Bioethics and Psoriasis Herbert B. Allen * , Rina Allawh, Lauren Ogrich, Neha Jariwala and Erum Ilyas Department of Dermatology, Drexel University College of Medicine, USA * Corresponding author: Herbert B. Allen, Department of Dermatology, Drexel University College of Medicine, 219 N. Broad St, 4th floor, Philadelphia, PA 19107, United States, Tel: 2157625550; Fax: 215762 5570; E-mail: Herbert.Allen@drexelmed.edu Received date: April 05, 2017; Accepted date: May 04, 2017; Published date: May 09, 2017 Copyright: © 2017 Allen HB, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract We have presented the clinical, epidemiological, microbiological, pathological, immunopathological, serological, and therapeutic studies showing how the streptococcus may be strongly linked to psoriasis. With this as background, we have presented three ethical arguments that are cogent for psoriasis. First, this microbial “pathogen” theory is both ignored and overlooked even with the abundance of evidence supporting it. That being the case, current treatments, consequently, are aimed not at the onset of the disease, but much later in the pathogenic cascade. Last, the continued use of “biologics” or costly immunosuppressives, which are not curative, presents bioethical challenges. We consider psoriasis a sequela of streptococcal infection similar to rheumatic fever, where treatment, at the earliest stages of the disease, has resulted in its disappearance. Keywords: Pathogen; Biologics; Serological; Streptococcal pharyngitis Psoriasis-discussion of Microbial Pathogenesis of the Disease We have recently completed an ethical analysis of Lyme disease and have found the ethics to be challenged in all aspects of that disease from diagnosis through laboratory evaluation to treatment and outcomes [1]. Psoriasis difers from Lyme disease in that many fewer targets for ethical discussion are present. Tere are still some that are worthy of evaluation from an ethical standpoint. First and foremost, in the ethics discussion is whether the cause of psoriasis is the streptococcus or not. We have previously presented fndings from clinical, microbiological, immunopathological, serological, epidemiological and therapeutic studies that all point to a streptococcal origin for the disease [2]. A brief discussion of each of those aspects follows. It is well known that guttate psoriasis follows streptococcal pharyngitis. Bacterial cultures and ASO titers may be positive for streptococcus, and the patients routinely beneft from a course of penicillin (or a penicillin derivative) added to their treatment regimen [3]. Plaque psoriasis, however; has no apparent link to streptococcal pharyngitis. Recent observations may illuminate this apparent situation and demonstrate how the bacterium is still present and involved. Streptococci have been shown to internalize in tonsillar epithelial cells, live inside the cells for up to a year, then externalize and recolonize [4]. When they are inside the cells, their presence is not detectable either by culture or serology. Tus, they can be present in the disease but not visible. Another way the organism escapes detection is by forming bioflms. Tese have been shown to be present in tonsillar tissue in psoriasis [5]. Te streptococcal organisms spin out a polysaccharide (slime) coating providing a means to evade the immune system as well as a shield of protection. Periodically, “exporter” cells leave the bioflm, recolonize, and subsequently make new bioflms. Trough internalization and bioflm external formation, the streptococcus has the unique capability to “hide in plain sight” despite having a known presence in psoriasis. Immunopathology provides further insight on the role and impact of bioflms. We have recently found Toll-like receptor 2 (TLR2) in the upper dermal capillaries in biopsies of psoriatic plaques [2]. Located here, in the blood supply of the psoriatic plaques, TLR2 is in a prime location to cause the changes in psoriasis. It is well established that TLR2 activates the MyD88 pathway which has TNFα as its endpoint [2]. TNFα is the “prime” mode by which TLR2 destroys organisms. TLR2 also upregulates IL 17 and IL 12/23 [6,7]. Te TNFα, IL 17 and IL 12/23 are all well-known cytokines involved in the pathogenesis of psoriatic lesions. Inhibition of the above cytokines, results in ultimate clearing of the psoriatic lesions [8] TLR2 targets the bioflms via receptor sites within the bioflm itself [9]. We have shown its presence surrounding the bioflms in the eccrine sweat ducts in eczema and associated with the plaques in the brains of Alzheimer’s disease patients [10,11]. Interestingly, TLR2 has also been found by Carrasco in circulating monocytes in psoriatic arthritis [12]. Te serological fndings in plaque psoriasis are indeed compelling: anti-streptococcal IgG has been shown to be markedly elevated in plaque psoriasis [13]. Of note, the presence of IgG is diferent from ASO titer which is the ordinary serologic marker for streptococcal disease. One might also broadly consider the TLR2 found in the dermal capillaries and the TLR2 on circulating monocytes as part of the serologic response to streptococcus. Te epidemiologic fndings strongly point to streptococcus as the etiology of psoriasis. Most noteworthy in this regard is where there is no streptococcus in the environment (northernmost Europe and certain Pacifc islands), there is no psoriasis. Further, psoriasis becomes more prevalent as streptococcus increases with decreasing latitude [14]. Allen et al., J Clin Res Bioeth 2017, 8:3 DOI: 10.4172/2155-9627.1000304 Commentary Open Access J Clin Res Bioeth, an open access journal ISSN:2155-9627 Volume 8 • Issue 3 • 1000304 Journal of Clinical Research & Bioethics J o u r n a l o f C l i n i c a l R e s e a r c h & B i o e t h i c s ISSN: 2155-9627