Hyaluronic Acid – Yes, Size Does Matter! Being touted by some as a “better” hyaluronic acid (HA) for skin application, low molecular weight  hyaluronic acid (LMW- HA) is in fact a potent stimulus for inflammation and scarring. We at BFT have found a major disconnect between what the cosmetic industry says is true, and what actual scientists say is true. We find a number of products claiming to contain a new, improved form of HA that is “low molecular weight”. But, in keeping with  their usual habit, do the wrong experiments and then misinterpret the results to put a positive spin on the matter. Hyaluronic acid (HA) is ubiquitous in mammals, forming a key component of connective tissue in our bodies.

The average person has roughly 1. HA in the body, one- third of which is turned over (degraded and re- synthesized) every day. HA is an important structural molecule in the extracellular matrix of our skin. It is synthesized there by fibroblasts, fibrocytes, and by roving stem repair cells derived from bone marrow(MSC’s)  that show up in case of wounding and other forms of damage. HA is used therapeutically – it is the stuff of facial fillers, and can be applied topically as a humectant. Being a very large molecule it does not penetrate and instead sits of the skin surface where it binds to water to maintain hydration, and cross links with other HA molecules to knit together a temporary barrier. The size of these can vary from low(LMW- HA) to medium (MMW- HA) molecular weights.

HMW- HA has been shown to attenuate the inflammatory response, suggesting that HMW- HA promotes regenerative healing in adult wounds. Other scientific peer- reviewed publications peg LMW- HA as pro- inflammatory by multiple mechanisms: they stimulate macrophages to produce inflammatory chemokines, induce interferons, recruit T- cells, induce IL- 1.

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NO2. In both adults and fetuses, HA levels increase in response to wounding. However, unlike adults, fetuses produce much more HMW- HA in response to injury. A fine reticular pattern is produced in the non.

HMS- HA, whereas a more disorganized pattern is seen when HA fragments abound. So, in some ways, adding LMW- HA topically may replicate that cascade of events. Exposure of human melanoma cells to small HA fragments leads to nuclear factor k. B (NFk- B) activation followed by enhanced expression of matrix metalloprotease (MMP) 2 and interleukin (IL)- 8, factors that can contribute to melanoma progression. Make sure the formulator didn’t fall prey to marketing materials from one of those too- clever- by- half ingredients manufacturers who make up a good story but haven’t a clue about the real science.

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Caveat emptor! Jiang D1, Liang J, Noble PW. Hyaluronan as an immune regulator in human diseases. Physiol Rev. 2. 01. Jan; 9. 1(1): 2. 21- 6. PMID: 2. 12. 48. 16. Accumulation and turnover of extracellular matrix components are the hallmarks of tissue injury.

Fragmented hyaluronan stimulates the expression of inflammatory genes by a variety of immune cells at the injury site. Hyaluronan binds to a number of cell surface proteins on various cell types. Hyaluronan fragments signal through both Toll- like receptor (TLR) 4 and TLR2 as well as CD4. Targeting Inflammatory Cytokines and Extracellular Matrix Composition to Promote Wound Regeneration.

Adv Wound Care (New Rochelle). Apr 1; 3(4): 3. 44- 3. PMID: 2. 47. 57. 58. Significance: Delayed wound healing is one of the most challenging complications of several diseases, including diabetes.

There is a vast interest in finding efficient treatments that promote scarless wound healing. The ability of the fetus to regenerate skin wounds after injury has generated much interest in the fetus as a model of regeneration.

In this review, we evaluate the role and differential regulation of inflammation, extracellular matri . Hyaluronan fragments induce cytokine and metalloprotease upregulation in human melanoma cells in part by signalling via TLR4. Exp Dermatol. 2. 00. Feb; 1. 7(2): 1. 00- 7. PMID: 1. 80. 31. 54. Small fragments of the extracellular matrix component hyaluronic acid (s. HA) are typically produced at sites of inflammation and tissue injury and have been shown to be associated with tumor invasiveness and metastasis.

Here we report that exposure of human melanoma cells to s. HA leads to nuclear factor k.

B (NFk- B) activation followed by enhanced expression of matrix metalloprotease (MMP) 2 and interleukin (IL)- 8, factors that can contribute to mela . Goon Last Of The Enforcers (2017) Online. Contact sensitizers induce skin inflammation via ROS production and hyaluronic acid degradation.

PMID: 2. 28. 48. 46. Allergic contact dermatitis (ACD) represents a severe health problem with increasing worldwide prevalence. It is a T cell- mediated skin disease induced by protein- reactive organic and inorganic chemicals. A key feature of contact allergens is their ability to trigger an innate immune response that leads to skin inflammation. Previous evidence from the mouse contact hypersensitivity (CHS) model suggests a role for endogenous activators of innate i . Hyaluronan fragments induce IFN. J Inflamm (Lond).

May 3. 0; 1. 0(1): 2. PMID: 2. 37. 21. 39.

The extracellular matrix plays a critical role in insuring tissue integrity and water homeostasis. However, breakdown products of the extracellular matrix have emerged as endogenous danger signals, designed to rapidly activate the immune system against a potential pathogen breach. Type I interferons play a critical role in the immune response against viral infections.

In the lungs, hylauronan (HA) exists as a high molecular weight, biologically i . Hyaluronan fragments synergize with interferon- gamma to induce the C- X- C chemokines mig and interferon- inducible protein- 1. J Biol Chem. 1. 99. Dec 2. 5; 2. 73(5. PMID: 9. 85. 70. 43.

Hallmarks of chronic inflammation and tissue fibrosis are increased influx of activated inflammatory cells, mediator release, and increased turnover and production of the extracellular matrix (ECM). Recent evidence has suggested that fragments of the ECM component hyaluronan play a role in chronic inflammation by inducing macrophage expression of chemokines. Interferon- gamma (IFN- gamma), an important regulator of macrophage functions, has been sh . Induction of IL- 1. Sep 1; 1. 59(5): 2.

PMID: 9. 27. 83. 43. Components of the extracellular matrix (ECM) can regulate leukocyte activation and function at inflammatory sites. Low molecular weight fragments of the ECM glycosaminoglycan hyaluronan (LMW- HA) that accumulate in inflammation, but not the ubiquitous high molecular weight form of HA (HMW- HA), have been shown to induce cytokine and/or chemokine production by alveolar and bone- marrow derived macrophages.

To determine the cellular requirements for r . Hyaluronan fragments induce nitric- oxide synthase in murine macrophages through a nuclear factor kappa. B- dependent mechanism. J Biol Chem. 1. 99. Mar 2. 1; 2. 72(1.

PMID: 9. 06. 54. 73. Download The Show (2017) Movie In Hd. Activated macrophages play a critical role in controlling chronic tissue inflammation through the release of a variety of mediators including cytokines, chemokines, growth factors, active lipids, reactive oxygen, and nitrogen species. The mechanisms that regulate macrophage activation in chronic inflammation are poorly understood. A hallmark of chronic inflammation is the turnover of extracellular matrix components, and recent work has suggested .

Hyaluronan (HA) fragments induce chemokine gene expression in alveolar macrophages. The role of HA size and CD4. J Clin Invest. 1. Nov 1. 5; 9. 8(1. PMID: 8. 94. 16. 60.

Hyaluronan (HA) is a glycosaminoglycan constituent of extracellular matrix. In its native form HA exists as a high molecular weight polymer, but during inflammation lower molecular weight fragments accumulate. We have identified a collection of inflammatory genes induced in macrophages by HA fragments but not by high molecular weight HA. These include several members of the chemokine gene family: macrophage inflammatory protein- 1alpha, macrophage .