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Gene Knockout Technology and the Host Response to Endotoxin: Role of CD14 and Other Inflammatory Mediators
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
Resistance of mice deficient in ICAM-1 to the lethal effects of LPS is thought to be associated with a lack of cell-cell interaction. ICAM-1 (intercellular adhesion molecule 1) is an adhesion molecule expressed by leukocytes and vascular endothelium; it is a ligand for Mac-1 and LFA-1, members of the β2 subfamily of integrins expressed on leukocytes (44). ICAM-1 mediates at least one third of the binding of lymphocytes and monocytes to resting endothelial cells based on in vitro studies; stimulation of endothelial cells with LPS results in upregulation of ICAM-1 expression and an increase in the binding of leukocytes. Accordingly, ICAM-1–deficient mice have high blood leukocyte counts, with two- to sixfold more blood neutrophils and two- to threefold more blood lymphocytes than control mice. Administration of LPS results in a strong reduction in the number of neutrophils in the blood of both control and ICAM-1-deficient mice 2 hours after administration; however, 6 hours after administration of LPS, the ICAM-1–deficient animals show a major increase in the number of blood neutrophils (at least fivefold higher), which continues to increase to at least ninefold higher than controls by 24 hours. This increase of blood neutrophils is mirrored by a strongly reduced emigration of neutrophils to the liver in ICAM-1-deficient mice by 24 hours and an increase in neutrophils in the sinusoids (44). These studies show that the resistance to LPS seen in ICAM-1–deficient mice is not due to reduced levels of cytokines, but to a decrease in neutrophil transmigration.
Gene Therapy for Chronic Inflammatory Diseases of the Lungs
Published in Kenneth L. Brigham, Gene Therapy for Diseases of the Lung, 2020
Several of the same gene therapeutic strategies theoretically beneficial in IPF are applicable to asthma. Cyclo-oxygenase gene therapy and the consequent production of the PGE2 could mediate the inflammation present in the airways of asthmatics (82). Antisense gene therapy directed against cellular adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) could modulate leukocyte trafficking into the lungs. Modulation of the cytokine cascade is another possibility for gene therapy. This could include antisense gene therapy against several cytokines such as TNF-α, IL-4, or IL-5 or possibly gene therapy with interferon γ or IL-10 (83).
Interaction of Immune and Connective Tissue Cells
Published in Brian J. Nickoloff, Dermal Immune System, 2019
Joseph H. Korn, Theresa Piela-Smith
Intercellular adhesion molecule-1 (ICAM-1) is an important cell surface adhesive glycoprotein found on many different cell types, including endothelial cells, whose expression can be upregulated by many cytokines, including IL-1 and interferon (IFN)-γ.8 A circulating form of ICAM-1 has also been identified in normal human serum.9,10 ICAM-1 functions in intercellular adhesion reactions by binding to its principal leukocyte integrin ligand, lymphocyte function-associated antigen-1 (LFA-1), which is a heterodimer complex restricted to white blood cells.11,12 ICAM-1 is capable of binding to a second leukocyte integrin, MAC-1,13 albeit with lower avidity than to LFA-1,14 as well as serving as the obligate receptor for major group rhinoviruses.15,16 Structurally, the ICAM-1 molecule contains five extracellular immunoglobulin (Ig)-like domains, a single transmembrane region, and a short cytoplasmic tail, and therefore is included as a member of the Ig supergene family.17,18 The binding site for LFA-1, as well as for rhinovirus, has been localized primarily to the first Ig-like domain.19 ICAM-l/LFA-1 interaction is only one of many mechanisms by which lymphocytes can adhere to endothelial cells.
Novel nano-carriers with N-formylmethionyl-leucyl-phenylalanine-modified liposomes improve effects of C16-angiopoietin 1 in acute animal model of multiple sclerosis
Published in Drug Delivery, 2023
Xiao-Xiao Fu, Han Qu, Jing Wang, Hua-Ying Cai, Hong Jiang, Hao-Hao Chen, Shu Han
As targets of the C + A compound, the expression of Tie2 and integrin αVβ3 was significantly upregulated in vascular ECs (Jiang et al., 2014). Previous studies indicated that Ang-1 may be involved in maintaining EC integrity of blood vessels, promoting survival of ECs, and preventing vascular leakage through the Ang-1-Tie2 system (López-Vales and David, 2019). However, it can also prevent inflammatory cells from adhering together through the inhibition of adhesion factors, including intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) (Liang et al., 2015). The major machinery of C16 functions in a competitive manner to disturb the binding of αVβ3 integrin and inflammatory cells to the endothelium, and ultimately attenuate the transmigration of leukocytes (Jiang et al., 2014). Although Ang-1 and C16 have some overlapping functions, together the C + A compound has been shown to prevent edema in the CNS and improve the function of tight junctions between ECs in the CNS of EAE animals. In the vehicle group of EAE rats, there was reduced ECR staining and MBP immunoreactivity, and the myelin sheath with abundant loose, fused, and fragmented spires, suggesting extensive demyelination. The CNS is susceptible to axonal injury, which can result in defective conduction and functional loss. In addition, electrophysiological recordings also indicated one reduced amplitude and delayed latency of c-SEP responses (to sensory stimuli) and c-MEP responses (for motor function), suggesting focal demyelination and axonal damage.
Heterogeneity of T cells and macrophages in chlorine-induced acute lung injury in mice using single-cell RNA sequencing
Published in Inhalation Toxicology, 2022
Chen-qian Zhao, Jiang-zheng Liu, Meng-meng Liu, Xiao-ting Ren, De-qin Kong, Jie Peng, Meng Cao, Rui Liu, Chun-xu Hai, Xiao-di Zhang
T-helper lymphocytes (Th) can reflect the balance between pro-inflammatory and anti-inflammatory (Zedler et al. 1999). The conversion of the Th1 phenotype to T-helper 2 (Th2) at the onset of ALI suggests that the anti-inflammatory response tends to be enhanced at the onset of ALI, and the enhancement of the anti-inflammatory response induces a depressed cellular immune function in the body. In this study, we identified many genes and signaling pathways associated with activation of T cell immune response by top10 marker gene. Ets1, Elf1 and Elk3 expression were upregulated. Ets1 has an important role as a key transcriptional repressor in blocking the differentiation of Th2 and Th17 cells, thus inhibiting the onset and progression of inflammation (Lee et al. 2019). Elf1 not only regulates CD25, which is involved in T cell activation, but also CD247, which couples antigen recognition of T cell receptors to several intracellular signaling pathways (Goudy et al. 2013; Ben Khalaf et al. 2019). Intercellular adhesion molecule-1 (ICAM-1) is a major factor in the damage of inflammatory organs (Zhang et al. 2010). Interestingly, over-expression of Elk3 suppresses the protein levels of (Radbel et al. 2020; Cao et al. 2021). Therefore, these genes are expected to be a target gene for the treatment of ALI caused by Cl2. The mechanism of Ets1, Elf1 and Elk3 in Cl2 injury needs further study.
High serum sICAM-1 is correlated with cerebral microbleeds and hemorrhagic transformation in ischemic stroke patients
Published in British Journal of Neurosurgery, 2018
Bo-Na Wu, Jing Wu, Dong-Lin Hao, Lun-Lin Mao, Jin Zhang, Ting-Ting Huang
Intercellular adhesion molecule 1 (ICAM-1) is a glycoprotein which belongs to the immunoglobulin superfamily, and is constitutively expressed on endothelium and plays a variety of functions, such as inflammatory responses, cellular stresses, reactive oxygen species production, and cell proliferation.8,9 Membrane-bound ICAM-1 protein can be cleaved and released to form soluble ICAM-1 (sICAM-1) into the bloodstream where it acts as a marker of ICAM-1.10 High circulating sICAM-1 levels have been observed in many diseases, such as atherosclerosis, coronary heart disease, systemic lupus erythematosus, idiopathic pulmonary fibrosis, and cancers.11–15