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ООО "ИЦ КОМКОН"

ФГБУ НКЦТ им. С.Н. Голикова ФМБА России




Адрес редакции и реквизиты

192012, Санкт-Петербург, ул.Бабушкина, д.82 к.2, литера А, кв.378

Свидетельство о регистрации электронного периодического издания ЭЛ № ФС 77-37726 от 13.10.2009
Выдано - Роскомнадзор

ISSN 1999-6314

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«
Vol. 26, Art. 12 (pp. 304-345)    |    2025       
»

Recognition of bacterial quorum sensing signals by G-protein coupled receptors of human cells in the innate immune response (Review article)
Laletin V.S.1,2
1Irkutsk State Medical University of the Ministry of Health of Russia,
664003, Russian Federation, Irkutsk, st. Krasnogo vosstaniya 1
2St. Petersburg State Pediatric Medical University, 194100, Russian Federation, St. Petersburg, Litovskaya str., 2



Brief summary

Biofilms are produced in the majority of bacterial infectious diseases. Biofilm formation is regulated by bacterial quorum sensing systems allowing bacteria to coordinate gene expression in synchrony. Quorum sensing is mediated by mobile intercellular signal molecules secreted by bacterial cells. After reaching a certain threshold levels of quorum sensing signals, bacterial population activates biofilm formation and production of virulence factors collectively. Quorum sensing signaling molecules are substances of the various chemical nature. Gram-negative bacteria use small signaling molecules, such as acyl-homoserine lactones and 2-alkyl-4-quinolones. Gram-positive bacteria use predominantly peptide signaling molecules. Quorum sensing signals can be detected not only by bacterial cells, but by cells of other organisms, as well as by cells of the human body. Recent studies have revealed that G-protein coupled receptors of T2R- and MRGPR-families play a key role in recognition of quorum sensing signaling molecules. These receptors are expressed by human cells participating in innate immune response. The first family receptors, T2R bitter taste receptors, initially found in taste buds, are expressed by a number of cells, including macrophages, monocytes, neutrophils, natural killer cells and epithelial cells of different localizations. The representative of the second family, MRGPRX2 receptor, is expressed by mast cells, basophils and eosinophils. Activation of these receptors by quorum sensing signaling molecules mediates intracellular calcium mobilization and functional responses of the target cell. Several effects of T2R receptors activation by quorum sensing signaling molecules have been revealed. Activation of T2R receptors of macrophages mediates activation of NO-synthase, generation of NO and enhancement of phagocytosis. Activation of T2R receptors of neutrophils stimulates chemotaxis, phagocytosis and expression of CD11b. Activation of T2R receptors of airway ciliated epithelial cells increases mucociliary clearance, activates NO-synthase, generation of NO in bactericidal levels and elimination of bacteria. Activation of T2R receptors of gingival epithelial cells mediates secretion of tumor necrosis factor-α, interleukin-6 and -8, and β-defensin-2. Activation of MRGPRX2 by quorum sensing signaling molecules mediates degranulation of mast cells, release of tumor necrosis factor-α and prostaglandin D2, generation of reactive oxygen species, inhibition of bacterial growth and prevention of biofilm formation. Thus, alongside the canonical pattern recognition receptors, activation of G-protein coupled receptors by bacterial quorum sensing signaling molecules appears to be one of the universal mechanisms of pathogen recognition by the key cells of the innate immune response.


Key words

quorum sensing; biofilms; signal-transduction system; G-protein coupled receptors; phagocytosis; cytokines; macrophages; neutrophils; epithelial cells; mast cells





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