References

mimmun

Медицинская иммунология

Medical Immunology (Russia)

1563-06252313-741X

SPb RAACI

10.15789/1563-0625-IOL-3019

mimmun-3019

Research Article

ОБЗОРЫ

REVIEWS

Дисбаланс липополисахарид-связывающих систем как потенциальное звено патогенеза ревматоидного артрита

Imbalance of lipopolysaccharide-binding systems as a potential link in pathogenesis of rheumatoid arthritis

https://orcid.org/0000-0002-8960-602X

Яцков

И. А.

Yatskov

I. A.

Яцков И.А. – к.м.н., доцент кафедры внутренней медицины № 2

295051, Республика Крым, г. Симферополь, б-р Ленина, 5/7

Yatskov I.A., PhD (Medicine), Associate Professor, Department of Internal Medicine No. 2

5/7 Lenin Blvd, Simferopol, Republic of Crimea 295051

https://orcid.org/0000-0001-9640-754X

Белоглазов

В. А.

Beloglazov

V. A.

Белоглазов В.А. – д.м.н., профессор, заведующий кафедрой внутренней медицины № 2

295051, Республика Крым, г. Симферополь, б-р Ленина, 5/7

Beloglazov V.A., PhD, MD (Medicine), Professor, Head, Department of Internal Medicine No. 2

5/7 Lenin Blvd, Simferopol, Republic of Crimea 295051

https://orcid.org/0000-0002-5486-7262

Бублей

К. В.

Bubley

K. V.

Бублей К.В. – ассистент/ординатор кафедры внутренней медицины № 2

295051, Республика Крым, г. Симферополь, б-р Ленина, 5/7

Bubley K.V., Assistant Professor, Department of Internal Medicine No. 2

5/7 Lenin Blvd, Simferopol, Republic of Crimea 295051

bubley.99@mail.ru

Ордена Трудового Красного Знамени Медицинский институт имени С.И. Георгиевского ФГАОУ ВО «Крымский федеральный университет имени В.И. Вернадского»РоссияS. Georgievsky Medical Institute, V. Vernadsky Crimean Federal UniversityRussian Federation

2025

04102024

272265274

2025

Яцков И.А., Белоглазов В.А., Бублей К.В.

Yatskov I.A., Beloglazov V.A., Bubley K.V.

This work is licensed under a Creative Commons Attribution 4.0 License.

https://www.mimmun.ru/mimmun/article/view/3019

Липополисахарид (LPS, эндотоксин) грамнегативной флоры является одним из сильнейших активаторов нативной иммунной системы и индуктором системного и локального воспаления. В связи с увеличением количества факторов, способствующих транслокации LPS в системный кровоток, будь то неадекватная антибиотикотерапия, применение энтеро- и гепатотоксичных лекарственных препаратов, а также повышение доли углеводной и жирной пищи в рационе современного человека, роль LPS в поддержании воспалительного фона, в том числе низкоинтенсивного растет. Взаимодействия эндотоксина с организмом человека опосредованы целым рядом рецепторов и молекул переносчиков, многие из которых можно выделить в группу так называемых «липополисахарид-связывающих систем», а именно липополисахарид-связывающий белок (LBP) и бактерицидный белок повышенной проницаемости бактерий (BPI). Характер ответа на повышение циркулирующего в крови пула LPS во многом зависит от данных молекул, а также дополнительных молекул, взаимодействующих с LPS и LPS-связывающими системами, в частности – липопротеидов низкой (LDL) и высокой плотности (HDL). Учитывая имеющиеся в литературе данные о регистрации повышенных уровней LPS у пациентов с ревматоидным артритом (РА), а также наличия у данных пациентов в подавляющем большинстве дислипидемических состояний, LPS потенциально является патогенетически важным фактором при РА. В данном обзоре представлены основные данные о биологии и роли LPS и «липополисахарид-связывающих систем» в развитии и поддержании воспаления при РА. Поиск информации проводился по ключевым словам «ревматоидный артрит и липополисахарид», «ревматоидный артрит и липополисахарид-связывающий белок», «ревматоидный артрит и BPI» в зарубежных и отечественных наукометрических базах, в том числе e-Library и PubMed. Представленные данные дают право считать сочетание дисбаланса «липополисахаридсвязывающих систем» и дислипидемии важным отягощающим провоспалительным фактором при РА, а поиск механизмов влияния на эти состояния по отдельности и в комбинации перспективным научным и клиническим направлением.

Lipopolysaccharide (LPS, endotoxin) of Gram-negative bacteria is a strong activator of innate immune system and inducer of systemic and local inflammation. Due to increasing number of factors contributing to the translocation of LPS into the systemic bloodstream, e.g., non-adequate antibiotic therapy, usage of entero- and hepatotoxic drugs, as well as increased proportion of carbohydrate and fatty foods in the diet of modern people, the role of LPS is growing, in view of maintaining low-grade inflammatory background. Interactions of endotoxin within human body are mediated by a number of receptors and carrier molecules, many of which can be distinguished into a group of so-called “LPS-binding systems”, i.e., lipopolysaccharidebinding protein (LBP) and bactericidal/permeability-increasing protein (BPI). The character of response to increased LPS pool in blood circulation depends largely on these molecules, as well as additional substances that interact with LPS and LPS-binding systems, in particular, low-density lipoproteins (LDL) and high-density lipoproteins (HDL). Given current publications reporting elevated LPS levels in patients with rheumatoid arthritis (RA), and persistence of dyslipidemias in the vast majority of these patients, LPS is potentially a pathogenetically important factor in RA. This review presents basic data on the biology and role of LPS and “lipopolysaccharide-binding systems” in development and maintenance of inflammation state in RA. Information was searched using the keywords “rheumatoid arthritis and lipopolysaccharide”, “rheumatoid arthritis and lipopolysaccharide-binding protein”, “rheumatoid arthritis and BPI” in foreign and Russian scientific databases, including e-Library and PubMed. The presented data allow us to consider the combination of “lipopolysaccharide-binding systems” imbalance and dyslipidemia a sufficient aggravating pro-inflammatory factor in RA, and the search for potential mechanisms influencing these conditions, either separately, or in combined manner, as a promising field for clinical research.

LPSревматоидный артритBPILBPэндотоксин

LPSrheumatoid arthritisBPILBPendotoxin

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The authors declare that there are no conflicts of interest present.