Escherichia coli K1 induces pterin production for enhanced expression of Fcγ receptor I to invade RAW 264.7 macrophages

Shanmuganathan, Muthusamy V.; Krishnan, Subramanian; Fu, Xiaowei; Prasadarao, Nemani V.

doi:10.1016/j.micinf.2013.10.013

Cited by 9 publications

(5 citation statements)

References 16 publications

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“…The expression of OmpA is critical for survival inside PMNs after phagocytosis as OmpA − E. coli failed to survive. The phagocytosis of OmpA − E. coli by PMNs produces an enormous amount of reactive oxygen species (ROS) [ 122 ]. In contrast, OmpA + E. coli suppressed the release of ROS even in the presence of external stimuli such as LPS, indicating that E. coli overrides PMN machinery to prevent antimicrobial activity.…”

Section: Escherichia Coli K1-induced Neonatal Meningitismentioning

confidence: 99%

Host–pathogen interactions in bacterial meningitis

et al. 2016

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Bacterial meningitis is a devastating disease occurring worldwide with up to half of the survivors left with permanent neurological sequelae. Due to intrinsic properties of the meningeal pathogens and the host responses they induce, infection can cause relatively specific lesions and clinical syndromes that result from interference with the function of the affected nervous system tissue. Pathogenesis is based on complex host–pathogen interactions, some of which are specific for certain bacteria, whereas others are shared among different pathogens. In this review, we summarize the recent progress made in understanding the molecular and cellular events involved in these interactions. We focus on selected major pathogens, Streptococcus pneumonia, S. agalactiae (Group B Streptococcus), Neisseria meningitidis, and Escherichia coli K1, and also include a neglected zoonotic pathogen, Streptococcus suis. These neuroinvasive pathogens represent common themes of host–pathogen interactions, such as colonization and invasion of mucosal barriers, survival in the blood stream, entry into the central nervous system by translocation of the blood–brain and blood–cerebrospinal fluid barrier, and induction of meningeal inflammation, affecting pia mater, the arachnoid and subarachnoid spaces.

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Section: Escherichia Coli K1-induced Neonatal Meningitismentioning

confidence: 99%

Host–pathogen interactions in bacterial meningitis

et al. 2016

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“… 128 Polybacterial infection inhibited the level BH4 in the mesenteric artery and colon, worsening atherosclerotic vascular disease. 130 However, Escherichia coli K1 increased GCH1 131 or BH4 132 expression in human brain microvascular endothelial cells and macrophage to evade surveillance by the immune system.…”

Section: Intestinal Microorganisms Act On Ferroptosismentioning

confidence: 98%

The influence of microbiota on ferroptosis in intestinal diseases

Yao,

2023

Gut Microbes

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Ferroptosis is a distinctive form of iron-dependent necrotic cell death, characterized by excessive lipid peroxidation on cellular membranes and compromised cellular antioxidant defenses. Multiple metabolic pathways, including iron and lipid metabolism, as well as antioxidant systems, contribute to the execution of ferroptosis. The gut microbiota exerts regulatory effects on ferroptosis through its microbial composition, biological functions, and metabolites. Notably, most pathogenic bacteria tend to promote ferroptosis, thereby inducing or exacerbating diseases, while most probiotics have been shown to protect against cell death. Given microbiota colonization in the gut, an intimate association is found between intestinal diseases and microbiota. This review consolidates the essential aspects of ferroptotic processes, emphasizing key molecules and delineating the intricate interplay between gut microbiota and ferroptosis. Moreover, this review underscores the potential utility of gut microbiota modulation in regulating ferroptosis for the treatment of intestinal diseases.

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“…Leib and colleagues have found that ROS was produced from predominantly polymorphonuclear leukocytes in the subarachnoid and ventricular space, cortical vessels, endothelial cells in group B streptococci meningitis [ 128 , 129 ]. There is also a large generation of ROS from microglia, neurons, and astrocytes induced by E. coli lipopolysaccharides, cytokines (TNF-α and interleukin-1β [IL-1] β) [ 130 , 131 , 132 , 133 ]. Oxidative stress or free radicals increasingly became a vital event in promoting the development of neuronal injury during bacterial meningitis.…”

Section: Neuroprotective Properties Of Melatonin Against Bacterialmentioning

confidence: 99%

The Potentials of Melatonin in the Prevention and Treatment of Bacterial Meningitis Disease

et al. 2021

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Bacterial meningitis (BM) is an acute infectious central nervous system (CNS) disease worldwide, occurring with 50% of the survivors left with a long-term serious sequela. Acute bacterial meningitis is more prevalent in resource-poor than resource-rich areas. The pathogenesis of BM involves complex mechanisms that are related to bacterial survival and multiplication in the bloodstream, increased permeability of blood–brain barrier (BBB), oxidative stress, and excessive inflammatory response in CNS. Considering drug-resistant bacteria increases the difficulty of meningitis treatment and the vaccine also has been limited to several serotypes, and the morbidity rate of BM still is very high. With recent development in neurology, there is promising progress for drug supplements of effectively preventing and treating BM. Several in vivo and in vitro studies have elaborated on understanding the significant mechanism of melatonin on BM. Melatonin is mainly secreted in the pineal gland and can cross the BBB. Melatonin and its metabolite have been reported as effective antioxidants and anti-inflammation, which are potentially useful as prevention and treatment therapy of BM. In bacterial meningitis, melatonin can play multiple protection effects in BM through various mechanisms, including immune response, antibacterial ability, the protection of BBB integrity, free radical scavenging, anti-inflammation, signaling pathways, and gut microbiome. This manuscript summarizes the major neuroprotective mechanisms of melatonin and explores the potential prevention and treatment approaches aimed at reducing morbidity and alleviating nerve injury of BM.

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Escherichia coli K1 induces pterin production for enhanced expression of Fcγ receptor I to invade RAW 264.7 macrophages

Cited by 9 publications

References 16 publications

Host–pathogen interactions in bacterial meningitis

Host–pathogen interactions in bacterial meningitis

The influence of microbiota on ferroptosis in intestinal diseases

The Potentials of Melatonin in the Prevention and Treatment of Bacterial Meningitis Disease

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