Features of the pathogenetic mechanisms of tuberculous peritonitis in an experiment

About authors

1 Moscow Research and Clinical Center for TB Control, Moscow, Russia

2 Pirogov Russian National Research Medical University, Moscow, Russia

3 Saint-Petersburg State Research Institute of Phtisiopulmonology, St. Petersburg, Russia

Correspondence should be addressed: Dmitry Vladimirovich Plotkin
Ostrovityanova, 1, Moscow, 117997; ur.tsil@31nk

About paper

Author contributions: Plotkin DV, Vinogradova TI, Sinitsyn MV, Bogorodskaya EM — study concept and design development; Plotkin DV, Reshetnikov MN, Zhuravlev VYu, Zyuzya YuR — material collection; Reshetnikov MN, Zhuravlev VYu — statistical processing; Plotkin DV, Vinogradova TI, Ariel BM, Yablonsky PK — analysis of the data obtained; Plotkin DV, Ariel BM, Sinitsyn MV, Bogorodskaya EM — text preparation; Vinogradova TI, Zyuzya YuR, Yablonsky PK — editing.

Compliance with ethical standards: the study was approved by the Ethics Committee of the Saint Petersburg Research Institute of Phthisiopulmonology (protocol № 73 of December 23, 2020). All manipulations with animals conformed to the requirements of the European Convention for the Protection of Vertebral Animals Used for Experimental and Other Scientific Purposes (CETS # 170) and followed guidelines provided in GOST 33216-2014 Rules for Working with Laboratory Rodents and Rabbits.

Received: 2021-06-30 Accepted: 2021-07-21 Published online: 2021-08-04

The prevalence of tuberculous peritonitis that has been observed in the recent decades is the result of lymphohematogenous spread of Mycobacterium tuberculosis (MBT) from lungs and other extrapulmonary sources. It is still unclear why certain organs and anatomical regions get involved in the inflammatory process during generalization of the tuberculosis infection. Why do some cases develop into peritoneal tuberculosis and other into kidney tuberculosis? Thus study aimed to investigate the pathogenesis of tuberculous peritonitis in a reproducible biological model. Tuberculous peritonitis was modeled in 18 rabbits (10 in the test group, 8 in control) by intraperitoneal inoculation of the MBT suspension. In order to suppress peritoneal macrophages and major cytokines, test group rabbits were injected with the TNFα inhibitor and iron (III) hydroxide sucrose complex before being infected, while control group rabbits received no immunosuppressive drugs. Autopsy of the control group animals revealed changes characteristic of pulmonary tuberculosis in 37.5% of cases, with no damage to other organs and systems registered. Conversely, test group rabbits had the signs of tuberculous peritonitis in their abdominal cavities. The results of this study suggest that it is the local immunity of an anatomical area that largely determines whether a secondary focus of extrapulmonary tuberculosis infection will develop there or not. For the peritoneum, a smaller pool of peritoneal macrophages and weaker cytokine production is a necessary and sufficient condition to have tuberculous peritonitis developing therein.

Keywords: peritonitis, tumor necrosis factor, animal model, tuberculous peritonitis, abdominal tuberculosis, TNFα, rabbit