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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 generation of chemotactic factors and the subsequent mobilization of leukocytes in reaction to a chemoattractant are essential elements of host defense in response to various stimuli, including tissue injury, infection, or cancer. The nature of the stimulus and the subsequent spectrum of chemotactic factors produced, determines the specific leukocyte population elicited to the inflammatory lesion. For example, a specific antigenic stimulus leading to cell-mediated immunity will result in the production of chemotactic factors that recruit exclusively mononuclear immune cells, leading to either lymph node enlargement or an expanding granulomatous inflammation. In contrast, the stimuli associated with acute tissue injury may result in the production of a different set of chemotactic factors, with a profile for recruiting predominantly PMNs. Thus, a diversity of leukocyte chemotactic factors exist, with different target cell specificity.
Specific Host Restance: The Effector Mechanisms
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Chemotactic factors are substances that attract leukocytes. Under their influence polymorphonuclear leukocytes are induced to adhere to vascular endothelial cells, pass through the spaces between the endothelial cells of the capillaries (extravasation), and move into the inflamed site by moving up the concentration gradient of the factor. The presence of additional leukocytes increases the likelihood of phagocytosis of any parasites present. and 67 are weakly chemotactic; is strongly chemotactic.
Inflammation
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Defective chemotaxis may also be due to impaired synthesis of chemotactic factors. Various components of the complement also play a part as endogenous chemotactic factors. Genetic deficiencies in the synthesis of these components are associated with recurrent infections.206 Such deficiencies have been described in Clr, C2, C3, and C5 components.509 In case of homozygous C3 deficiency, recurrent pneumonia, impetigo, and otitis media are often manifest, and supplementation of C3 factor to the serum can correct this impairment.10
Advances in viral oncolytics for treatment of multiple myeloma – a focused review
Published in Expert Review of Hematology, 2021
Ayesha Sarwar, Laila Hashim, Muhammad Salman Faisal, Mobeen Zaka Haider, Zahoor Ahmed, Tehniat Faraz Ahmed, Moazzam Shahzad, Iqraa Ansar, Sundas Ali, Muhammad Muaaz Aslam, Faiz Anwer
Macrophages commonly infiltrate the tumor cells. They are of two subtypes, M1 and M2 [100]. They differ in the fact that M1 macrophages and M2 macrophages suppress and promote tumor growth, respectively. M2 macrophages are the common subtype of the macrophages in tumor tissue by secreting growth factors that positively influence angiogenesis and tumor matrix remodeling [101]. Many tumors, including multiple myeloma, release various monocytic chemotactic factors like monocyte chemo-attractant protein-1 (MCP-1) and vascular endothelial growth factor (VEGF). The monocytes that are recruited because of these chemotactic factors then differentiate into macrophages. Myeloma cells secrete VEGF that stimulates the production of IL-6 by the bone marrow stromal cells (BMSCs). Both VEGF and IL-6 stimulate myeloma growth. IL-6 is also responsible for increasing the MCP-1 release by the myeloma cells. As a result, IL-6 promotes myeloma growth both directly as well as indirectly by recruiting tumor-associated macrophages.
Protective Effects of Alpha-Lipoic Acid on Methotrexate-Induced Oxidative Lung Injury in Rats
Published in Journal of Investigative Surgery, 2018
Huseyin Arpag, Mehmet Gül, Yusuf Aydemir, Nurhan Atilla, Birgül Yiğitcan, Tugrul Cakir, Cemal Polat, Özer Þehirli, Muhammet Sayan
IL-1β and TNF-α are primary inflammatory cytokines produced by monocytes and macrophages in response to a range of stimuli including various microbial products, activated T cells, immune complexes, and the combined action of other cytokines. They cause leucocytes to move out of capillaries and accumulate at sites of injury or infection. This is because of their stimulating production of chemotactic factors and inducing adhesion molecules for leucocytes on vascular endothelium. The up-regulation of surface molecules such as E-selectin and intercellular adhesion molecule 1 (ICAM-1) causes leucocytes to attach to the endothelium, and then they move out into the extravascular space in response to chemotactic stimuli. Systemic inflammatory response indicators; IL-1β and TNF-α levels were also found increased in the serum of MTX group. Treatment with ALA decreased the level of plasma IL-1β and TNF-α.
Inhibition of CDC42 reduces macrophage recruitment and suppresses lung tumorigenesis in vivo
Published in Journal of Receptors and Signal Transduction, 2021
Bo Zhang, Jian Zhang, Lilong Xia, Jing Luo, Lei Zhang, Yanhui Xu, Xinhai Zhu, Guoping Chen
CDC42 plays an important role in the regulation of cytoskeleton [1] and is in connection with macrophage chemotaxis [24]. Macrophages can not only stimulate angiogenesis, but also enhance the invasion of tumor cells at the primary tumor sites [13]. It has been shown that macrophages can induce nitric oxide synthase to increased inflammation and promote lung cancer [25]. In the tumor microenvironment of metastasis, macrophages prime to the metastatic site and create a suitable environment for tumor extravasation and growth [26,27]. In addition, macrophages can protect tumors from attack by suppressing immune surveillance cells [28]. Therefore, our study further investigated whether macrophages were recruited to the primary tumor site in the allograft lung cancer model. The number of invasive macrophages was significantly reduced in the lung tumor site inoculated with CDC42 knockdown cells. In addition, the level of macrophage chemotactic factors was also decreased, indicating the number of macrophages in the tumor site inoculated with CDC42 knockdown LLC1 cells may be positively related with the level of chemotactic factor. In summary, our study demonstrated a correlation between CDC42 and lung cancer cell proliferation and invasion in a mouse model. To our knowledge, the reduction of CDC42 level was verified to prevent the pathogenesis and development of lung tumor in vivo for the first time. Moreover, CDC42 is partially responsible for the production of chemotactic factors. Lack of chemotactic factors can result in a significant decrease in macrophage recruitment at the primary tumor site. Above all, our study uncovered the key role of CDC42 in the tumorigenesis and development of lung cancer in vitro and in vivo which might provide a novel therapeutic target and potential strategy for lung cancer treatment in the future.