Febriana Catur Iswanti
Department Of Biochemistry And Molecular Biology, Faculty Of Medicine, Universitas Indonesia, Jakarta, Indonesia/Center Of Hypoxia And Oxidative Stress Study, Faculty Of Medicine, Universitas Indonesia, Jakarta, Indonesia

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Journal : Universa Medicina

Chemokines in allergic asthma inflammation Sulfiana Sulfiana; Febriana Catur Iswanti
Universa Medicina Vol. 41 No. 3 (2022)
Publisher : Faculty of Medicine, Universitas Trisakti

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18051/UnivMed.2022.v41.289-301

Abstract

Asthma is the most frequent noncommunicable disease and one of the leading causes of years lived with disability. Asthma has a severe impact on a patient's life, being able to disturb the activities of both children and adults. The morbidity and mortality of asthma may depend on the severity and progressiveness of the symptoms experienced by the patient. Different and complex pathomechanisms underline the pathology of asthma, in which the regulation of innate and adaptive immune responses plays a role. There is a complex interaction between immune cells including chemokines involved in the pathogenesis of asthma. Immune cell trafficking is orchestrated by a family of small proteins called chemokines. Leukocytes express cell-surface receptors that bind to chemokines and trigger transendothelial migration. This review article outlines the main role of chemokines in inflammatory reactions that occur in allergic asthma, based on the latest literature studies that have been published previously. The allergic reaction in asthma expresses various chemokines and their receptors. Chemokines including eotaxins (CCL11, CCL24, and CCL26), CCL2, CCL5, CCL17, and CCL22 regulate immune cells that under pathological conditions travel to the inflammatory site, mainly in the lung, to protect the body from pathogen invasion. Chemokines are released by a number of immune cells such as monocytes, dendritic cells, mast cells, and epithelial cells in the airway. The biological effects of chemokine production are enhanced by secreted cytokines when an allergic reaction occurs in asthma, such as IL-4, IL-5, and IL-13. Chemokines cause an accumulation of different inflammatory cells at the site of inflammation, which ultimately results in tissue damage to the airway. The inhibition of the reactions evoked by the interaction between chemokines and their receptors is considered a candidate for the development of potent therapeutic drugs for asthma in the future.
Macrophage modulation in activation process induced immune thrombocytopenia Mahdaleny, Mahdaleny; Bustami, Arleni; Iswanti, Febriana Catur
Universa Medicina Vol. 43 No. 1 (2024)
Publisher : Faculty of Medicine, Universitas Trisakti

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18051/UnivMed.2024.v43.76-87

Abstract

The immune system operates like an orchestra that harmoniously maintains the homeostasis balance while protecting from external or internal pathogens attack. Inflammation is one of the key critical immune defenses to eradicate pathogens and encourage tissue repair and recovery by activating the host’s immune and non-immune cells. As a part of the immune response during inflammation, blood platelets serve various functions; however, their activation and involvement in inflammation can also contribute to pathological conditions, such as thrombosis, which results in myocardial infarction, stroke, and venous thromboembolism. Activated platelets can mobilize and release intracellular granules (alpha and dense granules), which include secondary mediators like chemokine PF4/CXCL4. In contrast to most other chemokines, PF4 participates in several long-term regulatory processes, such as cell differentiation, survival, and proliferation. However, recent findings suggest that PF4 is also responsible for modulating macrophage polarization, which can substantially impact the development of induced immune thrombotic thrombocytopenia. This review aims to explain how PF4 induced vascular problems by modulation of macrophage development during immunological thrombocytopenia. A literature search using the keywords PF4, CXCL4, macrophage M4, platelet macrophage M4, and induced immune thrombocytopenia was done using the following databases: Google Scholar, ProQuest, ScienceDirect, and Scopus for articles published from 2000 to 2023. The literature study was done to find the connection between platelet activation, macrophage modulation, and vascular problems such as atherosclerosis and thromboembolism in induced immune thrombotic thrombocytopenia. Several recent studies on PF4, macrophage modulation, and vaccine-induced thrombotic thrombocytopenia were carefully reviewed. This review concludes that macrophage polarization modulation is promising in managing vascular problems in patients with induced immune thrombotic thrombocytopenia.