Ceramides and Programmed Cell Death
I'm not promoting TriCeram by Osmotics or EpiCeram by Ceragenix ... not because they cost and arm and a leg, but because they are just trying to do the job of sebum and we know your own sebum is better. We also know that putting oils on your skin causes your skin to produce less oils. Dr. Peter Elias, M.D., Professor of Dermatology at the University of
California, San Francisco and Ceragenix' Chief Scientific Officer has even published on this very phenomenon. He discovered that the skin works as a bio sensor and actually perceives that an occlusive film barrier downregulates the production of barrier lipids so that once the cream is gone, you are left with dry skin ... but I'm sure they don't advertise that.
Ceragenix/EpiCeram does, however, advertise that people with atopic dermatitis have decreased ceramides. They themselves even told me that staph makes an enzyme that feeds on ceramides. So, why not just control staph, build and protect your own sebum, and increase glutamine instead for cellular proliferation and lipogenesis by human sebaceous glands. (Sebum is produced when the sebaceous gland disintegrates.) Note that sebum is antimicrobial, which is another one of EpiCeram's boasts about ceramides.
Research seems to point towards avoiding ceramide accumulation anyway ...
LINKS
- Ceramidase Activity in Bacterial Skin Flora as a Possible Cause
of Ceramide Deficiency in Atopic Dermatitis
 In the present study, we provide evidence that CDase is
present in the skin of patients with AD, secreted from P.
aeruginosa and/or related strains, suggesting that such exogenous
enzymes may be involved in the pathogenesis of AD. The
enzyme activities may result in ceramide deficiency, thus disturbing
the permeability barrier function of the stratum corneum
while accelerating the immune reaction and eventually
resulting in the predominance of S. aureus in the skin of patients
with AD. The finding that the skin of patients with AD is colonized by ceramidase-secreting bacteria
thus suggests that microorganisms are related to the deficiency of ceramide in the horny layer of the epidermis,
which increases the hypersensitivity of skin in AD patients by impairing the permeability barrier.
- Journal of Investigative Dermatology on Ceramides In addition to being a major factor in both the permeability barrier and the maintenance of the water reservoir of the skin, ceramide, and/or its metabolites appear to be involved in the proliferation, differentiation, and apoptosis of epidermal keratinocytes
- Ceramides inhibit cell growth and are potent inducers of apoptosis, a form of programmed cell death
- Ceramide accumulation mediates inflammation, cell death and infection susceptibility in cystic fibrosis. The accumulation of ceramide causes Cftr-deficient mice to suffer from constitutive age-dependent pulmonary inflammation, death of respiratory epithelial cells, deposits of DNA in bronchi and high susceptibility to severe Pseudomonas aeruginosa infections
- Ceramides or their metabolites could contribute to adverse effects of long-chain fatty acids on insulin resistance and inflammation.
- They show that the lipid mediator ceramide mediates apoptosis of cells in the lungs of mice, leading to pulmonary emphysema. The authors further support the relevance of these findings to humans, showing that ceramide is upregulated in the lungs of patients with bronchitis and emphysema. Ceramide is a highly regulated sphingolipid second messenger. The molecule is produced by a variety of tissues in response to a number of stimuli including endotoxin, oxidative stress and cytokines. Ceramide coordinates stress responses, modulates oxidative and proliferative responses and is a potent inducer of apoptosis.
- Ceramide regulates SR protein phosphorylation during adenoviral infection. The use of inhibitors of ceramide synthesis resulted in a significant delay in cell lysis, suggesting that ceramide was necessary for the lytic phase of the infection.
Ceramide in bacterial infections and cystic fibrosis.
Department of Molecular Biology, University of Duisburg-Essen, Hufelandstrasse 55, D-45122 Essen, Germany.
Ceramide is formed by the activity of sphingomyelinases, by degradation of complex sphingolipids, reverse ceramidase activity or de novo synthesized. The formation of ceramide within biological membranes results in the formation of large ceramide-enriched membrane domains. These domains serve the spatial and temporal organization of receptors and signaling molecules. The acid sphingomyelinase-ceramide system plays an important role in the infection of mammalian host cells with bacterial pathogens such as Neisseria gonorrhoeae, Escherichia coli, Staphylococcus aureus, Listeria monocytogenes, Salmonella typhimurium and Pseudomonas aeruginosa. Ceramide and ceramide-enriched membrane platforms are also involved in the induction of apoptosis in infected cells, such as in epithelial and endothelial cells after infection with Pseudomonas aeruginosa and Staphylococcus aureus, respectively. Finally, ceramide-enriched membrane platforms are critical regulators of the release of pro-inflammatory cytokines upon infection. The diverse functions of ceramide in bacterial infections suggest that ceramide and ceramide-enriched membrane domains are key players in host responses to many pathogens and thus are potential novel targets to treat infections. PMID: 18783339 [PubMed - indexed for MEDLINE]
Activation of bacterial ceramidase by anionic glycerophospholipids: possible involvement in ceramide hydrolysis on atopic skin by Pseudomonas ceramidase.
Since both P. aeruginosa and S. aureus (staph) are suspected of being present in microflora of atopic skin, we speculate that S. aureus-derived glycerophospholipids stimulate the hydrolysis of Ceramide in atopic skin by bacterial ceramidase.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1222425/
See: Proliferation of Sebaceous Glands for Sebum
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