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Inflammation and Infection
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Judith Hall, Christopher K. Harding
P. mirabilis urease is expressed during growth in urine:Hydrolysis of urea to carbon dioxide and ammonia.Creates alkaline urine → calcium crystal (apatite) formation and magnesium ammonium phosphate precipitates (struvite)Crystals become trapped within polysaccharides produced by attached bacterial cells → crystalline biofilms on tissues/cathetersAmmonia is toxic to urothelial cells.The urinary tract is limited in iron (an essential element for bacterial growth).Uropathogens synthesise siderophores to scavenge, chelate, and transport iron (Fe3+).Siderophores synthesised include the proteins aerobactin, yersiniabactin, and enterobactin.
Production of Neurochemicals by Microorganisms
Published in Akula Ramakrishna, Victoria V. Roshchina, Neurotransmitters in Plants, 2018
Alexander V. Oleskin, Boris A. Shenderov
Accordingly, one of the potentially important effects of microbial neurochemicals is based on their capacity to help the plant organism maintain Fe homeostasis. Catecholamines can chelate ferric iron, removing it from catecholamine-binding proteins that, in the animal organism, are exemplified by lactoferrin and transferrin of the blood serum and other biological fluids. Catecholamine-bound iron becomes available to bacterial cells that use specific carriers—siderophores (such as enterobactin in E. coli) to transfer it into the cell (see review Oleskin et al., 2016, p. 7). For instance, catecholamines stimulate the growth of some strains of lactobacilli and bifidobacteria on the serum-containing SAPI medium (Yunes, 2017) and not on the serum-free BS medium. It seems likely, therefore, that the catecholamines serve as iron chelators in this system (reviewed, Oleskin et al., 2017b).
Uropathogens and the Lower Urinary Tract
Published in Linda Cardozo, Staskin David, Textbook of Female Urology and Urogynecology - Two-Volume Set, 2017
leAd to AlterAtions in host response to pAthogens [23]. In the Urinary trAct, severAl tLr polymorphisms Are AssociAted with either increAsed susceptibility to or greAter protection from UTI As well As number of UTI episodes [24]. There Are severAl known toxins thAt modulAte the host inflAmmAtory response, induce cytopAthic effects, And cAuse tissue dAmAge. AlphA-hemolysin promotes cell lysis, AppeArs to AttenuAte the host inflAmmAtory response, And is AssociAted with clinicAl severity [25,26]. Cytotoxic necrotizing fActor 1 (CnF1) hAs been shown to cAuse membrAne chAnges thAt fAcilitAte bActeriAl internAlizAtion into host cells [27] And inhibit neutrophil Activity in AnimAl models [28]. Iron is required for bActeriAl cellulAr processes And survivAl, And the competition for AvAilAble iron stores highlights the impressive Ability of uPeC to evAde host defenses. one host defense is to limit iron AvAilAbility viA trAnsferrin, An iron cArrier protein thAt cAn move iron stores in And out of cells. However, uPeC cAn utilize enterobActin, which hAs A higher Affinity for iron thAn trAnsferrin And cAn therefore scAvenge iron from the environment [29]. An AdditionAl host protein cAlled lipocAlin 2 specificAlly binds enterobActin And is upregulAted in urotheliAl cells contAining uPeC [30,31]; however, uPeC hAve yet AdditionAl iron Acquisition systems thAt Are not recognized by lipocAlin And cAn therefore work Around this host defense As well [32].
Identification of gut microbiome and transcriptome changes in ulcerative colitis and pouchitis
Published in Scandinavian Journal of Gastroenterology, 2022
Xin Gao, Di Huang, Li-Sheng Yang, An-Qi He, Kai-Yu Li, Tong Liu, Gang Liu
In contrast, KEGG analysis showed that many pathogens enriched in pouchitis were related to numerous pathways associated with infectious diseases (such as vibrio cholerae infection, hepatitis, influenza A and pathogenic Escherichia coli infection). That means infectious bacteria play an important role in the occurrence of pouchitis. What is more, we found that, enterobactin, a siderophore secreted by many pathogens, will confer a survival advantage upon E. coli in the inflammatory bowel [32], was associated with many pathogens enriched in pouchitis. Therefore, we concluded that the proliferation of these pathogenic bacteria could be the direct cause of UC-pouchitis, which likely explains why the use of antibiotic monotherapy can achieve clinical remission in most patients with pouchitis.
Genotypic validation of extended-spectrum β-lactamase and virulence factors in multidrug resistance Klebsiella pneumoniae in an Indian hospital
Published in Pathogens and Global Health, 2019
Rajesh Kumar Sahoo, Aradhana Das, Mahendra Gaur, Ankita Pattanayak, Saubhagini Sahoo, Nagen Kumar Debata, Pattanathu K.S.M. Rahman, Enketeswara Subudhi
Genomic DNA extraction was carried out using a modified ROSE method (Rapid one-step extraction) [9]. The concentration and purity of DNA was measured using UV-VIS spectrophotometer (Thermo Scientific, USA). ESBL positive isolates were tested for the presence of blaTEM, blaCTX-M, and blaSHV genes using gene-specific primers (Table S1) through a PCR-based method. About 25 ng of template DNA was mixed with PCR master mix, which contained 12.5 μL of 2X Taq PCR master mix (QIAGEN, India); 1 μL each forward and reverse primers and 9.5 μL of nuclease-free water. PCR amplification reactions were performed with the BIORAD thermal cycler (T100) using 30 cycles of 94°C for 1 min, 55°C for 45 s, and 72°C for 1 min, with initial denaturation at 94°C for 5 min and a final extension at 72°C for 10 min. Similarly, virulence-associated genes encoding type 1, type 3 adhesins (fimH-1, mrkD), enterobactin biosynthesis (entB), yersiniabactin biosynthesis (irp), and capsule serotypes (K1 and K2) were screened through PCR assays. The PCR conditions were similar to those of ESBL genes except the annealing temperature described in Table S1. The amplified products were run with 1% (w/v) agarose gel and visualized under UV trans-illuminator.
Hypervirulence and carbapenem resistance: two distinct evolutionary directions that led high-risk Klebsiella pneumoniae clones to epidemic success
Published in Expert Review of Molecular Diagnostics, 2019
Yi-Chyi Lai, Min-Chi Lu, Po-Ren Hsueh
During infection, K. pneumoniae releases siderophores, which are small but high-affinity iron-chelating compounds, to chelate iron away from transferrin and lactoferrin, and form soluble Fe3+ complexes that can be actively transported into bacterial cells. Four types of siderophores, enterobactin, yersiniabactin, salmochelin, and aerobactin, have been identified in K. pneumoniae. Both the classical K. pneumoniae and HvKP express enterobactin. However, lipocalin-2 (neutrophil gelatinase-associated lipocalin), a protein stored in the granules of human neutrophils, sequesters enterobactin that in turn inhibits the growth of K. pneumoniae strains producing enterobactin as the only type of siderophore [54]. In addition to enterobactin, most of the HvKP strains express the other three types of siderophores. Yersiniabactin, aerobactin, and salmochelin, encoded by the irp-ybt-fyu, iucABCDiutA, and iroBCDN loci, respectively, are impervious to lipocalin-2 neutralization, and thus allow HvKP to grow to high bacterial loads during infection [55]. Using isogenic mutants, Russo et al. demonstrated that HvKP produced aerobactin as the primary type of siderophore under in vivo iron-limiting conditions. The production of aerobactin, but not yersiniabactin or salmochelin, was required for the full virulence of HvKP1 (ST86, K2-type HvKP) in intraperitoneal and subcutaneous infection mouse models [56].