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Interleukin-8
Published in Jason Kelley, Cytokines of the Lung, 2022
Robert M. Strieter, Theodore J. Standiford, Mark W. Rolfe, Steven L. Kunkel
The microvascular aggregation of PMNs, followed by adherence to vascular endothelium, set the stage for PMN activation and transendothelial diapedesis to the subendothelial space. Subsequently, the PMN must migrate through the basement membrane and recognize chemical signals that serve as a homing mechanism to precisely target these cells to an area of inflammation. The complete understanding of the innumerable steps culminating in chemotaxis remains an enigma of the inflammatory response. Many questions are unanswered concerning PMN recruitment, including the cellular source(s) of the early response or proximal cytokines, IL-1 and TNF; the mechanism(s) whereby inflammatory cells bind reversibly to the endothelium; the mechanism(s) associated with PMN diapedesis through the endothelium; the ability of the PMN to breach the basement membrane barrier; the cellular sources for the local generation of chemotactic signals, and finally, the mechanism(s) of PMN migration along chemotactic gradients. Although we have only superficially introduced a variety of significant steps, which are necessary for successful leukocyte chemotaxis, the remainder of this chapter will be devoted to a discussion of a novel chemotactic cytokine: interleukin-8 (IL-8).
Cellular Components of Blood
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Chemotaxis is brought about by cell mobilization and migration. Neutrophils and monocytes migrate through pores in the endothelium of blood vessels by diapedesis and by amoeboid movement through tissues. These phagocytes are attracted to bacteria or inflammatory areas by chemicals released by damaged tissues, and by complement or leukocyte cohesion molecules interacting with damaged tissues.
The Immune System During HIV-1 Infection
Published in Niel T. Constantine, Johnny D. Callahan, Douglas M. Watts, Retroviral Testing, 2020
Niel T. Constantine, Johnny D. Callahan, Douglas M. Watts
Cytokines are produced by many cell types, including macrophages and T lymphocytes. Their production follows many types of cellular injury, including that caused by infectious agents, and is the primary mechanism by which the CMI response is orchestrated. Immediately following any injury, inflammatory cells are recruited to the injured site by a process known as Chemotaxis. Once the inflammatory cells are in the area, these cells then act to help eliminate the cause of injury, while growth factors from other cells begin the healing process. Once the injury is resolved, cytokine levels usually fall below detectable limits, as in healthy individuals.
Elevated Levels of Interleukins, Leukocyte Protein and Cathelicidin Antimicrobial Peptide are Strongly Associated with Early to Mid-Stage of Pythium insidiosum Infection in Rabbit Corneas
Published in Current Eye Research, 2022
Lalit Kishore Ahirwar, Savitri Sharma
The chemokine IL-8, which was significantly higher on 7th day compared to 3rd and 9th day post infection studied by RT-qPCR also showed significantly higher expression in infected tissue compared to control by mELISA on three of these time points. It is one of the chemokines, which has specificity to activate and recruit neutrophils to the local site of inflammatory region.34 As it is well known for chemotaxis, it also plays a crucial role as potent pro-inflammatory immune mediator.35 Although not statistically significant, the expression of other chemokine CCL4/MIP-1β demonstrated by RT-qPCR and mELISA was higher on 3rd followed by 7th and 9th day post infection studied by RT-qPCR. It was higher in infected tissue (mELISA) in comparison to control in all of the time points. It is a chemotactic immune mediator which induces recruitment of eosinophils at the site of inflammation. The eosinophils play important role in innate and adaptive immunity and maintain tissue homeostasis in human mucosal surface.36 The histopathology of corneal tissue infected with P. insidiosum of rabbits included in this study also showed predominant infiltration with eosinophils and other polymorphonuclear cells.11
Comparison of Chemokine CXCL-1 and Interleukin-6 Concentrations in the Subretinal Fluid and Vitreous in Rhegmatogenous Retinal Detachment
Published in Ocular Immunology and Inflammation, 2021
Chrysanthos Symeonidis, Tryfon Rotsos, Artemis Matsou, Maria Dermenoudi, Ilias Georgalas, Ioannis Tsinopoulos, Olga Makri, Efimia Souliou, Stavros A. Dimitrakos
In this milieu, chemotaxis is a significant prerequisite for membrane formation. Chemokines, a group of small molecular weight (8–10 kDa) proteins, are involved in chemotaxis, cell activation, hematopoiesis, and angiostasis.10,11 Chemokine classification (CC, CXC, XC, CX3C subgroups) is based on a two cysteine-residue structure with the possible interjection of one or more amino-acid residues.12 A constituent of the CXC subgroup, CXCL-1 is a human analog of the mouse keratinocyte-derived chemokine, also known as growth-related oncogene (GRO)-alpha. CXCL-1 is considered as a potent neutrophil chemoattractant and a contributor to the acute inflammatory reaction.13 Moreover, the inflammatory aspect of PVR has been shown to involve interleukins as regulators. Of them, elevated interleukin(IL)-6 production has been reported to enhance the proliferation of vascular endothelial cells thus contributing to the pathophysiology of proliferative vitreoretinal diseases such as PVR.14 IL-6 expression and activity are also significantly increased during RRD with or without PVR.15,16
Altered Expression of CXCL13 and Its Chemokine Receptor CXCR5 on B Lymphocytes during Active Graves’ Orbitopathy
Published in Current Eye Research, 2021
Shangtao Wan, Miaoli Lin, Yuxiang Mao, Xiaoqing Chen, Dan Liang
Our in vitro data further support the contribution of CXCL13 in recruiting B cells and the preferential memory B-cell subset. The serum of patients with active GO exerted a stronger chemotactic activity on B cells in this study. Using neutralizing antibodies against CXCL13 or CXCR5 reduced the migration by 20%, demonstrating that a specific interaction between CXCL13 and CXCR5 was involved in chemotaxis. Moreover, adding a low concentration of rhCXCL13 (100 pg/mL) to the serum of HC subjects or of patients with inactive GO enhanced the chemotactic response, while rhCXCL13 (100 pg/mL) alone did not exert a chemotactic effect. These results suggest that additional factors in the serum may have a synergistic effect on chemotaxis. In support of this hypothesis, a previous study showed that B cell survival factor increases the chemotactic response of primary and memory human B cells to CXCL13.41