Vol 22, No 3 (2025)

Being one of the leading causes of mortality, sepsis is a global healthcare and social issue. Sepsis is a life-threatening organ dysfunction caused by dysregulated immune response to infection. The current understanding of its pathophysiology has shifted from studying the pathogen to analyzing the patient’s immune response, which is very different and unique. In general, sepsis is the simultaneous or sequential development of hyperinflammation and immunosuppression, which ultimately determines the clinical outcome.

This paper emphasizes the need for a personalized approach to sepsis treatment based on the diagnosis of impaired immune status in the patient. We propose the complete blood count assessment using leukocyte analysis matrices allowing to determine the type and nature of immune response as an accessible, reproducible, and pathogenetically substantiated tool, even in a regular hospital setting. The paper presents a method for interpreting leukocyte matrices using the sepsis immunotyping technology allowing to identify the activation of innate or adaptive immunity and the nonimmunity or immunosuppression state. A conclusion is made on the clinical importance of the proposed approach for predicting the course of the disease, timely therapy correction, and the selection of a balanced, immune-oriented therapy. Thus, clinical integration of this approach contributes to the transition from empirical to pathogenetically substantiated therapy.

BACKGROUND: The oral cavity is constantly exposed to antigens. Local humoral immunity, mediated primarily by secretory immunoglobulin A (sIgA), plays a pivotal role by binding these antigens. The relationship between sIgA levels and the intensity of chronic inflammation is actively studied. Given that smoking is a factor of chronic oral inflammation, it is important to evaluate the local humoral immunity (sIgA) status and its association with inflammation activity (IL-6) in the oral fluid of smokers.

AIM: To assess the local humoral immunity and chronic inflammation activity using sIgA and IL-6 levels in the oral fluid of smokers.

METHODS: A smoking history survey was conducted among third-year students of the Dentistry Department at the Pavlov First Saint Petersburg State Medical University. The study also included a detailed history of the local oral mucosa status (acute infections, chronic diseases of the oral mucosa and throat) and immunity disorder and allergy history. The levels of sIgA and IL-6 in oral fluid were determined by enzyme immunoassay.

RESULTS: A total of 29 respondents were included in the study: 11 smokers and 17 non-smokers (control group). One respondent was excluded from the study due to acute respiratory viral infection. The average smoking history was 3 years; 54.5% of smokers (n = 6) and 66.7% of non-smokers (n = 12) had an allergy history. No immunodeficiencies were observed. Chronic gingivitis (K05.1) was diagnosed in one smoker. Chronic tonsillitis (J35.0) was diagnosed in two smokers. Oral fluid sIgA levels were lower in smokers than in non-smokers (31.25 [15.43; 96.20] vs 89.04 [64.73; 120.36] ng/mL, p = 0.04 [negligible]). There was no significant difference in the IL-6 level (12.74 [8.63; 17.56] vs 9.69 [7.90; 20.61], p = 0.36). For statistical analysis, the median and quartiles were used, as the groups were small and the distribution was different from normal (as assessed by the Shapiro–Wilk test). For comparative analysis, we used the Mann–Whitney U test. Enzyme immunoassay was performed using Vector-Best kits (Russia).

CONCLUSION: The findings indicate that smokers have lower levels of sIgA in oral fluid than non-smokers, which may contribute to chronic inflammatory diseases of the oral mucosa and throat in smokers.

BACKGROUND: Chronic coronary heart disease (CHD) is accompanied by low-grade inflammation, with platelet-leukocyte aggregates (PLAs) being important mediators. Their formation may depend on many factors, but the relationship between PLAs and metabolic hormones in coronary atherosclerosis (CA) of different severity has been understudied.

AIM: To study the relationship between PLA levels and basal and postprandial levels of hormones in patients with CHD based on the CA severity.

METHODS: The study included 32 patients with chronic CHD grouped based on the CA severity by the median Gensini Score index, a group with more severe CA (GS ≥  42.5; n = 18) and less severe CA (GS < 42.5; n = 14). Blood PLAs were determined by flow cytometry with visualization. Insulin, C-peptide, glucagon, glucagon-like peptide-1 (GLP-1), and leptin were measured by multiplexed immunoassay.

RESULTS: Patients with GS ≥  42.5 demonstrated an increased proportion of lymphocyte aggregates with more than three platelets [0.6 (0.3; 1.6) vs 0.1 (0.0; 0.5)%, p = 0.042] and a lower basal glucagon [25.9 (16.9; 47.2) vs 57.9 (23.2; 69.3) pg/mL, p = 0.049] than patients with GS < 42.5. PLAs correlated only with postprandial hormone levels, whereas these relationships were determined by the severity of atherosclerosis. Thus, in patients with GS < 42.5, negative relationships were found between the level of GLP-1 and CD62P⁺-PLA (r_s = −0.850; p = 0.004 and r_s = −0.733; p = 0.024), insulin and the proportion of large platelete-mononuclear leukocyte aggregates (r_s = −0.750; p = 0.020 and r_s = −0.766; p = 0.016), and positive relationships were found between leptin and the proportion of small PLAs (r_s = 0.700; p = 0.036 and r_s = 0.753; p = 0.019). In patients with GS ≥  42.5, positive relationship was recorded between the level of GLP-1 and CD62P⁺-PLA (r_s = 0.636; p = 0.045), whereas leptin positively correlated with the proportion of large PLAs (r_s = 0.663; p = 0.037 and r_s = 0.657; p = 0.039).

CONCLUSION: The study was the first to show a relationship between PLAs and postprandial hormone levels in patients with chronic CHD. The findings indicate the need for further research into the role of PLAs and hormones in immune inflammatory activity in patients with CHD.