From NSAIDs to Glucocorticoids and Beyond

Our interest in inflammation and its treatment stems from ancient times. Hippocrates used willow bark to treat inflammation, and many centuries later, salicylic acid and its derivative aspirin’s ability to inhibit cyclooxygenase enzymes was discovered. Glucocorticoids (GC) ushered in a new era of treatment for both chronic and acute inflammatory disease, but their potentially dangerous side effects led the pharmaceutical industry to seek other, safer, synthetic GC drugs. The discovery of the GC-inducible endogenous anti-inflammatory protein annexin A1 (AnxA1) and other endogenous proresolving mediators has opened a new era of anti-inflammatory therapy. This review aims to recapitulate the last four decades of research on NSAIDs, GCs, and AnxA1 and their anti-inflammatory effects.

Kawasaki Syndrome in Germany: Historical Aspects and Current Update

Through his analytical powers of observation, the Japanese physician Kawasaki became aware of a rare childhood disease that his colleagues mistook for scarlet fever. Even more than five decades later, there is only conjecture as to the cause, despite intensive research. Kawasaki syndrome even made it into the American blockbuster medical series Dr. House. For the Japanese pediatrician Tomisaku Kawasaki, who was regarded as very modest, it must have come as a great surprise when his name became established in medical circles worldwide at the end of the 1970s as the term for the acute inflammatory disease of the blood vessels in young children that he discovered

Levels of high‑sensitivity C‑reactive protein in young and middle‑aged individuals and their association with hypertension

Background. Chronic systemic inflammation plays a key role in the development of cardiovascular disease. However, the causal relationship between inflammation and arterial hypertension (AH) is not fully determined.Objective. To assess the levels of high-sensitivity С-reactive protein (hs-CRP) in young and middle-aged individuals and their association with АН. Materials and methods. The study involved 427 patients aged 30 to 55 years (41 [35; 48] years) undergoing a periodic medical examination on the basis of Gazprom Transgaz Moscow’s Centre for Diagnostics and Rehabilitation from November 2018 to February 2020. 169 patients were evaluated in dynamics after a year. Patients with acute inflammatory disease or chronic exacerbation, taking hypolipidemic, anti-inflammatory, hormone replacement therapy were excluded from the study. The hs-CRP level was determined by an immunoturbodimetric method with latex gain, with a lower detection limit of 0.1 mg/l. Statistical processing of the results was carried out in Statistica 10 program. Differences were considered statistically significant at p < 0.05.Results. Among young and middle-aged individuals increase in the level of hs-CRP ≥ 2 mg/l was found in 26.9 % of participants of the research. Protein concentrations were most significantly associated with body mass index (r = 0.53; p < 0.05) and systolic blood pressure (r = 0.28; p < 0.05). Persons with hs-CRP ≥ 2 mg/l had a frequency of identification of AH above, then at persons with normal levels of a marker (65.2 against 40.1 %; р = 0.000004). There was a statistically significant association between an increase in the level of hs-CRP and hypertension (OR = 2.8; 95 % CI: 1.8–4.4; p = 0.000004).Conclusions. The findings indicate that elevated hs-CRP levels are associated with AH in young and middle-aged individuals, and also suggest that chronic systemic inflammation is an independent contributor to the development of AH.

Leukocyte immunoglobulin-like receptor B4 deficiency exacerbates acute lung injury via NF-κB signaling in bone marrow-derived macrophages

Acute lung injury (ALI) is an acute inflammatory disease. Leukocyte immunoglobulin-like receptor B4 (LILRB4) is an immunoreceptor tyrosine-based inhibitory motif (ITIM)-bearing inhibitory receptor that is implicated in various pathological processes. However, the function of LILRB4 in ALI remains largely unknown. The aim of the present study was to explore the role of LILRB4 in ALI. LILRB4 knockout mice (LILRB4 KO) were used to construct a model of ALI. Bone marrow cell transplantation was used to identify the cell source of the LILRB4 deficiency-aggravated inflammatory response in ALI. The effect on ALI was analyzed by pathological and molecular analyses. Our results indicated that LILRB4 KO exacerbated ALI triggered by LPS. Additionally, LILRB4 deficiency can enhance lung inflammation. According to the results of our bone marrow transplant model, LILRB4 regulates the occurrence and development of ALI by bone marrow-derived macrophages (BMDMs) rather than by stromal cells in the lung. The observed inflammation was mainly due to BMDM-induced NF-κB signaling. In conclusion, our study demonstrates that LILRB4 deficiency plays a detrimental role in ALI-associated BMDM activation by prompting the NF-κB signal pathway.

DIAGNOSIS SEPSIS MENGGUNAKAN PROCALCITONIN

Sepsis can be difficult to distinguish from non-infections conditions in critically ill patients with clinical signs of inflammation.Diagnosis of sepsis by conventional methods (erythrocyte sedimentation rate, CRP) are difficult to be confirmed. Procalcitonin (PCT)was found in 1990s, which number was enhanced in bacterial and fungi infections. Procalcitonin (PCT) is calcitonin (PCT) prohormonwhich presence increasing in sepsis and severe diseases. Procalcitonin (PCT) can be measured in serum and plasma by immunolometricmethods (immunoassay). The process needs 30 minutes to 1.5 hours depends on the selected method. It can be hope in the future,that methods of Procalcitonin (PCT) measurement can used as a means for early sepsis detection and can distinguish between systemicinfection and acute inflammatory disease.