Bacteria are microscopic organisms that have the capacity to infect our body. Although most bacteria do not create harm in our body, those that do may develop into diseases, ones that create discomfort or even death. If you develop a bacterial infection, it is important that you provide treatment for your infection as some infections have the capacity to worsen, or worse, spread towards other body parts. If you have such an infection, the use of antibiotics will be the key in helping you get rid of the infection you have developed. Read more…
Monday, September 17
Wednesday, July 11
|LPS general structure. Supplemental Material: Annu. Rev. Biochem. 2011. 80:917-941. Link.|
|TLR4/MD-2 complex. Annu. Rev. Biochem. 2011. 80:917-941.|
|Fisher-Wellman & Bloomer|
- Altering the composition of lipid rafts. This, in turn, influences protein-protein interactions, as well as coupling ligand-receptor interaction with scaffold and intracellular signaling proteins.
- Producing intermediate molecules, such as prostaglandins. The final effect is difficult to assess, but there seem to be clear differences between the action of metabolites produced from omega 6 (O6) vs. omega 3 (O3).
- Altering membrane permeability. A higher unsaturation index (that is, the degree of unsaturation of phospholipid chains) renders a more fluid membrane, being the opposite true for a low unsaturation index. Increasing the proportion of SFA in cell membranes decreases permeability because unsaturated fatty acids chains form a "kink", increasing the degrees of freedom of the molecules and its physicochemical characteristics (both individually and as a group).
- Providing energy.
- Increased dietary intake of EPA (2.7g/day) has shown to reduce PGE2 production (a metabolite of arachidonic acid) in human mononuclear cells (MNCs).
- Fish oil ingestion has shown to increase the production of 5-series leukotrienes, products derived from EPA.
- EPA/DHA or fish oil also induces the production of resolvins, which have anti-inflammatory properties.
- Increasing membrane permeability by increasing the unsaturation index might increase phagocytosis by MNCs. The phagocytic index of neutrophils and monocytes has shown to be negatively correlated with palmitic acid content, but positively correlated with the content of PUFAs, specifically O3. In healthy humans, 1.5g/day of EPA+DHA for 6 months increased the phagocytic activity in monocytes and neutrophils by 200% and 40%, respectively.
- Arachidonic acid, EPA and DHA have shown to inhbit T-cell proliferation and IL-2 production in vitro. This has been replicated in animal models with fish oil and/or EPA/DHA in high doses. O3 might also affect the composition (and hence function) of lipid rafts, as treatment of T-cells with O3 displaces acylated proteins anchored to the inner lipid leaflet from lipid rafts, but not GPI-anchored proteins. This displacement (probably as a direct consequence of incorporation of EPA and DHA into membranes) affects the intracellular signaling pathway associated with the protein being displaced, such as LAT.
- Increasing the amount of dietary fish oil in rats causes a reduction in MHC II expression on dendritic cells, as well as levels of CD2, CD11a and CD18. Arachidonic acid and DHA, by slowing the transit of new MHC I molecules from the endoplasmic reticulum to Golgi, have shown to decrease surface MHC I expression, decreasing cytotoxic T-cell mediated lysis of target cells enriched in these fatty acids.
Albumin binds fatty acids and LPS
- Saturated fatty acids (SFAs) activate TLR4 and the downstream signaling pathway, ultimately leading to the activation of NFkB, which increases the expression of pro-inflammatory molecules (TNFa, IL-6, etc.).
- SFAs might contribute directly (by interacting with LPS and/or TLR4-MD-2) or indirectly (by reorganizing lipid rafts). In either case, an increase in the level of SFA promotes the activation of this pathway.
- The activation of TLR4 has been shown to be important for the onset and development of metabolic diseases such as obesity, diabetes and non-alcoholic hepatic steatosis.
- LPS uptake is mediated through chylomicrons and is promoted by a loss of barrier function of the small intestine.
- The level of endotoxemia correlates with baseline and post-prandial triglyceride levels.
- O3 PUFAs (EPA and DHA) have shown an inhibitory effect on LPS and LPS plus SFA-induced TLR4 activation.
- The oxidation of O3 PUFAs seems to be necessary for their anti-inflammatory effects.
- The level of SFA in the bloodstream is controlled by diet as well as the cellular energy status.
- MUFAs, in most studies, seem to be neutral. However, there is some evidence linking excess oleate and SCD-1 activity to cellular dysfunction, particularly beta-cell abnormalities. EPA has opposite effects and reduces SCD-1 expression.
- Albumin binds both fatty acids and LPS, and modulates the inflammatory response to a given LPS load. The relative proportion of individual fatty acids bound to albumin might influence the binding of LPS to TLR4, thus affecting the activation of the downstream signaling pathway.
- Reduce and control the amount of O6 PUFA, specially from vegetable sources (linoleic acid).
- Control the amount of SFAs. Consumption of dairy fat seems to be protective against endotoxemia (45). Ghee might be a better option than butter. Better to avoid protein-rich dairy.
- Increase the amount of marine EPA and DHA (O3 PUFAs). This should work best increasing the consumption of marine foods, but might be a problem for those with leaky gut given the presence of some metals in seafood. Individual tolerance must be assessed. If very sensitive, start with dietary supplements. A high dose (3-5g/day of EPA + DHA) might work first, and the those should be lowered afterwards (46). The higher the baseline triglyceride levels, the higher the dose. Additionally, the worse the inflammatory/immune status, the higher and longer the supplementation. This can be assessed using traditional blood markers (C-reactive protein, etc.) and symptoms. It has been shown that the effects of O3 supplementation are influenced by the O3 status of the subject (47). High inflammatory markers and/or symptoms might reflect O3 status.
- Avoid industrial trans-fatty acids.
* Work was presented in the conference. More information when available.
Thursday, July 5
|WD-milk promotes alopecia.|
|Fasting improves metabolic alterations induced by high-fat diets in mice. Copyright © 2012 Elsevier Inc. All rights reserved.|
|Fungi levels are an important part of the murine gut microbiota. This probably occurs also in humans. © 2012 American Association for the Advancement of Science. All Rights Reserved.|
|Copyright © 2012 Elsevier Inc. All rights reserved.|
|Fluorescence imaging of the process of DNA ejection to a single E.coli cell. Copyright © 2012 Elsevier Inc. All rights reserved.|
** It was also lower in PUFA (12.2% in WD vs. 61.8% in chow), but much higher in sucrose (152.8g/kg in WD vs. 0g/kg in chow).
*** Nevertheless, some inflammatory cytokines were still increased compared to control.
Iliev ID, Funari VA, Taylor KD, Nguyen Q, Reyes CN, Strom SP, Brown J, Becker CA, Fleshner PR, Dubinsky M, Rotter JI, Wang HL, McGovern DP, Brown GD, & Underhill DM (2012). Interactions between commensal fungi and the C-type lectin receptor Dectin-1 influence colitis. Science (New York, N.Y.), 336 (6086), 1314-7 PMID: 22674328
Wednesday, March 14
|Relationship between nutrition and the immune system. See text for details.|
- Nutrition influences the composition and function of adipose tissue (AT): Energy intake regulates fat mass, affecting the function and differentiation of pre- and mature adipocytes (direct effect). The concentration of specific fatty acids in AT is proportional to their abundance in the diet (indirect effect). The dietary fatty acid profile also affects membrane lipid composition on other cell types, which regulates cell functioning.
- Adipose tissue is an immune organ: There are several immune cells present in AT from different body sites, differing each one in the proportion of cell types. Lymph nodes present in AT are sorrounded by perinodal adipocytes, which have a higher proportion of polyunsaturated fatty acids (PUFA) than adipocytes far from the nodes. Lymphoid clusters within AT include milky spots (MS) and fat-associated lymphoid clusters (FALCs), which have an active role determining whole-body immune responses. Adipocytes are also able to secrete adipocytokines (leptin, resistin, adiponectin, etc.) and classical cytokines (IL-6, TNF-a, etc.).
- Adipose tissue regulates energy intake: Cytokines secreted by AT regulate appetite and energy balance, acting through neural pathways involved in energy homeostasis.
- Nutrition affects the gut flora: Microbial composition of the human gut flora is very responsive to diet. Small changes in either macronutrient distribution or food choices affect differently not only the relative proportion of certain species, but also their metabolism and gene expression patterns.
- Gut flora regulates fat mass and metabolism: Digestion of plant cell walls, oligosaccharides and other food components by gut bacteria increases the energy yield of food, contributing to energy intake. Acetate and propionate, produced by the fermentation of soluble fiber, are metabolized (predominantly) in skeletal muscle and the liver, respectively. Gut microbiota also supress FIAF activity and promotes hepatic triglyceride synthesis. Metabolism of drugs and xenobiotics is dependent on the composition of the gut flora.
- Gut flora regulates immunity: The presence of specific bacteria shapes the immune system and regulates mucosal and peripheral immune responses. The gut flora also competes with enteropathogens directly and by the action of antimicrobial peptides. Evolutionary co-adaptation has given gut bacteria and other microorganisms essential roles for mammalian health.
- Nutrition regulates immunity: Energy availability and macronutrients regulate the function, maturation and differentiation of immune cells.
Relevant factors for the protocol
Mode of birth
Hygiene practices during childhood
Family diet, diet history and maternal environment
Monday, March 12
- The study identified a "core" atherosclerotic plaque microbiota, comprising higher levels of Proteobacteria and fewer Firmicutes, compared with the gut and oral samples.
- The AP microbiota contained specific OTUs not shared with the analyzed body sites.
- The abundance of some OTUs in the gut and oral cavity was correlated with CVD markers.
- Shared OTUs among sites included Streptococcus and Veillonella, the correlation being stronger among the oral cavity and the AP, and these OTUs were also found in the gut samples from some patients. Across patients, the abundance of both were correlated in the oral cavity and the AP.
Koren O, Spor A, Felin J, Fåk F, Stombaugh J, Tremaroli V, Behre CJ, Knight R, Fagerberg B, Ley RE, & Bäckhed F (2011). Human oral, gut, and plaque microbiota in patients with atherosclerosis. Proceedings of the National Academy of Sciences of the United States of America, 108 Suppl 1, 4592-8 PMID: 20937873
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