About model of psoriasis pathogenesis (simplified)
A few words about the model of psoriasis pathogenesis. According to this model, psoriasis is a consequence of increased kPAMP levels (specific bacterial products) in blood flow. Two main factors for the increased kPAMP levels in blood flow:
SP1. Small intestinal hyperpermeability for bacterial products with PAMP .
SP2. Small intestinal bacterial overgrowth (SIBO) with PsB-bacteria.
SP1 determines the amount of bacterial products that can penetrate into blood through small intestinal wall (conventionally, every minute through every cm2).
SP2 determines the quantity and range of bacterial products constantly formed in parietal biofilm of small intestine (conventionally, every minute on every cm2).
Composition of small intestinal parietal microbiome determines the range of bacterial products formed. Among bacteria that can inhabit the small intestine, there are PsB, which are presumable psoriagenic. Their peptidoglycan is similar to that of a well-known pathogen – Streptococcus pyogenes.
It is assumed that antigen causing inadequate response of skin immune system originates from fragments of peptidoglycan forming cell wall of psoriagenic bacteria.
And when this antigen gets into skin, it is taken up by blood neutrophils, which, firstly, endocytose bacterial products in blood, secondly, are attracted to inflamed skin, and thirdly, may undergo NETosis (self-destruction) in inflamed skin. Action of one from two factors SP1 and SP2 is sufficient for chronically elevated level of kPAMP in blood (and, consequently, psoriasis maintenance). A long-term and stable remission of psoriasis is possible only with normalization of kPAMP concentration in blood.
And such normalization is only possible when both small intestine permeability for bacterial products and small intestinal bacterial overgrowth (SIBO) level are within normal limits.
Small intestinal bacterial overgrowth (SIBO) in psoriatic patients.
An excess concentration of parietal small intestine microbiome above norm is called SIBO (small intestinal bacterial overgrowth syndrome). The first studies of small intestinal microbiome in psoriatic patients were conducted back in 2009-11. A classic small intestinal bacterial overgrowth (SIBO) test was performed on 121 psoriatic patients and a control group of 43 healthy persons. Small intestinal bacterial overgrowth (SIBO) was detected in 78% of patients. Average total microbial count was 3x10e6, which is significantly higher than in the control group – 1,1x10e3. Correlation was found between small intestinal bacterial overgrowth (SIBO) level and the type, severity and duration of psoriasis.
Pathogenic and presumable psoriagenic bacteria were detected in the majority of patients. In 65% of patients, bacteria of genus Enterococcus (mainly Enterococcus faecalis) were found – on average 2x10e5, in 9% – Streptococcus pyogenes, in 30% – viridans streptococci. In the control group, these types of bacteria were not detected (Peslyak 2012c, Gumayunova 2009a, Gumayunova 2016, Nesterov 2009). In the following years, such studies were performed on many psoriatic patients. SIBO with pathogenic and/or presumable psoriagenic bacteria was almost always found.
Abbreviations and terms
| PAMP | Pathogen-associated molecular patterns (in particular kPAMP ) |
| PsB | Presumable psoriagenic bacteria – species of bacteria with PG-Y peptidoglycan |
| kPAMP | LPS, PG, bacDNA |
| LPS | Lipopolysaccharide |
| PG | Peptidoglycan |
| bacDNA | Bacterial DNA |
| SIBO | Small intestine bacterial overgrowth |
Detailed in (Peslyak & Korotky 2020).
Bibliography
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