http://www.ncbi.nlm.nih.gov/pubmed/1795112...Pubmed_RVDocSumA study on zincs effects on inhibiting Toll-like receptors, thus reducing imflammation. This was a topical study, but oral usage of zinc is also used to treat acne. THere is a prescription acne medication for acne called NICOMIDE, since zinc works so well for acne. Guess what, there are TONS of toll like receptors in the gut. Coincidence?
Guardians of the gut: newly appreciated role of epithelial toll-like receptors in protecting the intestine.
http://www.ncbi.nlm.nih.gov/pubmed/1861996...Pubmed_RVDocSumImmune-non immune networks in intestinal inflammation.
http://www.ncbi.nlm.nih.gov/pubmed/1847376...Pubmed_RVDocSumA review on the various mechanisms between bacteria in the gut and gastrointestinal and overall immunity.
http://www.ncbi.nlm.nih.gov/pubmed/1824882...Pubmed_RVDocSumWe analyzed the gut immune stimulation induced by Gram-positive bacteria: non probiotic Lactobacillus acidophilus CRL 1462 and Lactobacillus acidophilus A9; two potentially probiotic strains: L. acidophilus CRL 924 and Lactobacillusdelbrueckii subsp. bulgaricus CRL 423; comparatively with a probiotic strain: Lactobacillus casei CRL 431. We also studied Gram-negative bacteria: Escherichia coli 129 and E. coli 13-7 in BALB/c mice. All the strains increased the number of IgA+ cells. We analyzed the cytokines IFNgamma, TNFalpha, IL-17, IL-12, IL-6 and MIP-1alpha. The Gram(+) strains increased the number of IL-10+ cells. Gram(-) strains did not increase IL-10+ cells, but they increased the number of IL-12+ cells. The probiotic strain increased mainly IFNgamma and TNFalpha. In the study of the receptors TLR-2, TLR-4 and CD-206, we demonstrated that only the probiotic strain increased the number of CD-206+ cells.
All the Gram(+) strains increased the number of TLR-2+ cells and the Gram(-) strains of the TLR-4+ cells. The probiotic strain induced the release of IL-6 by a preparation enriched in intestinal epithelial cells (IEC). Gram(+) and Gram(-) bacteria activated different immune receptors and induced a different cytokine profile. The probiotic strain showed a great activity on the immune cells and the enriched population in IEC, activating mainly cells of the innate immune system.
http://www.ncbi.nlm.nih.gov/pubmed/1737971...Pubmed_RVDocSumHelicobacter hepaticus colonizes the murine intestine and has been associated with hepatic inflammation and neoplasia in susceptible mouse strains. In this study, the catalase of an enterohepatic Helicobacter was characterized for the first time. H. hepaticus catalase is a highly conserved enzyme that may be important for bacterial survival in the mammalian intestine. Recombinant H. hepaticus catalase was expressed in Escherichia coli in order to verify its enzymic activity in vitro. H. hepaticus catalase comprises 478 amino acids with a highly conserved haem-ligand domain. Three conserved motifs (R-F-Y-D, RERIPER and VVHAKG) in the haem-ligand domain and three surface-predicted motifs were identified in H. hepaticus catalase and are shared among bacterial and mammalian catalases. H. hepaticus catalase is present in the cytoplasmic and periplasmic compartments. Mice infected with H. hepaticus demonstrated immune responses to murine and H. hepaticus catalase, suggesting that Helicobacter catalase contains conserved structural motifs and may contribute to autoimmune responses. Antibodies to H. hepaticus catalase recognized murine hepatocyte catalase in hepatic tissue from infected mice. Antibodies from sera of H. hepaticus-infected mice reacted with peptides comprising two conserved surface-predicted motifs in H. hepaticus catalase.
Catalases are highly conserved enzymes in bacteria and mammals that may contribute to autoimmune responses in animals infected with catalase-producing pathogens.An example of how a single strain of bacteria found in the gut (in mice) can produce a product which can cross react with the mice's own enzymes. More importantly, this article shows that autoimmunity may have ties to various types of bacteria in the gut. If it can happen in mice, there is no reason a similar effect can't happen in humans. In fact, this is the case in arthritis induced by Lyme disease.
Immunopathology of Lyme arthritis
http://www.ncbi.nlm.nih.gov/pubmed/1804434...Pubmed_RVDocSumLyme borreliosis (Lyme disease) is the most prevalent tick-borne disease caused by spirochaetes of the Borrelia species complex. Arthritis is one of the common manifestations of B. burgdorferi infection. The pathomechanism of articular changes in Lyme arthritis has not yet been elucidated. Histopathological studies of synovia and immunological changes are similar to rheumatoid arthritis. In the early stage of inflammation B. burgdorferi interact with polynuclear granulocytes and epithelial cells, triggering production of reactive oxygen species, lipid peroxidation products and other inflammatory mediators. The imbalance between anabolic and catabolic processes in inflamed joints results in the progressive destruction of articular cartilage and disintegration of extracellular matrix.
Molecular mimicry between OspA (outer surface protein A) and adhesion molecule LFA-1alpha seems to be responsible for chronic arthritis.Another example of how cross reactivity between a bacteria can cause "seemingly unrelated" arthritis issues.
An abstract from an article which shows how different bacteria can manipulate toll like receptors in the gut
Autoimmunity results from the dysregulation of the immune system leading to tissue damage. Th1 and Th17 cells are known to be cellular mediators of inflammation in autoimmune diseases. The specific cytokine milieu within the site of inflammation or within secondary lymphatic tissues is important during the priming and effector phases of T cell response. In this review, we will address the nature of the inflammatory response in the context of autoimmune disease, specifically we will discuss the role of dendritic cells following stimulation of their innate pathogen recognition receptors in directing the development of T cell responses. We will focus on how dendritic cell subsets change the balance between major players in autoimmunity, namely Th1, Th17 and regulatory T cells. Th17 cells, once thought to only act as pathogenic effectors through production of IL-17, have been shown to have regulatory properties as well with co-production of the anti-inflammatory cytokine IL-10 by a subset now referred to as regulatory Th17 cells. IL-17 is important in the induction of autoimmune diseases such as experimental autoimmune encephalomyelitis (EAE) and inflammatory bowel disease (IBD). Study of the inflammatory process following encounter with agents that stimulate the innate immune responses such as adjuvants opens a new horizon for the discovery of therapeutic agents including those derived from microorganisms.
Microbial products such as adjuvants that function as TLR ligands may stimulate the immune system by interacting with Toll-like receptors (TLR) on antigen-presenting cells.]Microbial agents such as Bacille Calmette-Guérin (BCG) or Freund's adjuvant (CFA) that induce a Th17 response are protective in models of autoimmune diseases particularly EAE and type 1 diabetes (T1D). The induction of innate immunity by these microbial products alters the balance in the cytokine microenvironment and may be responsible for modulation of the inflammation and protection from autoimmunity.I have read many of these papers. They are all from high quality journals, all from 2008 or 2007. This is just an example of just SOME of the information on the connection between toll receptors in acne, toll receptors in autoimmunity, regulation of toll receptors within the gut, and how bacteria can use many methods such as molecular mimicry to cause human pathogenisis.. I found all of these articles within 15 minutes on Pub Med. I can find dozens of other articles which can connect intestinal health with acne. I have read many of them. I can do this all day. I many not know everything, but I do work in a lab, have a deal of experience reading scientific journals so I understand what they are talking about, and am working on my masters in biomolecular sciences.
If you guys want more information which supports the idea connecting intestinal inflammation with skin, I'll be more than happy to dig up more on pub med. I would post the whole journal articles if it was practical.
Other thoughts: As I said before, bacteria aren't the only things which can effect gut health. I don't know much in this area, but there is a growing amount of research of the enteric nervous system (huge nervous network within the intestine that we hardly know anything about. It is also connected to the central nervous system) regulation and gut health. This may be how other factors like mood and sleep can lead to acne. Certain SSRI antidepressants have been shown to be helpful in relieving some bowel related disorders. Considering the fact that there are a high level of neurons within the gut, it is certainly reasonable that there may be SOME connection between gut health and neurotransmitters, and vica versa.Thats why many people with chronic adult acne may also experience issues with depression and chronic fatigue. One more journal entry, just for shits and giggles.
Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
http://www.ncbi.nlm.nih.gov/pubmed/1574047...Pubmed_RVDocSumStress, defined as an acute threat to homeostasis, evokes an adaptive or allostatic response and can have both a short- and long-term influence on the function of the gastrointestinal tract. The enteric nervous system is connected bidirectionally to the brain by parasympathetic and sympathetic pathways forming the brain-gut axis. The neural network of the brain, which generates the stress response, is called the central stress circuitry and includes the paraventricular nucleus of the hypothalamus, amygdala and periaqueductal gray. It receives input from the somatic and visceral afferent pathways and also from the visceral motor cortex including the medial prefrontal, anterior cingulate and insular cortex. The output of this central stress circuit is called the emotional motor system and includes automatic efferents, the hypothalamus-pituitary-adrenal axis and pain modulatory systems. Severe or long-term stress can induce long-term alteration in the stress response (plasticity). Corticotropin releasing factor (CRF) is a key mediator of the central stress response. Two CRF receptor subtypes, R1 and R2, have been described. They mediate increased colonic motor activity and slowed gastric emptying, respectively, in response to stress. Specific CRF receptor antagonists injected into the 0 block these visceral manifestations of stress. Circulating glucocorticoids exert an inhibitory effect on the stress response by receptors located in the medial prefrontal cortex and hippocampus. Many other neurotransmitters and neuroimmunomodulators are being evaluated.
Stress increases the intestinal permeability to large antigenic molecules. It can lead to mast cell activation, degranulation and colonic mucin depletion. A reversal of small bowel water and electrolyte absorption occurs in response to stress and is mediated cholinergically. Stress also leads to increased susceptibility to colonic inflammation, which can be adaptively transferred among rats by sensitized CD4(+) lymphocytes.
The association between stress and various gastrointestinal diseases, including functional bowel disorders, inflammatory bowel disease, peptic ulcer disease and gastroesophageal reflux disease, is being actively investigated. Attention to the close relation between the brain and gut has opened many therapeutic avenues for the future.I haven't read this one yet, but I mean to.