Psoriasis as a consequence of incorporation of beta-streptococci into the microbiocenosis of highly permeable intestines (a pathogenic concept)

TL;DR

This paper reviews evidence linking intestinal permeability and beta-streptococci to psoriasis, proposing a new pathogenic model emphasizing gastrointestinal origin and secondary skin symptoms, supported by clinical data.

Contribution

It introduces a novel pathogenic concept that psoriasis originates from intestinal hyperpermeability and bacterial incorporation, shifting focus to gastrointestinal factors in disease development.

Findings

Beta-streptococci presence correlates with psoriasis.

Intestinal hyperpermeability may trigger skin manifestations.

Clinical validation supports the proposed model.

Abstract

A review of recent investigations into pathogenesis of psoriasis summarizing data on the relationship between the presence {\beta}-streptococci in the organism and the cutaneous immune reaction. Results of the studies on gastrointestinal pathology in psoriatic patients are presented. The authors propose a hypothesis that advocates the primary origin of psoriatic gastrointestinal pathology and secondary nature of skin manifestations. A chronic plaque psoriasis model is developed on the basis of the assumption on the key role of two psorafactors, i.e. hyperpermeability of intestinal walls for certain proteins and incorporation of beta-streptococci in the microbiocenosis of intestinal mucosa. The validity of the model is confirmed by the results of practical clinical work.