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Infection and Inflammation
Published in Michael Ljungberg, Handbook of Nuclear Medicine and Molecular Imaging for Physicists, 2022
Erik H. J. G. Aarntzen, Andor W. J. M. Glaudemans
Macrophage derived pro-inflammatory cytokines, mainly TNFα, IL-6 and IL-1β, act not only on immune cells with professional antigen presenting capacity, but also systemically. The liver responds by producing acute-phase proteins, stimulating the activation of complement system, and fibrinogen. In case of a systemic inflammatory response, called sepsis, there is widespread leakage from blood vessels, leading to edema, decreased blood volume, collapse of vessels and disseminated intravascular coagulation [15]. This eventually may lead to organ failure and even death.
Ozone-induced acute phase response in lung versus liver: the role of adrenal-derived stress hormones
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Devin I. Alewel, Andres R. Henriquez, Catherine H. Colonna, Samantha J. Snow, Mette C. Schladweiler, Colette N. Miller, Urmila P. Kodavanti
The acute-phase response (APR) is a rapid host defense system characterized by the synthesis of specialized proteins that drive physiological changes to counteract stressful events (Gruys et al. 2005). Immediately following the encounter of common stressors like tissue injury or infection, pro-inflammatory cytokines, such as interleukin-6 (IL-6), interleukin-1 (IL-1), and tumor necrosis factor-α (TNF-α), are proposed to trigger the production of acute-phase proteins (APPs) (Gulhar, Ashraf, and Jialal 2020) to augment tissue repair processes and reestablish homeostasis (Cray, Zaias, and Altman 2009). The APR may also be induced by homeostatic imbalances in response to inhaled environmental pollutant exposures (Elder et al. 2004; Shannahan et al. 2012). In addition, acute psychosocial pressures that activate the hypothalamus-pituitary-adrenal (HPA) stress axis act through neuroendocrine mechanisms to induce an acute-phase event (Marsland et al. 2017). Previous reviews of APR identified the liver as the primary target of cytokine signaling and subsequent APP synthesis and regulation (Cray, Zaias, and Altman 2009; Kuscuoglu et al. 2018).
Reallocating sitting time to standing or stepping through isotemporal analysis: associations with markers of chronic low-grade inflammation
Published in Journal of Sports Sciences, 2018
Joseph Henson, Charlotte L. Edwardson, Danielle H. Bodicoat, Kishan Bakrania, Melanie J. Davies, Kamlesh Khunti, Duncan C. S. Talbot, Thomas Yates
Low-grade inflammation has been proposed to be involved in the underlying pathogenesis of type 2 diabetes mellitus (T2DM) (Wang et al., 2013). This manifestation is thought to be a result of an ongoing acute-phase response, primarily characterised by alterations in acute-phase proteins, such as C-reactive protein (CRP) (Pradhan, Manson, Rifai, Buring, & Ridker, 2001). More specifically, mediators of inflammation which include the interleukin 6 (IL-6) family of cytokines have been proposed to affect glucose homeostasis and metabolism directly and indirectly by action on skeletal muscle cells (Kristiansen & Mandrup-Poulsen, 2005). Previous studies have established an inverse relationship between the amount of physical activity and proinflammatory cytokines in obesity, T2DM, and the metabolic syndrome (Hamer et al., 2012; Kasapis & Thompson, 2005). Therefore, the beneficial effects of physical activity may be partly mediated by changes in the adipokines profile.
On the interpretation of bioaerosol exposure measurements and impacts on health
Published in Journal of the Air & Waste Management Association, 2019
Hamza Mbareche, Lidia Morawska, Caroline Duchaine
Health markers used to evaluate the health impact of bioaerosol exposure have not been standardized. Here, we present a summary of the measures typically used when health impact was included in the experimental design of bioaerosol studies. Cardiopulmonary markers including blood pressure, pulse, and heart rate variability are often considered (Cole-Hunter et al. 2018). Lung function is evaluated using spirometry and often the Tiffeneau-Pinelli index (FEV1/FVC; forced expiratory volume in the first second/forced vital capacity) to compare exposed subjects with nonexposed controls (Farokhi, Heederik, and Smit 2018; Magzamen et al. 2018). Blood samples from exposed subjects are commonly used to investigate inflammatory mechanisms or as exposure markers, either by measuring total and specific immunoglobins (IgE and IgG) or by determining blood levels of neutrophils, cytokines (tumor necrosis factor-α [TNF-α], interleukin-1β [IL-1β], or interleukin-6 [IL-6]). and the acute-phase proteins serum amyloid A (SAA) and C-reactive protein (CRP) (Blais-Lecours et al. 2011; Bønløkke et al. 2009; Brauner et al. 2017; Cormier et al. 1997, 2000; Eduard 1995; Faridi et al. 2017; Madsen et al. 2016; Müller et al. 2006; Van Kampen et al. 2016). However, these biomarkers of exposure indicating health, biological effects, or susceptibility of individuals do not always give clear information about workers’ exposure (Douwes et al. 2003). In some cases, there are no differences in IgG antibodies levels to molds detected in the air between workers and unexposed controls (Zhang et al. 2012). Likewise, sputum, BAL, and nasal lavage can also be used for inflammatory cell quantification (Bønløkke et al. 2012b; Hoffmann et al. 2005; Huijskens et al. 2016).