scholarly journals The role of TNFRSF7 and TNFRSF9 receptors in the development of systemic inflammation in patients with viral pneumonia

Author(s):  
А.В. Малярчиков ◽  
К.Г. Шаповалов

Актуальность. Системный про- и противовоспалительный каскад реакций является одним из патофизиологических компонентов развития критического состояния различного генеза. Поиск биологических маркёров и патогенетических механизмов влияния на макроорганизм систем рецепторов, участвующих в реализации реакций врожденного и адаптивного иммунитета, вследствие повреждения или инфекции, остается актуальным научным направлением. Цель исследования. Оценить активность системы рецепторов TNFRSF7 и TNFRSF9, определив их плазменную концентрацию у больных пневмониями на фоне гриппа A/H1N1. Материалы и методы. Обследовали 85 больных пневмонией на фоне гриппа A/H1N1. Из них 30 пациентов с тяжёлой пневмонией, 55 - с нетяжёлой пневмонией. Методом проточной цитофлуометрии определяли плазменную концентрацию молекул TNFRSF7 и TNFRSF9. Результаты. Установили, что что у больных тяжёлой пневмонией на фоне гриппа A/H1N1 плазменная концентрация рецепторов TNFRSF7 и TNFRSF9 увеличивалась в 1,8 и в 2,3 раза соответственно. Заключение. Увеличение концентрации TNFRSF7 и TNFRSF9 у больных пневмониями на фоне гриппа A/H1N1 свидетельствует о вовлечении в реализацию реакций врожденного и адаптивного иммунитета суперсемейства рецепторов TNF и ассоциировано с тяжестью состояния. Background. Systemic pro- and anti-inflammatory cascades of reactions are pathophysiological components of various critical states. It remains relevant to search for biological markers and pathogenetic mechanisms of effects on the macro-organism of receptor systems involved in innate and adaptive immunity induced by damage or infection. Aim of the study. To evaluate the activity of the TNFRSF7 and TNFRSF9 receptor systems by determining their plasma concentrations in pneumonia patients with influenza A (H1N1). Materials and methods. 85 patients with pneumonia associated with influenza A (H1N1) were examined. Among them, 30 patients had severe pneumonia, and 55 patients had non-severe pneumonia. Plasma levels of TNFRSF7 and TNFRSF9 were measured by flow cytometry. Results. In patients with severe pneumonia and underlying influenza A (H1N1), the plasma concentrations of TNFRSF7 and TNFRSF9 receptors increased 1.8-fold and 2.3-fold, respectively. Conclusion. The significant increase in plasma TNFRSF7 and TNFRSF9 receptors in patients with pneumonia associated with influenza A (H1N1) indicates the involvement of the TNF receptor superfamily in innate and adaptive immunity reactions and is related with severity of the disease.

2021 ◽  
Vol 6 ◽  
pp. 70-73
Author(s):  
A.V. Malyarchikov ◽  
◽  
K.G. Shаpovаlov ◽  

Aim of study. To evaluate the role of the CD27/CD70 signalling pathway in development of systemic inflammatory response in patients with pneumonia associated with influenza A (H1N1). Material and methods. A total of 85 patients with pneumonia associated with influenza A (H1N1) were examined. Among them, 30 patients had severe pneumonia and 55 patients had non-severe pneumonia. The patients’ age was 48±15 years. Men accounted for 47.8% and women 52.2% of the sample. The exclusion criteria were: unstable haemodynamics, BMI>30, diabetes mellitus, HIV, tuberculosis, oncopathology. The control group was constituted by 15 healthy donors. The diagnosis of influenza A (H1N1) was confirmed by a positive PCR test. The CURB / CRB-65 scales were used to diagnose and assess the severity of pneumonia; SMART-COP as well as the Federal Clinical Guidelines of the Ministry of Health of the Russian Federation «Community-acquired pneumonia in adults» 2019 and the IDSA / ATS criteria (in the presence of one «major» or three «minor» criteria, the pneumonia was regarded as «severe»). The plasma level of CD27 was evaluated via flow cytometry using the Beckman Coulter analyser (USA) using the LEGENDplex™ HU Immune Checkpoint Panel 1 Beckman Coulter (USA) kit for multiplex analysis. Results. It has been established that the plasma level of CD27 increased 1.8-fold in patients with severe pneumonia and underlying influenza A (H1N1) and 1.5-fold in patients with non-severe pneumonia compared to the control group, which is associated with the severity of the condition and the mortality rate. Conclusion. The CD27/CD70 signalling pathway is actively involved in the cascade of innate and adaptive immunity reactions in patients with pneumonia associated with influenza A (H1N1). CD27 activity is associated with the severity of the disease and the increase in mortality


2021 ◽  
Vol 23 (4) ◽  
pp. 799-804
Author(s):  
M. A. Levkovich ◽  
L. V. Kravchenko ◽  
A. A. Afonin ◽  
I. I. Krukier ◽  
A. Yu. Levkovich ◽  
...  

Subject: to assess a role of factors of innate and adaptive immunity in the development of intrauterine generalized cytomegalovirus infection.The study included 47 newborns with congenital generalized cytomegalovirus infection comprising group I. Based on the data of clinical and laboratory examination, all newborns studied were divided into two subgroups. Subgroup 1.1 (29 subjects) consisted of newborns with severe CMVI and subgroup 1.2 (18 subjects) – newborns with moderate CMVI. The control group included 26 newborns without herpesvirus infection.Determination of the number of monocytes expressing Toll receptors (TLR) was performed by laser flow cytometry (Beckman Coulter) using Beckman Coulter, HyCultBiotechnology reagents: FITC-CD282+, CD284+, CD286+, and PE-CD14+. The newborn serum concentration of IFNγ, IFNα, IL-6, IL-8 was determined by ELISA using BenderMedsistems test systems.Intrauterine generalized CMVI with complete clinical symptoms in newborns was characterized by a decrease in the number of monocytes expressing TLR-2 and TLR-6, which was associated with a decrease in the level of IFNα, IFNγ, an increase in the level of IL-6, IL-8 and MCP-1. The subgroup with incomplete clinical symptoms CMVI was characterized by a decrease in the level of IFNα, in combination with an increase in the level of IL-6. The identified immune disorders lead to a reduction in the antiviral immune response and determine the severity of the disease in prenatally infected newborns. 


2011 ◽  
Vol 300 (5) ◽  
pp. L781-L789 ◽  
Author(s):  
Szabolcs Bertok ◽  
Michael R. Wilson ◽  
Anthony D. Dorr ◽  
Justina O. Dokpesi ◽  
Kieran P. O'Dea ◽  
...  

TNF plays a crucial role in the pathogenesis of acute lung injury. However, the expression profile of its two receptors, p55 and p75, on pulmonary endothelium and their influence on TNF signaling during lung microvascular inflammation remain uncertain. Using flow cytometry, we characterized the expression profile of TNF receptors on the surface of freshly harvested pulmonary endothelial cells (PECs) from mice and found expression of both receptors with dominance of p55. To investigate the impact of stimulating individual TNF receptors, we treated wild-type and TNF receptor knockout mice with intravenous TNF and determined surface expression of adhesion molecules (E-selectin, VCAM-1, ICAM-1) on PECs by flow cytometry. TNF-induced upregulation of all adhesion molecules was substantially attenuated by absence of p55, whereas lack of p75 had a similar but smaller effect that varied between adhesion molecules. Selective blockade of individual TNF receptors by specific antibodies in wild-type primary PEC culture confirmed that the in vivo findings were due to direct effects of TNF receptor inhibition on endothelium and not other cells (e.g., circulating leukocytes). Finally, we found that PEC surface expression of p55 dramatically decreased in the early stages of endotoxemia following intravenous LPS, while no change in p75 expression was detected. These data demonstrate a crucial in vivo role of p55 and an auxiliary role of p75 in TNF-mediated adhesion molecule upregulation on PECs. It is possible that the importance of the individual receptors varies at different stages of pulmonary microvascular inflammation following changes in their relative expression.


2009 ◽  
Vol 14 (22) ◽  
Author(s):  
G M Nava ◽  
M S Attene-Ramos ◽  
J K Ang ◽  
M Escorcia

To gain insight into the possible origins of the 2009 outbreak of new influenza A(H1N1), we performed two independent analyses of genetic evolution of the new influenza A(H1N1) virus. Firstly, protein homology analyses of more than 400 sequences revealed that this virus most likely evolved from recent swine viruses. Secondly, phylogenetic analyses of 5,214 protein sequences of influenza A(H1N1) viruses (avian, swine and human) circulating in North America for the last two decades (from 1989 to 2009) indicated that the new influenza A(H1N1) virus possesses a distinctive evolutionary trait (genetic distinctness). This appears to be a particular characteristic in pig-human interspecies transmission of influenza A. Thus these analyses contribute to the evidence of the role of pig populations as “mixing vessels” for influenza A(H1N1) viruses.


2019 ◽  
Vol 73 (9) ◽  
pp. 1867
Author(s):  
Maria Cristina Izar ◽  
Waleria Fonzar ◽  
Francisco Fonseca ◽  
Henrique Fonseca ◽  
Tuany P. Silva ◽  
...  

2018 ◽  
Vol 51 ◽  
pp. 02007
Author(s):  
Anna Mihailova ◽  
Indrikis Krams

There is evidence of the relation of sex steroid hormones and sexual dimorphism in immune system response to infectious diseases. The aim of this review was to identify the role of sex hormones in immune function and sexual dimorphism of immune reactions. Gonadal hormones together with the immune system play an important role in process of immune responses to the disease [1]. Estrogens, progesterone and testosterone have different impacts on immune cells and different gonadal hormones are of high importance for responses of innate and adaptive immunity [1, 2]. Estrogens mainly enhance immune function while testosterone has a suppressive role. Higher progesterone during pregnancy leads to autoimmune disease remission and an elevated susceptibility toward certain infectious diseases [2, 3, 4]. The intensity and prevalence of viral infections are typically higher in males, whereas disease outcome could be worse for females [5]. Sexual dimorphism of immune function is based on different concentrations of sex hormones in males and females and on a specific mediating role of these hormones in immune function and response along with differences in innate and adaptive immunity.


2000 ◽  
Vol 165 (8) ◽  
pp. 4544-4551 ◽  
Author(s):  
De’Broski R. Herbert ◽  
James J. Lee ◽  
Nancy A. Lee ◽  
Thomas J. Nolan ◽  
Gerhard A. Schad ◽  
...  

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