111 research outputs found
StopCOVID cohort : An observational study of 3,480 patients admitted to the Sechenov University hospital network in Moscow city for suspected COVID-19 infection
Β© 2020 Oxford University Press. This is a pre-copyedited, author-produced PDF of an article accepted for publication in Clinical Infectious Diseases following peer review. The version of record is available online at: https://doi.org/10.1093/cid/ciaa1535.BACKGROUND: The epidemiology, clinical course, and outcomes of COVID-19 patients in the Russian population are unknown. Information on the differences between laboratory-confirmed and clinically-diagnosed COVID-19 in real-life settings is lacking. METHODS: We extracted data from the medical records of adult patients who were consecutively admitted for suspected COVID-19 infection in Moscow, between April 8 and May 28, 2020. RESULTS: Of the 4261 patients hospitalised for suspected COVID-19, outcomes were available for 3480 patients (median age 56 years (interquartile range 45-66). The commonest comorbidities were hypertension, obesity, chronic cardiac disease and diabetes. Half of the patients (n=1728) had a positive RT-PCR while 1748 were negative on RT-PCR but had clinical symptoms and characteristic CT signs suggestive of COVID-19 infection.No significant differences in frequency of symptoms, laboratory test results and risk factors for in-hospital mortality were found between those exclusively clinically diagnosed or with positive SARS-CoV-2 RT-PCR.In a multivariable logistic regression model the following were associated with in-hospital mortality; older age (per 1 year increase) odds ratio [OR] 1.05 (95% confidence interval (CI) 1.03 - 1.06); male sex (OR 1.71, 1.24 - 2.37); chronic kidney disease (OR 2.99, 1.89 - 4.64); diabetes (OR 2.1, 1.46 - 2.99); chronic cardiac disease (OR 1.78, 1.24 - 2.57) and dementia (OR 2.73, 1.34 - 5.47). CONCLUSIONS: Age, male sex, and chronic comorbidities were risk factors for in-hospital mortality. The combination of clinical features were sufficient to diagnoseCOVID-19 infection indicating that laboratory testing is not critical in real-life clinical practice.Peer reviewe
Micro-Raman study of crichtonite group minerals enclosed into mantle garnet
We report the first comprehensive micro-Raman study of crichtonite group minerals (CGM) as inclusions in pyropic garnet grains from peridotite and pyroxenite mantle xenoliths of the Yakutian kimberlites as well as in garnet xenocrysts from the Aldan shield lamprophyres (Russia). The CGM form (i) morphologically oriented needles, lamellae, and short prisms and (ii) optically unoriented subhedral to euhedral grains, either single or intergrown with other minerals. We considered common mantle-derived CGM species (like loveringite, lindsleyite, and their analogues), with Ca, Ba, or Sr dominating in the dodecahedral A site and Zr or Fe in the octahedral B site. The Raman bands at the region of 600β830 cmβ1 are indicative of CGM and their crystal-chemical distinction, although the intensity and shape of the bands appear to be dependent on laser beam power and wavelength. The factor-group analysis based on the loveringite crystal structure showed the octahedral and tetrahedral cation groups with 18f and 6c Wyckoff positions, namely, dominantly TiO6 and to a lower extent CrO6, MgO4, and FeO4 groups, to be the major contributors to the Raman spectral features. The ionic groups with dodecahedral (M0) and octahedral (M1) coordination are inactive for Raman scattering while active in infrared absorption. A number of observed Raman modes in the CGM spectra are several times lower than that predicted by the factor group analysis. The noticed broadening of modes in the CGM Raman spectra may result from a combining of bands at the narrow frequency shift regions. Solid solution behavior, luminescence, and partial metamictization of the CGM may exert additional influence on the Raman band shape. The Raman spectral features showed CGM to be accurately identified and distinguished from other Ti-, Fe-, Cr-, and Zr-containing oxides (e.g., ilmenite or those of spinel and magnetoplumbite groups) occurring as accessory mantle minerals. Β© 2020 The Authors. Journal of Raman Spectroscopy published by John Wiley & Sons LtdRussian Science Foundation,Β RSF: 18β77β10062Council on grants of the President of the Russian FederationThis study was supported by the Russian Science Foundation (Grant 18β77β10062). The equipment of the Ural Center for Shared Use Β«Modern NanotechnologyΒ», Ural Federal University, and the Analytical Center for Multiβelemental and Isotope Research, IGM, was used. Sampling was supported by the Russian Federation state assignment project of IGM. We are grateful to Nikolai V. Sobolev for Samples Oβ173, Oβ39, and Oβ264. Vladimir N. Korolyuk, Elena N. Nigmatulina (IGM), and Allan Patchen (UT) are highly appreciated for the help with EMP analyses. We express our sincere thanks to F. Nestola and an anonymous reviewer for their thorough reviews and helpful suggestions, and to C. Marshall for regardful editorial handling of the manuscript on every stage of its revision
An oribatid mite (Arachnida: Acari) from the Oxford Clay (Jurassic: Upper Callovian) of South Cave Station Quarry, Yorkshire, UK
A single specimen of a new species of oribatid mite belonging to the genus Jureremus Krivolutsky, in Krivolutsky and Krassilov 1977, previously described from the Upper Jurassic of the Russian Far East, is described as J. phippsi sp. nov. The mite is preserved by iron pyrite replacement, and was recovered by sieving from the Oxford Clay
Formation (Jurassic: Upper Callovian) of South Cave, Yorkshire. It is the first record of a pre-Pleistocene mite, and the second species record of the family Cymbaeremaeidae, from the British Isles; also, it is only the third record of Acari from the Jurassic Period. The presence of a terrestrial mite in a sedimentary sequence of open marine origin is noteworthy, and suggestions for its mode of transport to the site of deposition are discussed
Purinergic signalling links mechanical breath profile and alveolar mechanics with the pro-inflammatory innate immune response causing ventilation-induced lung injury
Severe pulmonary infection or vigorous cyclic deformation of the alveolar epithelial type I (AT I) cells by mechanical ventilation leads to massive extracellular ATP release. High levels of extracellular ATP saturate the ATP hydrolysis enzymes CD39 and CD73 resulting in persistent high ATP levels despite the conversion to adenosine. Above a certain level, extracellular ATP molecules act as danger-associated molecular patterns (DAMPs) and activate the pro-inflammatory response of the innate immunity through purinergic receptors on the surface of the immune cells. This results in lung tissue inflammation, capillary leakage, interstitial and alveolar oedema and lung injury reducing the production of surfactant by the damaged AT II cells and deactivating the surfactant function by the concomitant extravasated serum proteins through capillary leakage followed by a substantial increase in alveolar surface tension and alveolar collapse. The resulting inhomogeneous ventilation of the lungs is an important mechanism in the development of ventilation-induced lung injury. The high levels of extracellular ATP and the upregulation of ecto-enzymes and soluble enzymes that hydrolyse ATP to adenosine (CD39 and CD73) increase the extracellular adenosine levels that inhibit the innate and adaptive immune responses rendering the host susceptible to infection by invading microorganisms. Moreover, high levels of extracellular adenosine increase the expression, the production and the activation of pro-fibrotic proteins (such as TGF-Ξ², Ξ±-SMA, etc.) followed by the establishment of lung fibrosis
Π‘ΡΠ±ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΈ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΊΡΠΎΠ²ΠΈ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ Ρ Π³Π΅Π½Π΅ΡΠ°Π»ΠΈΠ·ΠΎΠ²Π°Π½Π½ΠΎΠΉ Π³ΠΈΠΏΠΎΠΊΡΠΈΠ΅ΠΉ
The aim of the work is to establish general regularities and features of differentiation of blood monocytes into 4 subpopulations in diseases associated with circulatory and respiratory hypoxia.Materials and methods. 18 patients with ischemic heart disease (IHD), 12 patients with ischemic cardiomyopathy (ICMP), 14 patients with chronic obstructive pulmonary disease (COPD), 15 patients with newly diagnosed infiltrative pulmonary tuberculosis (PTB) and 12 healthy donors were examined. In whole blood, we determined the relative number of different subpopulations of monocytes by flow cytometry. The results were analyzed by statistical methods.Results. It is shown that an increase in the number of classical (80.56 [77.60; 83.55]%) and the deficit of intermediate (10.38 [9.36; 11.26]%), non-classical (6.03 [5.24; 6.77]%) and transitional (2.14 [1.41; 3.92] %) monocytes in the blood is determined in patients with COPD when compared with the group of healthy donors (p < 0.05). In groups of patients with PTB and IHD, an increase in the number of intermediate monocytes (26.24 respectively [22.38; 42.88] % and 25.27 [15.78; 31.39]%) and the lack of transitional cells (1.77 [1.36; 3.74]% and 2.68 [2.63; 4.0]%) at the normal content of classical and non-classical forms of monocytes (p < 0.05) is detected. In patients with ICMP, a decrease in the number of non-classical monocytes (up to 5.05 [4.08; 6.58]%) is combined with the normal cell content of other subpopulations (p < 0.05). The interrelation between the number of classical and intermediate monocytes in patients with COPD (r = β0.63; p < 0.05), PTB (r = β0.72; p < 0.01), IHD (r = β0.59; p < 0.05), ICMP (r = β0.58; p < 0.05) was established.Conclusion. In COPD associated with generalized hypoxia, an increase in the number of classical monocytes is combined with a deficiency of their other subpopulations in the blood. In PTB and IHD, antigenic stimulation of the immune system mediates accelerated differentiation of monocytes from classical to intermediate forms with a decrease in the number of transitional cells regardless of the etiology of the disease (infectious or non-infectious) and the type of hypoxia (respiratory or circulatory).Π¦Π΅Π»Ρ ΡΠ°Π±ΠΎΡΡ β ΡΡΡΠ°Π½ΠΎΠ²ΠΈΡΡ ΠΎΠ±ΡΠΈΠ΅ Π·Π°ΠΊΠΎΠ½ΠΎΠΌΠ΅ΡΠ½ΠΎΡΡΠΈ ΠΈ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠΈ Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΡΠΎΠ²ΠΊΠΈ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΊΡΠΎΠ²ΠΈ Π½Π° ΡΠ΅ΡΡΡΠ΅ ΡΡΠ±ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΈ (ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ (CD14hiCD16-), ΠΏΡΠΎΠΌΠ΅ΠΆΡΡΠΎΡΠ½ΡΠ΅ (CD14hiCD16lo), Π½Π΅ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ (CD14loCD16lo) ΠΈ ΠΏΠ΅ΡΠ΅Ρ
ΠΎΠ΄Π½ΡΠ΅ (CD14loCD16-)) ΠΏΡΠΈ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡΡ
, Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½ΡΡ
Ρ ΡΠΈΡΠΊΡΠ»ΡΡΠΎΡΠ½ΠΎΠΉ ΠΈ Π΄ΡΡ
Π°ΡΠ΅Π»ΡΠ½ΠΎΠΉ Π³ΠΈΠΏΠΎΠΊΡΠΈΠ΅ΠΉ.ΠΠ°ΡΠ΅ΡΠΈΠ°Π»Ρ ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ. ΠΠ±ΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Ρ 18 Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ Π±ΠΎΠ»Π΅Π·Π½ΡΡ ΡΠ΅ΡΠ΄ΡΠ° (ΠΠΠ‘), 12 Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠ΅ΠΉ (ΠΠΠΠ), 14 Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΎΠ±ΡΡΡΡΠΊΡΠΈΠ²Π½ΠΎΠΉ Π±ΠΎΠ»Π΅Π·Π½ΡΡ Π»Π΅Π³ΠΊΠΈΡ
(Π₯ΠΠΠ), 15 Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ Π²ΠΏΠ΅ΡΠ²ΡΠ΅ Π²ΡΡΠ²Π»Π΅Π½Π½ΡΠΌ ΠΈΠ½ΡΠΈΠ»ΡΡΡΠ°ΡΠΈΠ²Π½ΡΠΌ ΡΡΠ±Π΅ΡΠΊΡΠ»Π΅Π·ΠΎΠΌ Π»Π΅Π³ΠΊΠΈΡ
(Π’ΠΠ) ΠΈ 12 Π·Π΄ΠΎΡΠΎΠ²ΡΡ
Π΄ΠΎΠ½ΠΎΡΠΎΠ². Π ΡΠ΅Π»ΡΠ½ΠΎΠΉ ΠΊΡΠΎΠ²ΠΈ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΠΈ ΠΎΡΠ½ΠΎΡΠΈΡΠ΅Π»ΡΠ½ΠΎΠ΅ ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²ΠΎ ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
ΡΡΠ±ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΉ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΏΡΠΎΡΠΎΡΠ½ΠΎΠΉ ΡΠΈΡΠΎΠΌΠ΅ΡΡΠΈΠΈ. ΠΠΎΠ»ΡΡΠ΅Π½Π½ΡΠ΅ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΡ Π°Π½Π°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°Π»ΠΈ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ ΠΌΠ΅ΡΠΎΠ΄Π°ΠΌΠΈ.Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. ΠΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
Π₯ΠΠΠ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ΅ΡΡΡ ΡΠ²Π΅Π»ΠΈΡΠ΅Π½ΠΈΠ΅ Π΄ΠΎΠ»ΠΈ ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
(80,56 [77,60; 83,55]%) ΠΈ Π΄Π΅ΡΠΈΡΠΈΡ ΠΏΡΠΎΠΌΠ΅ΠΆΡΡΠΎΡΠ½ΡΡ
(10,38 [9,36; 11,26]%), Π½Π΅ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
(6,03 [5,24; 6,77]%) ΠΈ ΠΏΠ΅ΡΠ΅Ρ
ΠΎΠ΄Π½ΡΡ
(2,14 [1,41; 3,92]%) ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² Π² ΠΊΡΠΎΠ²ΠΈ ΠΏΠΎ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ Ρ Π³ΡΡΠΏΠΏΠΎΠΉ Π·Π΄ΠΎΡΠΎΠ²ΡΡ
Π΄ΠΎΠ½ΠΎΡΠΎΠ² (Ρ < 0,05). Π Π³ΡΡΠΏΠΏΠ°Ρ
Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ Π’ΠΠ ΠΈ ΠΠΠ‘ ΠΎΠ±Π½Π°ΡΡΠΆΠΈΠ²Π°Π΅ΡΡΡ ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΠ΅ ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²Π° ΠΏΡΠΎΠΌΠ΅ΠΆΡΡΠΎΡΠ½ΡΡ
ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² (ΡΠΎΠΎΡΠ²Π΅ΡΡΡΠ²Π΅Π½Π½ΠΎ 26,24 [22,38; 42,88]% ΠΈ 25,27 [15,78; 31,39]%) Π½Π° ΡΠΎΠ½Π΅ Π΄Π΅ΡΠΈΡΠΈΡΠ° ΠΏΠ΅ΡΠ΅Ρ
ΠΎΠ΄Π½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ (1,77 [1,36; 3,74]% ΠΈ 2,68 [2,63; 4,0]%) ΠΏΡΠΈ Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΠΎΠΌ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠΈ ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈ Π½Π΅ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠΎΡΠΌ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² (Ρ < 0,05). Π£ Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΠΠΠ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠ΅ ΡΠΈΡΠ»Π΅Π½Π½ΠΎΡΡΠΈ Π½Π΅ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² (Π΄ΠΎ 5,05 [4,08; 6,58]%) ΡΠΎΡΠ΅ΡΠ°Π΅ΡΡΡ Ρ Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΡΠΌ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ΠΌ ΠΊΠ»Π΅ΡΠΎΠΊ ΠΎΡΡΠ°Π»ΡΠ½ΡΡ
ΡΡΠ±ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΉ (Ρ < 0,05). Π£ΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½Π° Π²Π·Π°ΠΈΠΌΠΎΡΠ²ΡΠ·Ρ ΠΌΠ΅ΠΆΠ΄Ρ ΡΠΈΡΠ»Π΅Π½Π½ΠΎΡΡΡΡ ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈ ΠΏΡΠΎΠΌΠ΅ΠΆΡΡΠΎΡΠ½ΡΡ
ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
Π₯ΠΠΠ (r = β0,63; p < 0,05), Π’ΠΠ (r = β0,72; p < 0,01), ΠΠΠ‘ (r = β0,59; p < 0,05), ΠΠΠΠ (r = β0,58; p < 0,05).ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΡΠΈ Π₯ΠΠΠ, Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ Ρ Π³Π΅Π½Π΅ΡΠ°Π»ΠΈΠ·ΠΎΠ²Π°Π½Π½ΠΎΠΉ Π³ΠΈΠΏΠΎΠΊΡΠΈΠ΅ΠΉ, ΡΠ²Π΅Π»ΠΈΡΠ΅Π½ΠΈΠ΅ ΡΠΈΡΠ»Π° ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΡΠΎΡΠ΅ΡΠ°Π΅ΡΡΡ Ρ Π΄Π΅ΡΠΈΡΠΈΡΠΎΠΌ ΠΎΡΡΠ°Π»ΡΠ½ΡΡ
ΠΈΡ
ΡΡΠ±ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΉ Π² ΠΊΡΠΎΠ²ΠΈ. ΠΡΠΈ Π’ΠΠ ΠΈ ΠΠΠ‘ Π°Π½ΡΠΈΠ³Π΅Π½Π½Π°Ρ ΡΡΠΈΠΌΡΠ»ΡΡΠΈΡ ΠΈΠΌΠΌΡΠ½Π½ΠΎΠΉ ΡΠΈΡΡΠ΅ΠΌΡ ΠΎΠΏΠΎΡΡΠ΅Π΄ΡΠ΅Ρ ΡΡΠΊΠΎΡΠ΅Π½Π½ΡΡ Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΡΠΎΠ²ΠΊΡ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΈΠ· ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
Π² ΠΏΡΠΎΠΌΠ΅ΠΆΡΡΠΎΡΠ½ΡΠ΅ ΡΠΎΡΠΌΡ ΠΏΡΠΈ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠΈ ΡΠΈΡΠ»Π° ΠΏΠ΅ΡΠ΅Ρ
ΠΎΠ΄Π½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ Π²Π½Π΅ Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΠΈ ΠΎΡ ΡΡΠΈΠΎΠ»ΠΎΠ³ΠΈΠΈ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ (ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΎΠ½Π½Π°Ρ ΠΈΠ»ΠΈ Π½Π΅ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΎΠ½Π½Π°Ρ) ΠΈ Π²ΠΈΠ΄Π° Π³ΠΈΠΏΠΎΠΊΡΠΈΠΈ (Π΄ΡΡ
Π°ΡΠ΅Π»ΡΠ½Π°Ρ ΠΈΠ»ΠΈ ΡΠΈΡΠΊΡΠ»ΡΡΠΎΡΠ½Π°Ρ)
P2 purinergic receptor modulation of cytokine production
Cytokines serve important functions in controlling host immunity. Cells involved in the synthesis of these polypeptide mediators have evolved highly regulated processes to ensure that production is carefully balanced. In inflammatory and immune disorders, however, mis-regulation of the production and/or activity of cytokines is recognized as a major contributor to the disease process, and therapeutics that target individual cytokines are providing very effective treatment options in the clinic. Leukocytes are the principle producers of a number of key cytokines, and these cells also express numerous members of the purinergic P2 receptor family. Studies in several cellular systems have provided evidence that P2 receptor modulation can affect cytokine production, and mechanistic features of this regulation have emerged. This review highlights three separate examples corresponding to (1) P2Y6 receptor mediated impact on interleukin (IL)-8 production, (2) P2Y11 receptor-mediated affects on IL-12/23 output, and (3) P2X7 receptor mediated IL-1Ξ² posttranslational processing. These examples demonstrate important roles of purinergic receptors in the modulation of cytokine production. Extension of these cellular observations to in vivo situations may lead to new therapeutic strategies for treating cytokine-mediated diseases
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