Infections in Cirrhosis in the Critical Care Unit
Cheston B. Cunha, Burke A. Cunha in Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Because enteric bacteria predominate in SBP, it is thought that the gut is the major source of organisms for this infection. Several mechanisms have been proposed to explain the movement of organisms from the intestinal lumen to the systemic circulation. Cirrhosis-induced depression of the hepatic reticuloendothelial system impairs the liver’s filtering function, allowing bacteria to pass from the bowel lumen to the bloodstream via the portal vein. Cirrhosis also is associated with a relative increase in aerobic gram-negative bacilli in the jejunum. A decrease in mucosal blood flow due to acute hypovolemia or drug-induced splanchnic vasoconstriction may compromise the intestinal barrier to enteric flora, thereby increasing the risk of bacteremia. Finally, bacterial translocation may occur with the movement of enteric organisms from the gut lumen through the mucosa to the intestinal lymphatics. From there bacteria can travel through the lymphatic system and enter the bloodstream via the thoracic duct. It is assumed that SBP caused by non-enteric organisms is also due to bacteremia secondary to another site of infection, with subsequent seeding of the peritoneum and ascitic fluid.
The patient with acute gastrointestinal problems
Ian Peate, Helen Dutton in Acute Nursing Care, 2014
Protection against harmful organisms is a responsibility shared between several components of the gastrointestinal system. The epithelial cells lining the gut prevent migration of organisms and the mucosa itself acts as a physical barrier. The intestinal walls contain lymphocytes and macrophages, with the mesentery hosting regional lymph nodes. Intraluminal Peyers patches secrete immunoglobulin A (IgA) to prevent adherence of bacteria to the mucosal cells. These gut actions supplement the activities of the Kupffer cells in the liver and the spleen’s role in trapping and phagocytosing bacteria. The acutely ill patient may thus suffer bacterial translocation if these functions are compromised as a result of altered permeability of the gut wall secondary to hypovolaemia, ischaemia or sepsis. Problems may occur also as a result of immunosuppression or increased bacterial growth in the gut secondary to overgrowth (e.g. blind loop syndrome) or intestinal stasis.
Nut Allergy
Andreas L. Lopata in Food Allergy, 2017
The specific roles gut flora play in gut development is less understood. Hooper and colleagues (Hooper et al. 2001) investigated the effect of inoculating germ free mice with a single microflora Bacterioides theaiotaomicron. This resulted in the increased expression of genes related to nutrient absorption, gut motility, barrier integrity and toxin metabolism. Interestingly, germ free mice are also more easily sensitised to the peanut allergen Ara h 1 compared to mice with normal intestinal microflora (Stefka et al. 2014). Indicating that microflora colonisation is necessary to protect against allergy, at least in mice. Also, treatment of two intestinal cell lines, LS-123 and IEC-6 respectively, with varying bacterial components (lipopolysaccharide from E. coli, K. pneuminia and P aeruginosa. Lipid A monophosphoryl from E. coli, lipothecoid acid from S. faecalis and peptidoglycan from S. aures) increased DNA expression in both cell types to variable degrees (Olaya et al. 2001). However, colonisation of the gut by certain bacteria have demonstrated direct interaction with tight junctions and thus modified barrier function by increasing intestinal permeability. Clostridium perfringens enterotoxin causes the delocalisation of the tight junction protein occludin in caco-2 tight junctions into larger more complex species within the cell (Singh et al. 2000). The same group also showed that the interaction caused cellular toxicity and that this toxicity permitted the access to additional tight junction proteins (Singh et al. 2001).
The human gut microbiota: Metabolism and perspective in obesity
Published in Gut Microbes, 2018
Aline Corado Gomes, Christian Hoffmann, João Felipe Mota
Besides acting on the maturation of GALT, the commensal bacteria also prevent the intestinal colonization by pathogens. The gut microbiota improves the function of the epithelial barrier, while its absence decreases the production of antimicrobial peptides by Paneth cells. This event causes intestinal barrier dysfunction and increases bacterial translocation.22 Furthermore, bacteria-induced myeloid differentiation factor 88 (MyD88) signaling in the intestine increases epithelial cell IgA secretion. In addition, bacterial flagellin activates Toll-like receptors 5 (TLR5) from dendritic cells, and promotes the differentiation of B lymphocytes into IgA-producing cells23 IgA binds to the microbial antigens, neutralizes the activity of the pathogens, and prevents infection.24
Zonulin levels in complicated pregnancy: a systematic review and meta-analysis
Published in Journal of Obstetrics and Gynaecology, 2022
Mojtaba Daneshvar, Anahita Yadegari, Davide Giuseppe Ribaldone, Mohaddeseh Hasanzadeh, Kurosh Djafarian
Moreover, diet composition is another possible contributing factor to circulating levels of zonulin (Mokkala et al. 2017b). In a number of studies on both pregnant and non-pregnant population higher dietary fibre has been shown to be associated with lower serum zonulin levels (Mokkala et al. 2016; Leech et al. 2019). In addition, some previous studies have reported an association between higher circulating levels of zonulin and higher anthropometric indices including body mass index and waist to hip ratio (Moreno-Navarrete et al. 2012; Żak-Gołąb et al. 2013). During the course of a normal pregnancy, various hormonal and immunological adaptations occur in order to ensure optimal growth and development of the foetus (Selma-Royo et al. 2021). These adaptations and also the process of implantation and placentation in early pregnancy result in a physiological low level inflammation. It is known that a precise balance between pro-inflammatory and anti-inflammatory cytokines and chemokines is crucial for a normal pregnancy (Kalagiri et al. 2016). Upregulation of zonulin can alter this balance by increasing pro-inflammatory cytokines as a result of the increased intestinal permeability and the immune response it triggers (Sturgeon and Fasano 2016). Another possible consequence of increased gut permeability is bacterial translocation. It has been shown that translocation of bacteria to placenta can result in local inflammation by invading epithelial cells (Chen et al. 2020). This added load of inflammation can predispose to onset of numerous complications for both mother and foetus (Tomsett et al. 2020).
Fungal lysozyme leverages the gut microbiota to curb DSS-induced colitis
Published in Gut Microbes, 2021
Ida Søgaard Larsen, Benjamin A. H. Jensen, Erica Bonazzi, Béatrice S. Y. Choi, Nanna Ny Kristensen, Esben Gjerløff Wedebye Schmidt, Annika Süenderhauf, Laurence Morin, Peter Bjarke Olsen, Lea Benedicte Skov Hansen, Torsten Schröder, Christian Sina, Benoît Chassaing, André Marette
Compared to obesity, gut health is further disrupted in IBD with clear genetic links to diminished HDP production.18,19 Bacterial translocation is well established in patients with IBD20,21 associating with reduced gut barrier function22 and a change in gut microbiota composition.23,24 Thus, obesity and IBD exhibit similar GI complications, although the links between the two phenotypes remain inadequately described.25 When the gut microbiota was evaluated by 16S rRNA gene amplicons, no similarities in microbiota composition changes within patients with obesity and IBD were reported.26 However, with more advanced network analysis, common regulation of specific enzymes involved in the phosphotransferase system or the nitrate reductase pathway has been identified between these patient groups27 supported by a change in bacterial co-abundances.28 Similarly, frameshift mutations in the pattern recognition receptor, nucleotide-binding oligomerization domain-containing protein 2 (NOD2), predispose for human IBD,29 while genetic ablation of the same protein promotes IR in HFD-fed mice.30 Patients with IBD exhibit increased prevalence of IR and nonalcoholic fatty liver disease (NAFLD), thus supporting a close connection between the mentioned diseases.31,32 Still, IR and IBD are rarely studied together, although both pathologies are increasing worldwide.33,34
Related Knowledge Centers
- Coeliac Disease
- Gastrointestinal Tract
- Intestinal Epithelium
- Mucous Membrane
- Toxin
- Antigen
- Gastrointestinal Wall
- Lumen
- Nutrient
- Electrolyte