China 
Africa 
Explore chapters and articles related to this topic
Gut Microbiome and Heavy Metals
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Ashfaque Hossain, Muhammad Manjurul Karim, Tania Akter Jhuma, Godfred A. Menezes
One of the major functions of gut microbiome that is beneficial to the host is fermentation of non-digestible carbohydrates such as resistant starches, cellulose, hemicellulose, gums, and pectins, resulting in the generation of SCFAs (acetic acid, propionic acid, butyric acid; Figure 6.4), which serve as energy source to colonic epithelial cells, which is characteristic of microbiome of type-1 enterotype (Arumugam et al., 2011; Terminology). In addition, SCFAs stimulate differentiation and proliferation of intestinal epithelial cells (Cummings and Macfarlane, 1991; Sharma and Devi, 2014; Hossain et al., 2015). SCFAs are considered as markers of eubiotic microbiome. Although proteins constitute an essential component of healthy diet, excessive consumption of protein and fat diet (for example, Western diet) leads to the development of dysbiotic microbiome (type-2 enterotype; Arumugam et al., 2011; Terminology) (Bifari et al., 2017; Hussain et al., 2019), especially in overweight individuals, which is characterized by excess production of BCAAs (valine, leucine, and isoleucine, Figure 6.4). Excess BCAA has been linked with insulin resistance and development of type-2 diabetes (Ley et al., 2006; Lynch and Adams, 2014; Karusheva et al., 2019). Enrichment of proteolytic bacterial population leads to enhanced degradation of gut mucin, and hence increased gut permeability and resultant inflammation due to translocation of lipopolysaccharide (LPS) and other bacterial products (Hossain et al., 2016; Hussain et al., 2019).
Cyanobacterial toxins
Published in Ingrid Chorus, Martin Welker, Toxic Cyanobacteria in Water, 2021
As discussed above, lipopolysaccharides (LPS) from bacterial heterotrophs becomes a critical health issue when it is released from tissue infections or inflammations and enters the bloodstream. Routes for exposure to cyanobacterial LPS are quite different from such clinical cases: systemic infections with cyanobacteria are very unlikely and have never been reported (in contrast to infections with green algae such as nonautotroph Prototheca spp.); thus, an increase of LPS from multiplication of cyanobacteria in the human body can be excluded.
Biological and Biochemical Analysis of Bacteria and Viruses
Published in Christopher S. Cox, Christopher M. Wathes, Bioaerosols Handbook, 2020
Andreas Hensel, Klaus Petzoldt
Lipopolysaccharides (LPS) are components of the outer membrane of all Gram-negative bacteria species (Gram-positive bacteria cannot be detected with this test). The lipid portion of the molecule, which is anchored in the cell membrane, is the strong, biologically active pyrogen. The pathophysiological effects of endotoxin, the whole LPS molecule, do not require living bacteria.117
Circulating markers of intestinal barrier injury and inflammation following exertion in hypobaric hypoxia
Published in European Journal of Sport Science, 2023
Zachary J. McKenna, Bryanne N. Bellovary, Jeremy B. Ducharme, Michael R. Deyhle, Andrew D. Wells, Zachary J. Fennel, Jonathan W. Specht, Jonathan M. Houck, Trevor J. Mayschak, Christine M. Mermier
Under normal physiological conditions the intestinal epithelium operates in a state of “physiologic hypoxia”, often characterized as a steep oxygen gradient from the submucosa to the intestinal lumen (Konjar et al., 2021; Singhal & Shah, 2020; Zheng et al., 2015). Indeed, this physiologic hypoxia allows for several intracellular adaptations that collectively promote intestinal barrier homeostasis via hypoxia inducible factors (Konjar et al., 2021; Singhal & Shah, 2020; Zheng et al., 2015). However, in some scenarios this hypoxia can become pathological resulting in intestinal injury and inflammation (Singhal & Shah, 2020). High altitude exposures can reduce splanchnic perfusion (Loshbaugh et al., 2006) and lower blood oxygen levels causing local hypoxic and oxidative stress in the gut (Dosek et al., 2007). These stressors can injure the intestinal barrier leading to increased intestinal permeability and bacterial endotoxin translocation (Lian et al., 2021; McKenna et al., 2022b). The translocation of Gram-negative bacteria which harbor lipopolysaccharides (LPS) on their outer membrane can activate innate immune cells via Toll like receptor-4 (TLR-4) to initiate local and systemic inflammatory responses (Ducharme et al., 2022). Indeed, residence at high altitude has been shown to damage the intestinal barrier and increase intestinal permeability (Karl et al., 2018). Subsequent LPS-mediated increases in pro-inflammatory cytokines could cross the blood brain barrier and contribute to central nervous system dysfunction which may be a contributing factor to development of AMS (Banks et al., 1995).
The influence of climate change on human cardiovascular function
Published in Archives of Environmental & Occupational Health, 2020
Milos Gostimirovic, Radmila Novakovic, Jovana Rajkovic, Vladimir Djokic, Dusko Terzic, Svetozar Putnik, Ljiljana Gojkovic-Bukarica
Severe consequences high temperatures have on human health are represented through direct effects of thermal stress. When the heat exceeds the ability of human protective mechanisms to cool the organism down, a cascade of pathological events will finally lead to the cardiovascular impairment. Mechanism of heat-induced cardiovascular dysfunction is further explained. After activating sweat glands, dilating blood vessels and increasing skin blood flow, consequent water loss leads to a dehydration followed by hemoconcentration and increased risk of an ischemic stroke and thromboembolism.15 Redirecting blood flow from the gut increases gut epithelial membrane permeability and allow more bacteria to get into systemic circulation. Once they get into the blood stream and after releasing different endotoxins and lipopolysaccharides (LPS), activated immune response starts to break down, developing syndrome of systemic inflammatory response (SIRS) and multiple organ dysfunction syndrome (MODS). On the other hand, thermal stress can directly damage vascular endothelium which can be an additional factor in the genesis of cardiovascular dysfunction.15,16 Common climate-associated diseases include hypertension, heart rate disturbances, acute/chronic kidney disease, ischemic heart disease, tromboembolic disease, obesity and metabolic syndrome.16 Various climate patterns across the world cause seasonal differences in frequency and severity of those diseases, but many of them have a higher incidence during summer, in tropic areas and during hot waves.
Targeting gap junctional intercellular communication by hepatocarcinogenic compounds
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Kaat Leroy, Alanah Pieters, Andrés Tabernilla, Axelle Cooreman, Raf Van Campenhout, Bruno Cogliati, Mathieu Vinken
Lipopolysaccharide (LPS) is an endotoxin located in the outer membrane of Gram-negative bacteria that initiates acute inflammation in animals. A number of studies reported marked reduction of Cx32 production in response to administration of LPS in vitro (Yang et al. 2019) and in vivo in both mice (Temme et al. 2000) and rats (Correa et al. 2004; Gingalewski et al. 1996; Gonzalez et al. 2002). This reduction may be attributed to enhanced protein degradation and inhibition of Cx32 mRNA expression (Yang et al. 2019). This is associated with lowered mRNA stability induced by alterations in posttranscriptional modifications of Cx32 gene expression, such as shortening of the poly(A)tail (Gingalewski et al. 1996; Theodorakis and De Maio 1999). Concurrently, Gonzalez et al. (2002) noted that GJIC was inhibited. Based upon data from rat hepatocytes, it was postulated that not LPS alone, but activated Kupffer cells and their secreted pro-inflammatory mediators are responsible for reduced number of GJIC. In contrast, GJIC is induced in rat hepatic stellate cell cultures and Kupffer cell cultures upon exposure to pro-inflammatory compounds because of enhanced protein and mRNA Cx43 expression (Eugenin et al. 2007; Fischer et al. 2005). Results for Cx26 are not consistent, as both upregulation (De Maio et al. 2000; Temme et al. 2000) and downregulation (De Maio et al. 2000; Gonzalez et al. 2002) of its protein and mRNA content were detected.