Assessment of cbiL gene expression and vitamin B12 levels in acne vulgaris: involvement of both in-vivo and in-vitro studies

Document Type : Original Article

Authors

1 Microbiology and Immunology Department, Faculty of Pharmacy, Sinai University, El Arish 45518, Egypt

2 Biochemistry Department, Faculty of Pharmacy, New Mansoura University, Egypt

3 Medical Microbiology and Immunology Department, Faculty of Medicine, Beni-Suef University, Egypt

4 Dermatology Department, Faculty of Medicine, Beni-Suef University, Egypt

Abstract

Acne vulgaris (AV) is a chronic inflammatory disease of the pilosebaceous follicles that affects nearly 90% of teenagers; half of them continue to experience symptoms as adults. There have been several reports of monomorphic acneiform eruptions in patients treated with intramuscular cobalamin injections. The eruptions resolved after the cessation of the therapy. Cyanocobalamin, pyridoxine (B6), and riboflavin (B2) have been reported to exacerbate existing acne. Moreover, it was reported that in acne patients, the serum level of vitamin B12 was significantly decreased after treatment, but no explanation was given. We propose a vitamin B12-mediated bacterial mechanism for acne pathogenesis on the evidence mentioned above. One hundred twenty AV patients were recruited.
     Our results proved that vitamin B12 was involved in the pathogenesis of AV; in vivo, it proved that AV patients had significantly higher serum levels of the vitamin than controls and showed a positive correlation to the disease duration and severity. In vitro, it proved that vitamin B12 supplementation to p. acnes cultures significantly raised the porphyrins produced in these cultures when compared to the non-supplemented ones. It also proved that this shift in the metabolism is secondary to inhibition of the cbiL gene of the vitamin B12 synthesis in the bacteria; as porphyrins and vitamin B12 share the same precursors, vitamin B12 does has a role in either elicitation or aggravation of AV.
 

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