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Bile Acids in the Pathogenesis of Necrotizing Enterocolitis
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
While the importance of ileal proinflammatory mediators in necrotizing enterocolitis (NEC) is well established, the gut–liver axis also contributes to disease development. Tumor necrosis factor-alpha (TNF-α) and interleukin-18 (IL-18) produced in the liver are correlated with the progression of intestinal damage in experimental NEC, and when Kupffer cells (KC), the resident hepatic macrophage, are inhibited, the incidence and severity of NEC are significantly decreased (1). These results suggest the importance of the liver in disease pathophysiology through the release of inflammatory mediators into the biliary system and initiated a search for other hepatic-derived mediators that might play a role in NEC.
Anti-infectious innate and adaptive immune responses
Published in Gabriel Virella, Medical Immunology, 2019
Carl Atkinson, Gabriel Virella
Interleukin-18. IL-18, produced primarily by macrophages and related cells, was initially named “interferon-γ inducing factor,” reflecting its major biological role. In many respects, it is similar to IL-1 and IL-12. IL-18 is produced and released by APCs, and its main targets are Th0/Th1 CD4+ T cells and NK cells. However, in combination with other cytokines and cell-cell interactions, it can also induce Th2 lymphocyte activation.
Cryptosporidium
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Una Ryan, Nawal Hijjawi, Lihua Xiao
CD4+ T lymphocytes and Th-1 immune responses play a key role in acquired immunity against cryptosporidiosis, but CD8+ T lymphocytes and dendritic cells contribute to the clearance of the parasite from the intestine.112,116,117 These protective immune responses appear to be mediated through TLR4/NF-κB–dependent nitric oxide production.114,118 TLR4/NF-κB–regulated responses are probably also involved in innate immunity against Cryptosporidium spp. For example, luminal release of exosomes from the biliary and intestinal epithelium is increased following infection with C. parvum, and the release of exosomes involves activation of TLR4/IKK2 signaling. As exosomes are involved in the transfer of epithelial antimicrobial peptides, it was suggested that TLR4 regulates luminal exosome release and shuttling of antimicrobial peptides from the gastrointestinal epithelium.119 Recently, it was further shown that let-7i–regulated SIRT1 expression could be involved in NF-κB–mediated epithelial innate immune responses to C. parvum.120 Natural killer cells are probably also involved in innate immune responses against C. parvum. In addition, they can rapidly drive the establishment of acquired immune responses through the early recruitment of CD8+ T cells,121 and interleukin-18 has been shown to be involved in innate immunity against C. parvum infection.121,122
IL18-family Genes Polymorphism Is Associated with the Risk of Myocardial Infarction and IL18 Concentration in Patients with Coronary Artery Disease
Published in Immunological Investigations, 2022
Anastasia V. Ponasenko, Anna V. Tsepokina, Maria V. Khutornaya, Maxim Yu. Sinitsky, Olga L. Barbarash
Interleukin 18 (IL18) is a pleiotropic proinflammatory cytokine stimulating the production of interferon-gamma (IFNγ), tumor necrosis factor-alpha (TNFα), interleukin 1 (IL1), interleukin 2 (IL2), cell adhesion molecules, and apoptosis-inducting factors, promoting proliferative activity of T-lymphocytes and lytic activity of natural killer cells (NK cells) (Nakanishi et al. 2001). It can be a pathogenetic factor in the development of the diseases accompanied by acute and chronic inflammation, including atherosclerosis (Varghese et al. 2016; Yasuda et al. 2019; Zykov et al. 2015). In addition, elevated IL18 levels are associated with other cardiovascular diseases (CVD), including acute coronary syndrome, type 2 diabetes, metabolic syndrome, and arterial hypertension. They are associated with CVD adverse prognosis and high mortality (Chalikias et al. 2005; Zhang et al. 2017). The relationship of IL18 gene polymorphism with adverse coronary events in coronary artery disease (CAD) patients has been recently reported (Opstad et al. 2013; Xie et al. 2015). Moreover, serum levels of IL18 are determined by IL18 gene polymorphism (Martinez-Hervas et al. 2015; Opstad et al. 2011).
Current concepts and advances in biomarkers of acute kidney injury
Published in Critical Reviews in Clinical Laboratory Sciences, 2021
Activation of inflammatory pathways and recruitment of inflammatory cells are early responses to kidney injury. Biomarkers of inflammation during AKI are depicted in Figure 2. During this process, interleukin-18 (IL-18) is synthesized as an inactive precursor at multiple sites, including bone marrow-derived macrophages, proximal tubular epithelial cells, and intercalated cells in the collecting duct [55]. IL-18 is then cleaved by caspase-1 and released into the tubular lumen and serum, leading to neutrophil infiltration and further tubular injury [56]. Urinary IL-18 was shown to be an early diagnostic marker of AKI and predicted mortality post-cardiac surgery and in ICU settings [57–60]. It is worth noting that although measurement of IL-18 is readily available via established enzyme-linked immunosorbent assays, sample storage at room temperature for a prolonged period of time may lead to measurement bias [61]. In reaction to proinflammatory cytokines such as IL-1β and tumor necrosis factor-α (TNF-α), kidney tubular cells produce monocyte chemoattractant protein-1 (MCP-1) to attract monocytes and tissue macrophages [62]. Urinary MCP-1 is likely produced locally by the kidney, as there is a lack of correlation between urinary and serum MCP-1 levels [7]. Urinary MCP-1, however, correlates well with AKI in cisplatin-induced nephrotoxicity or following cardiac surgery [63,64]. MCP-1 can be measured using a similar platform as UMOD [44].
Interleukin-18 is associated with the presence of interstitial lung disease in rheumatoid arthritis: a cross-sectional study
Published in Scandinavian Journal of Rheumatology, 2019
T Matsuo, M Hashimoto, I Ito, T Kubo, R Uozumi, M Furu, H Ito, T Fujii, M Tanaka, C Terao, H Kono, M Mori, M Hamaguchi, W Yamamoto, K Ohmura, S Morita, T Mimori
Interleukin-18 (IL-18) is a member of the IL-1 cytokine superfamily. It is produced mainly by macrophages and regulates the T-cell immune response during host defence (18). In the lung, IL-18 can be produced by resident macrophages. It has been reported that IL-18 levels are increased in ILD patients. Furthermore, serum IL-18 levels were associated with the presence of ILD in polymyositis and dermatomyositis patients (19, 20). Other reports have described that IL-18 levels in serum and bronchoalveolar lavage fluid were higher in patients with non-specific interstitial pneumonia (NSIP) or usual interstitial pneumonia (UIP) than in healthy controls (21, 22). Animal studies have also suggested pathogenic roles of IL-18 in the development of lung inflammation (23–25). Administration of IL-18 and IL-2 induces fatal acute ILD in mice (26). Based on these findings, it is possible that IL-18 is associated with the pathological mechanism of ILD in RA patients.