflammation patterns are there in inflammatory diseases of unknown etiology? If anyone has the time to contribute it would be appreciated. ReasonableLogicalMan(Talk 20:32, 18 November 2007 (UTC)

treatment options?[edit]

Shouldn't this page include a section on treatment options to be of service to those who suffer from chronic inflammatory conditions? FQ1513 (talk) 23:25, 22 December 2007 (UTC)

Not necessarily. Inflammation is a perfectly normal process. It doesn't necessarily need to be treated at all, and even when it does, the best treatment depends on the actual cause. A treatment section would basically boil down to "Inflammation normally goes away by itself, and when it doesn't, then you need to figure out the cause and treat the cause." A list of all possible treatments for all kinds of inflammation would be a mile long and basically useless. WhatamIdoing (talk) 19:45, 23 January 2008 (UTC)

pictures may detract from readability for some readers.[edit]

pictures may detract from readability for some readers. --Emesee (talk) 16:08, 25 January 2008 (UTC)

do we have to have the gross pictures right next to the text? i mean isn't there a picture of a stubbed toe we could use, rather than a scene from The Mummy Returns? [1] Makeswell (talk) 08:44, 15 March 2010 (UTC)

polymorphonuclear leukocytes[edit]

I don't believe the term "polymorphonuclear leukocytes" is used anywhere on the page as it is now. It might add to the page if the term was mentioned where appropriate. ReasonableLogicalMan(Talk 02:44, 26 February 2008 (UTC)

muscle strain inflammation[edit]

I was given COX-2 inhibitors to get rid of a painful inflammation in my hand that persist for several weeks (I lift weights, was on a month off, pulled a muscle when I came back).

I was surprised to find that muscle strain is not listed as causing inflammation. Indeed, the article implies such inflammation is either an external entity (virus) or autoimmune problem. From other inet sources I've learned that pulled muscles have broken fiber, leading to inflammation which is mostly self-sustained (in a way, an autoimmune problem) hence COX-2 inhibitors treatment resolve the issue. I'd like to see details added here by a professional. —Preceding unsigned comment added by 79.176.101.39 (talk) 17:25, 6 February 2009 (UTC)

It kills —Preceding unsigned comment added by 24.4.199.129 (talk) 03:59, 9 April 2009 (UTC)



You're right. Stress is an important initiator of inflammation. See "danger theory" —Preceding unsigned comment added by 71.67.101.104 (talk) 01:53, 6 October 2009 (UTC)

The first sentence[edit]

"Inflammation is the complex biological response of vascular tissues..." Vascular tissue seems to be a term from plant biology. Does this intro' sentence mean "blood vessels" or "tissue infused with blood vessels"? If you know, please clarify. Anthony (talk) 14:35, 7 October 2009 (UTC)


Agreed. While the cardinal signs of inflammation are mediated through changes in the vascular tissue (vasodilation, endothelial permeability), conceptually, contemporary understanding of inflammation is much broader than this and includes at least the immune system as well. —Preceding unsigned comment added by Gregnz (talkcontribs) 21:51, 25 November 2009 (UTC)

Pictures, Particularly the Greeting Photo[edit]

Some of the previous posters are correct. Particularly, the first picture detracts from the readability/digestibility of the article. If you (the reader) are in favor of this picture, please try not to take offense at the following remarks, but please try to look at the criticism objectively. The picture needs to be more "diplomatic", and not offensive to 30 to 50 to who-knows-what percentage of the readers. Just because the picture-insert-er and this article's favorite moderators have developed a stomach for such a picture (with extra-articular information such as necrotic tissue and puss in the middle) does not mean that they should show their stamina off to the rest of the population. Again, if you (the reader) are one such as this, please, try not to take offense at the anti-current-picture camp's remarks, but objectively look at the picture, the article's title, and what others have said before me.

This site is not intended to be a comprehensive, professional, medical resource per se, but is a reference for the general population of the world. It should not be forcing it's subscribers to high-tolerance-necessary, professional, overkill photos, just because someone found or created what was to them "the perfect photo" for what belongs to a more specialized topic than "Inflammation", or to a professional medical reference where the subscribers are expected -- by the nature of their career -- to have developed the tolerance/stomach for such images.

In summary, the previous objectors have a point, and it ought not be ignored only because of their potential lack of credentials. At least, the more offensive pictures should be found at the bottom of the article, if not instead as part of a more acute or specialized article on the subject to which "black rings of necrotic tissue surrounding pus" might more readily pertain, particularly as a greeting photo. It can be assumed that when the general population of the world goes looking for an article on "inflammation", they are likely not thinking of "black rings of necrotic tissue, surrounding central areas of pus", both of which are not even a component of "Inflammation". The picture that should be used as the greeting picture, should be one that has as it's prominent feature, the five "cardinal signs" of inflammation (necrotic tissue and pus "not" being members of this list). The current greeting picture clearly should be changed or removed.

Hypocritus (talk) 16:20, 16 June 2010 (UTC)

Would this be better? Anthony (talk) 09:40, 20 September 2010 (UTC)
Done. Anthony (talk) 04:30, 27 September 2010 (UTC)

New category/template for diseases with significant inflammatory factor but unknown/diverse etiology?[edit]

Trying to stick fibrosclerosis into some category, I noticed that eg sarcoidosis does not have the inflammation category either. How to add them into some template/category? Richiez (talk) 08:13, 20 September 2010 (UTC)

Question[edit]

Any reason that 'Interstitial Cystitis' in the list of inflammatory disorders is not linked to the page with that title? Seems like a no-brainer, to a layman anyway ... —Preceding unsigned comment added by Foolishearthling (talkcontribs) 15:16, 30 April 2011 (UTC)

Draft section, with footnotes - Neurogenic inflammation[edit]

Neurogenic inflammation is inflammation arising from the local release from afferent neurons of inflammatory mediators such as Substance P and Calcitonin Gene-Related Peptide (CGRP).

This process appears to play an important role in the pathogenesis of numerous diseases including psoriasis,[1] asthma, fibromyalgia, eczema, rosacea, dystonia, multiple chemical sensitivity,[2] and migraine.[3][4][5]

In migraine, stimulation of the trigeminal nerve causes neurogenic inflammation via release of neuropeptides including Substance P, nitric oxide, vasoactive intestinal polypeptide, 5-HT, Neurokinin A and CGRP.[6][7]

Treatment[edit]

The treatment of migraine with CGRP blockers show promise.[8] In early trials, the first oral nonpeptide CGRP antagonist, MK-0974 (Telcagepant), was shown effective in the treatment of migraine attacks,[9] but elevated liver enzymes in two participants were found. Other therapies and other links in the neurogenic inflammatory pathway for interruption of disease is under study, including migraine therapies.[10]

Noting that botulinum toxin has been shown to have an effect on inhibiting neurogenic inflammation, and evidence suggesting the role of neurogenic inflammation in the pathogenesis of psoriasis, the University of Minnesota has begun a clinical trial to follow up on the observation that dystonia patients treated with botulinum toxin had dramatic improvement in psoriasis symptoms.[11]

Astelin (Azelastine) "is indicated for symptomatic treatment of vasomotor rhinitis including rhinorrhea, nasal congestion, and post nasal drip in adults and children 12 years of age and older."[12]

Statins may be useful for treating diseases presenting with predominant neurogenic inflammation.[13]

References[edit]

  1. ^ Saraceno, R; Kleyn, CE; Terenghi, G; Griffiths, CE (2006). "The role of neuropeptides in psoriasis". The British journal of dermatology. 155 (5): 876–82. doi:10.1111/j.1365-2133.2006.07518.x. PMID 17034513.
  2. ^ Bascom, R; Meggs, WJ; Frampton, M; Hudnell, K; Killburn, K; Kobal, G; Medinsky, M; Rea, W (1997). "Neurogenic inflammation: with additional discussion of central and perceptual integration of nonneurogenic inflammation". Environmental health perspectives. 105 Suppl 2: 531–7. PMC 1469802. PMID 9167992.
  3. ^ Frediani, F; Villani, V; Casucci, G (2008). "Peripheral mechanism of action of antimigraine prophylactic drugs". Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology. 29 Suppl 1: S127–30. doi:10.1007/s10072-008-0903-8. PMID 18545913.
  4. ^ Peroutka, SJ (2005). "Neurogenic inflammation and migraine: implications for the therapeutics". Molecular interventions. 5 (5): 304–11. doi:10.1124/mi.5.5.10. PMID 16249526.
  5. ^ Geppetti, P; Capone, JG; Trevisani, M; Nicoletti, P; Zagli, G; Tola, MR (2005). "CGRP and migraine: neurogenic inflammation revisited". The journal of headache and pain. 6 (2): 61–70. doi:10.1007/s10194-005-0153-6. PMID 16362644.
  6. ^ Arun A Kalra, AA; Debra Elliott, D (2007). "Acute migraine: Current treatment and emerging therapies". Ther Clin Risk Manag. Dove Medical Press Limited. 3 (3): 449–459. PMC 2386351. PMID 18488069. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  7. ^ Andrea Stephanie Link, AS; Anikó Kuris, A; Edvinsson, L; et al. (2008). "Treatment of migraine attacks based on the interaction with the trigemino-cerebrovascular system". J Headache Pain. Biomedical Center Lund. 9 (1): 5–12. doi:10.1007/s10194-008-0011-4. PMC 2245994. PMID 18217201. Unknown parameter |month= ignored (help); Explicit use of et al. in: |last2= (help); |access-date= requires |url= (help)
  8. ^ Durham, PL; Vause, CV (2010). "Calcitonin gene-related peptide (CGRP) receptor antagonists in the treatment of migraine". CNS drugs. 24 (7): 539–48. doi:10.2165/11534920-000000000-00000. PMID 20433208.
  9. ^ Farinelli, I; Missori, S; Martelletti, P (2008). "Proinflammatory mediators and migraine pathogenesis: moving towards CGRP as a target for a novel therapeutic class". Expert review of neurotherapeutics. 8 (9): 1347–54. doi:10.1586/14737175.8.9.1347. PMID 18759547.
  10. ^ Farinelli, I; De Filippis, S; Coloprisco, G; Missori, S; Martelletti, P (2009). "Future drugs for migraine". Internal and emergency medicine. 4 (5): 367–73. doi:10.1007/s11739-009-0273-0. PMID 19551474.
  11. ^ Use of Botulinum Toxin to Treat Psoriasis
  12. ^ Product Information: Astelin®, azelastine. Wallace Laboratories, Cranbury, NJ. (PI Revised 08/2000) PI Reviewed 01/2001
  13. ^ Bucelli, RC; Gonsiorek, EA; Kim, WY; Bruun, D; Rabin, RA; Higgins, D; Lein, PJ (2008). "Statins decrease expression of the proinflammatory neuropeptides calcitonin gene-related peptide and substance P in sensory neurons". The Journal of pharmacology and experimental therapeutics. 324 (3): 1172–80. doi:10.1124/jpet.107.132795. PMID 18079356.

External links[edit]

There may be helpful research for expanding this article in the discussion section, http://en.wikipedia.org/wiki/Talk:Neurogenic_inflammation.


Ocdnctx (talk) 13:03, 1 May 2011 (UTC)

Perhaps a section is needed on role of inflammation in promoting diabetes? Inflammation and cancer?[edit]

The study of inflammation is exploding.

Perhaps sections are needed on role of inflammation in promoting

Diabetes?

Inflammation and cancer?

Inflammation and circulatory/cardiac disease (fairly recent recognution of the role of "unstable plaques").

Ocdnctx (talk) 20:05, 1 May 2011 (UTC)

section atherosclerosis[edit]

The complete section to atherosclerosis is barely a copy of the abstract of the paper by Libby, Ridker and Maseri, "Inflammation and atherosclerosis." published in circulation in 2002. — Preceding unsigned comment added by 145.100.194.53 (talk) 21:32, 7 November 2011 (UTC)

Sleep[edit]

Can somebody please add the benefit of sufficient and regular sleep for inflammation to this article - it is VERY surprising that, at time of writing, the word "sleep" doesn't even appear in it. --New Thought (talk) 20:00, 5 August 2012 (UTC)

Depression[edit]

Two claims are made: (1) that "negative cognition" causes inflammation and (2) that inflammation causes depression. While the latter is plausible (if not particularly interesting), the former is surprising and calls out for strong evidence. The citation given is a psychology paper about social prejudice and depression, and inflammation is not mentioned in the abstract. Even if the paper does claim thoughts cause inflammation, establishing this seems well beyond its scope. 216.239.45.130 (talk) 00:14, 9 July 2013 (UTC)

As someone who has both, I found the later particularly interesting! But to add to this area, I have found a paper named "From stress to inflammation and major depressive disorder: a social signal transduction theory of depression" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4006295/ - which appears to support the whole statement. I haven't read the whole article yet, but the sentence:

"Central to this social signal transduction theory of depression is the hypothesis that experiences of social threat and adversity up-regulate components of the immune system involved in inflammation"

in the abstract supports, if not the 1st claim directly, at least a similar statement - that stress has been shown to increase inflamation. It is further supported by the passage:

"A large number of naturalistic and laboratory-based studies have examined whether stress is associated with inflammation. As we review below, these studies strongly support such an association. Moreover, consistent with the CTRA model presented earlier (see Figure 1) and with the data just described linking social rejection and depression, associations between stress and inflammation appear to be particularly strong for stressors that indicate the presence of possible physical or social threat. To examine these effects, we first review studies showing that early life stress, adulthood life stress, and laboratory-based social stressors are associated with increased inflammatory activity. Then, we discuss neural, genetic, and genomic mechanisms that may be responsible for converting experiences of social stress into inflammation."

--Yyattt (talk) 16:50, 30 November 2017 (UTC)

Signal-to-noise theory[edit]

New user here, but anyway: Signal-to-noise section was added by only one user and has a video as source? Although the idea makes sense to me, can this section be considered a "real" information? — Preceding unsigned comment added by 130.234.128.196 (talk) 21:53, 25 November 2013 (UTC)

Assessment comment[edit]

The comment(s) below were originally left at Talk:Inflammation/Comments, and are posted here for posterity. Following several discussions in past years, these subpages are now deprecated. The comments may be irrelevant or outdated; if so, please feel free to remove this section.

*Requires far more reference diversity than just Robbins for an A-class grading I think -- Serephine talk - 09:44, 30 May 2007 (UTC)

Last edited at 09:44, 30 May 2007 (UTC). Substituted at 18:55, 29 April 2016 (UTC)

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The following Wikimedia Commons file used on this page has been nominated for deletion:

Participate in the deletion discussion at the nomination page. —Community Tech bot (talk) 02:01, 3 November 2018 (UTC)