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

TL;DR

This paper proposes that psoriasis originates from intestinal hyperpermeability allowing beta-streptococci to enter and influence the skin immune response, supported by clinical evidence and a new pathogenic model.

Contribution

It introduces a novel pathogenic concept linking intestinal microbiocenosis and permeability to psoriasis development, emphasizing the primary gastrointestinal origin.

Findings

Beta-streptococci presence correlates with psoriasis severity

Intestinal hyperpermeability is common in psoriatic patients

Clinical model supports gastrointestinal origin of psoriasis

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.