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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.
Eosinophil–Epithelial Interactions and Transepithelial Migration
Published in Bruce S. Bochner, Adhesion Molecules in Allergic Disease, 2020
Mary K. Schroth, James M. Stark, Julie B. Sedgwick, William W. Busse
The respiratory epithelium expresses a limited number of known adhesive ligands. Of these, only intercellular adhesion molecule-1 (ICAM-1, CD54) has been identified on the respiratory epithelium in vitro (84,85) and in vivo in biopsies from asthmatic subjects (86,87). ICAM-1 is a single-chain glycoprotein belonging to the immunoglobulin superfamily; it consists of five immunoglobulin-like extracellular domains, a single membrane-spanning domain, and a short cytoplasmic tail (88,89). Migratory inflammatory cells, including eosinophils (90–93), neutrophils (13,69), T lymphocytes (94), and basophils (95), bind to ICAM-1 via the β2 integrin family of proteins, which are heterodimers of two subunits containing a common β chain (CD18) and one of three alpha chains (CD11a, CD11b, CD11c) (96). Inflammatory cell-ICAM-1 adhesion is mediated by CD11a/CD18 (LFA-1) binding to the amino-terminal domain of ICAM-1 (domain 1, which also serves as a receptor for rhinovirus), and by CD11b/CD18 (Mac-1) binding to ICAM-1 domain 3 (71,89,97–102).
Pathophysiology of Spinal Cord Injury in a Rat Model of Decompression Sickness
Published in John J. Lemasters, Constance Oliver, Cell Biology of Trauma, 2020
The lack of detectable inflammatory reaction supports the notion that extensive ischemic injury or tissue trauma does not play a major role in the cord injury in rats with decompression sickness. In contrast with the lack of leukocyte and central nervous system effector cell reaction, evidence of endothelial cell activation (increased ICAM-1 immunostaining) was found in the rats subjected to diving. ICAM-1 can be induced in several cell types by a number of cytokines. In the central nervous system, increased ICAM-1 immunostaining has been found in areas of necrosis and inflammation.22 In the rat decompression sickness model, increased ICAM-1 immunostaining appears to be functionally unrelated to the cellular inflammatory reaction. The increased immunostaining may be a consequence of sublethal injury to endothelial cells caused by intravascular free gas.
Upregulation of claudin‑4 by Chinese traditional medicine Shenfu attenuates lung tissue damage by acute lung injury aggravated by acute gastrointestinal injury
Published in Pharmaceutical Biology, 2022
Yueliang Zheng, Mian Zheng, Jing Shao, Chengxing Jiang, Jian Shen, Rujia Tao, Yuqin Deng, Yingge Xu, Yuanqiang Lu
Next, we assessed the pathological state of the gastrointestinal tissue of the ALI model mice. ICAM-1 is a cell surface glycoprotein and an adhesion receptor known to play the central role in inflammation (Bui et al. 2020). WB of large intestine tissue showed that ICAM-I was upregulated in the ALI mice (Figure 6(A)). MPO activity is a very sensitive marker that reflects both neutrophil accumulation and neutrophil activation. It is regarded as one of the most sensitive markers of tissue inflammation available. MPO activity in the colonic mucosa was also analyzed for the biochemical evaluation of tissue damage. Consistent with the ICAM-1 expression results, MOP activity was elevated in the large intestine of the ALI mice, suggesting ALI was accompanied by gastrointestinal injury in these mice (Figure 6(B)). However, in the Shenfu-treated ALI mice, intestinal MOP activity and ICAM-1 expression were suppressed, implying diminished tissue inflammation and injury after Shenfu injection (Figure 6(A,B)).
The Overlap between Genetic Susceptibility to COVID-19 and Skin Diseases
Published in Immunological Investigations, 2022
Navid Jabalameli, Fateme Rajabi, Alireza Firooz, Nima Rezaei
The 9q34.2 locus and the rs657152 have not yet been linked to any type of cutaneous disease. The peak association signal within 9p34.2 contains the ABO blood group genes. Further analysis based on three blood group-determining SNPs showed that individuals with the O blood group had a lower risk for developing COVID-19 and individuals with the A blood group had a higher chance for hospitalization and respiratory failure. Several explanations have been provided for this association, but what grasped our attention is the impact of blood groups on the transcription level and concentration of soluble intercellular adhesion molecule‐1 (sICAM‐1) and soluble E-selectin (Blann et al. 1996; Paré et al. 2008). Both markers are increased in severe COVID-19; thus the link between disease severity and blood groups might be mediated by the effect of blood groups on these markers (Smadja et al. 2020, Tong et al. 2020). ICAM-1 and E-selectin are both expressed on endothelial cells and facilitate leukocyte adhesion and migration. ICAM-1 is implicated in the pathogenesis of many inflammatory diseases such as psoriasis (Bressan et al. 2018; Schopf et al. 1993), lichen planus (Lecewicz‐Toruń et al. 1997), atopic dermatitis (Koide et al. 1994), and cutaneous lupus erythematosus (Guo Liu et al. 2020; Witkowska and Borawska 2004). E-selectin also plays a role in the pathogenesis of psoriasis (Szepietowski et al. 1999), atopic dermatitis (Czech et al. 1996), and erythema nodosum (Amoli et al. 2004). Thus the presence of these dermatologic conditions can be a hint for having a higher risk for severe COVID-19.
The blood-gas barrier in COVID-19: an overview of the effects of SARS-CoV-2 infection on the alveolar epithelial and endothelial cells of the lung
Published in Tissue Barriers, 2021
Hypoxemia, defined as an oxygen saturation below 90%, is a common early clinical finding in patients with COVID-19. Low oxygen saturation in the absence of gross pulmonary pathology or respiratory dysfunction, as observed with COVID-19, is strongly indicative of an ongoing destructive process at the BGB; which mediates the exchange of O2 and CO2 in an otherwise healthy individual. It is suggested that the COVID-19-associated hypoxemia might be due to a dysfunctional BGB4 characterized by endothelial injury5 and extensive distortions in the pulmonary vascular bed6. These distortions could be attributed to the disintegration of ECM proteins and disruption of intercellular junctions that might result in the loosening of cell–matrix and cell–cell contact, respectively7. Endothelial injury, on the other hand, was suggested to be strongly associated with increased plasma levels of ‘intercellular adhesion molecule-1ʹ (ICAM-1) in patients with COVID-19 (Figure 1). Upregulated in response to inflammation, ICAM-1 is a marker of endothelial injury known to induce the release of pro-inflammatory cytokines in the alveoli5.