Background Information:
Psoriasis is an autoimmune disease that affects 1-3% of the world’s population and is influenced by both genetic and environmental factors, such as diet, stress-level, skin-care routine, etc. (Alekseyenko et al., 2013). People with psoriasis suffer from lesions (often called plaques) of dry, red, itchy, inflamed, and often “scaly’ skin (Langley et al., 2005). Lesions are created, in part, by an overactive inflammatory response in the skin, as well as the increased division of specific cells of the epidermis. In the recent past, researchers have specifically identified immune cells that play a role in this process by producing chemicals that increase inflammation (Chang et al., 2018; Lowes et al., 2008).
Today, it’s not uncommon knowledge that microbes live inside and on us, generating our microbiome (Turnbaugh et al., 2007). The microbiome is associated with many inflammatory diseases, such as irritable bowel syndrome, so it’s only logical to start looking for an association with psoriasis (Chang et al., 2018). “Alteration of the cutaneous microbiome in psoriasis and potential role in Th17 polarization’ stands out among other studies in this area of interest. This is due to the researchers’ discussion about a need for more stringent sampling protocols, through reviewing past studies and ultimately deciding on following the National Institute of Health Human Microbiome Project sampling protocol (Chang et al., 2018). Related studies have had wildly different sampling and analysis methods, such as using skin swabs vs. biopes, variability between anatomical sites sampled, and different DNA amplification primers being used (Alekseyenko et al., 2013; Chang et al., 2018; Fahlen et al., 2012; Gao et al., 2008; Kong et al., 2017). These highly varied sampling methods have generated conflicting results, such as opposing results on psoriatic skin sample diversity and microbial species abundance, giving rise to inconsistent data for researchers that are hoping to pool participant data across multiple studies (Chang et al., 2018).
Central Question:
Does the skin microbiome have any interaction with psoriasis? In “Alteration of the cutaneous microbiome in psoriasis and potential role in Th17 polarization’, Chang et al. (2018) wanted to look at the possible relationship between psoriasis and the skin microbiome, specifically microbes that may interact with the immune cells previously found to be connected to psoriatic lesions (Lowes et al., 2008). The researchers were motivated to conduct this study because past research indicates that the skin microbiome is important for skin health and that it may affect immune system function, both important factors in psoriasis (Belkaid & Tamoutounour, 2016; Chang et al., 2018; Naik et al., 2013).
Evidence:
Chang et al. (2018) found that healthy skin samples had increased levels of P. acnes and S. epidermis, while psoriasis skin samples had increased colonization of S. aureus and decreased amounts of P. acnes. After identifying these key microbial differences between participant groups, the researchers conducted a mouse model study in order to test if a specific microbial species could cause an increased inflammatory response similar to psoriasis.
The researchers found that only S. aureus, and not S. epidermis or the control, increased the concentration of the immune cells linked to psoriasis lesions. This finding shows that the increase of S. aureus on the skin does increase this inflammatory response. This finding may be linked back to psoriasis as this overactive immune cell plays a large role in the lesions that characterize the disease. The researchers also noted that P. acnes may be a key player in maintaining the balance and stability of the skin microbial community, based on it’s decreased presence in psoriatic samples.
My Questions for the Researchers:
My personal question for the researchers is how they intend to increase the generalizability of their results. I would be interested in their suggestions for possible methods of increasing their sample size, from both psoriatic and healthy populations, while also using more than one geographical location. I would also like to ask the researchers how they intend to build from the current findings. Do they intend to address the directionality of this relationship by exploring whether changes in the microbial community trigger, or exacerbate psoriasis, or whether these shifts in the microbial community are first driven by changes in the psoriatic skin environment?
Further Readings:
If you are particularly interested in psoriasis or it’s interactions with the skin microbiome, I encourage you to read the review, “Skin microbiome: An actor in the pathogenesis of psoriasis’, by Wen-Ming and Hong-Zhong (2018). More in depth information about psoriasis can be found at the National Psoriasis Foundation website and at the American Academy of Dermatology website. Future research on this topic is sure to hold exciting information. By following more stringent sampling and data analysis protocols, and improving generalizability, researchers can generate a more reliable data set as a whole. This is important for producing strong scientific research, as well as for cross-study comparisons and increasing our overall knowledge on the relationship between the skin microbiome and psoriasis (Chang et al., 2018; Kong et al., 2017).
References:
- Alekseyenko et al. (2013). Community differentiation of the cutaneous microbiota in psoriasis. Microbiome, doi: 10.1186/2049-2618-1-31
- Belkaid and Tamoutounour. (2016). The influence of skin microorganisms on cutaneous immunity. Nature Reviews Immunology, doi: 10.1038/nri.2016.48
- Chang et al. (2018). Alteration of the cutaneous microbiome in psoriasis and potential role in Th17 polarization. Microbiome, doi: 10.1186/s40168-018-0533-1
- Fahlen et al. (2012). Comparison of bacterial microbiota in skin biopsies form normal and psoriatic skin. Archives of Dermatological Research, doi: 10.1007/s00403-011-1189-x
- Gao et al. (2008). Substantial alterations of the cutaneous bacterial biota in psoriatic lesions. PLoS One, doi: 10.1371/journal.pone.0002719
- Kong et al. (2017). Performing skin microbiome research: A method to the madness. Journal of Investigative Dermatology, doi: 10.1016/j.jid.2016.10.033
- Langley et al. (2005). Psoriasis: Epidemiology, clinical features, and quality of life. Annals of the Rheumatic Diseases, doi: 10.1136/ard.2004.033217
- Lowes et al. (2008). Psoriasis vulgaris lesions contain discrete populations of Th1 and Th17 T cells. Journal of Investigative Dermatology, doi: 10.1038/sj.jid.5701213
- Naik et al. (2013). Compartmentalized control of skin immunity by resident commensals. Science, doi: 10.1126/science.1225152
- Turnbaugh et al. (2007). The human microbiome project: exploring the microbial part of ourselves in a changing world. Nature, doi: 10.1038/nature06244
- Wen-Ming and Hong-Zhong. (2018). Skin microbiome: An actor in the pathogenesis of psoriasis. Chinese Medical Journal, doi: 10.4103/0366-6999.221269