Effects of mycoplasma infection on the host organism response via p53/NF‐κB signaling

Borchsenius, Sergey N.; Daks, Alexandra; Fedorova, Olga; Чернова, О. А.; Barlev, Nikolai A.

doi:10.1002/jcp.26781

Cited by 17 publications

(16 citation statements)

References 100 publications

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“…In line with this hypothesis is that a protease-rich environment enhances the invasive properties of Mycoplasma Hyorhinis [ 44 ]. Under a molecular point of view, Mycoplasma triggers NF-KappaB (NF-kB) pathway activation [ 45 ] and ets has a coregulatory role in MMP-1 expression [ 46 , 47 ]. NF-kB stimulation has also been observed for Chlamydia [ 48 ] and Legionella [ 49 ]; in the latter study, moreover, a direct association between in vitro NF-kB expression and in vivo pathogenicity of the different strains could be demonstrated.…”

Section: Discussionmentioning

confidence: 99%

Genetic Variants of Matrix Metalloproteinase and Sepsis: The Need Speed Study

et al. 2022

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Many causal mechanisms in sepsis susceptibility are largely unknown and the functional genetic polymorphisms (GP) of matrix metalloproteinases (MMPs) and their natural tissue inhibitor of MMPs (TIMP1) could play a role in its development. GPs of MMPs and TIMP (namely MMP-1 rs1799750, MMP-3 rs3025058, MMP-8 rs11225395, MMP-9 rs2234681, and TIMP-1 rs4898) have been compared in 1058 patients with suspected sepsis to assess the association with susceptibility and etiology of sepsis. Prevalence of MMP8 rs11225395 G/G genotype was higher in sepsis patients than in those with non-infective Systemic Inflammatory Reaction Syndrome (35.6 vs. 26%, hazard ratio, HR 1.56, 95% C.I. 1.04–2.42, p = 0.032). G/G patients developed less hyperthermia (p = 0.041), even after stratification for disease severity (p = 0.003). Patients carrying the 6A allele in MMP3 rs3025058 had a higher probability of microbiologically-proven sepsis (HR 1.4. 95%C.I. 1.01–1.94, p = 0.044), particularly when due to virus (H.R. 2.14, 95% C.I. 1.06–4.31, p = 0.046), while MMP-1 G/G genotype patients carried a higher risk for intracellular bacteria (Chlamydia, Mycoplasma, and Legionella, H.R. 6.46, 95% C.I. 1.58–26.41, p = 0.003). Neither severity of sepsis at presentation, nor 30-day mortality were influenced by the investigated variants or their haplotype. MMP8 rs11225395 G/G carriers have lower temperature at presentation and a more than 50% increased susceptibility to sepsis. Among patients with sepsis, carriers of MMP1 rs1799750 G/G have an increased susceptibility for intracellular pathogen infections, while virus serology is more often positive in those with the MMP3 rs3025058 A/A genotype.

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Section: Discussionmentioning

confidence: 99%

Genetic Variants of Matrix Metalloproteinase and Sepsis: The Need Speed Study

et al. 2022

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“…Additionally, to underline the importance of this signaling pathway, binding of lipoprotein/lipopeptide with TLRs results in cellular activation and in the downstream expression of NF-κB. Some of the inflammatory diseases linked to infections by Mycoplasmas are mastitis, salpingitis, urethritis, arthritis atypical pneumonia, and bronchopulmonary dysplasia, which is particularly dangerous for newborns [ 40 ]. Such inflammation is elicited by the presence of specific immune mediators, released by target cells (epithelial cells and leukocytes) upon infection by Mycoplasmas.…”

Section: Mycoplasmas and Inflammationmentioning

confidence: 99%

Mycoplasmas–Host Interaction: Mechanisms of Inflammation and Association with Cellular Transformation

2020

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Mycoplasmas are the smallest and simplest self-replicating prokaryotes. Located everywhere in nature, they are widespread as parasites of humans, mammals, reptiles, fish, arthropods, and plants. They usually exhibiting organ and tissue specificity. Mycoplasmas belong to the class named Mollicutes (mollis = soft and cutis = skin, in Latin), and their small size and absence of a cell wall contribute to distinguish them from other bacteria. Mycoplasma species are found both outside the cells as membrane surface parasites and inside the cells, where they become intracellular residents as “silent parasites”. In humans, some Mycoplasma species are found as commensal inhabitants, while others have a significant impact on the cellular metabolism and physiology. Mollicutes lack typical bacterial PAMPs (e.g., lipoteichoic acid, flagellin, and some lipopolysaccharides) and consequently the exact molecular mechanisms of Mycoplasmas’ recognition by the cells of the immune system is the subjects of several researches for its pathogenic implications. It is well known that several strains of Mycoplasma suppress the transcriptional activity of p53, resulting in reduced apoptosis of damaged cells. In addition, some Mycoplasmas were reported to have oncogenic potential since they demonstrated not just accumulation of abnormalities but also phenotypic changes of the cells. Aim of this review is to provide an update of the current literature that implicates Mycoplasmas in triggering inflammation and altering critical cellular pathways, thus providing a better insight into potential mechanisms of cellular transformation.

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“…The primary contribution of mycoplasma to cancer and other diseases is most likely their inflammatory properties, which are mediated by the interaction of the lipopeptide MALP-2 with the Toll-like receptor, TLR2/6 [29][30][31][32][33][34][35][36][37][38] . Cultured cells infected with mycoplasma adopt more cancer-like phenotypes that include activated signaling pathways for proliferation, stimulated migration and the epithelial to mesenchymal transition 18,19,21,34,39,40 . Because mycoplasma infections are important in disease and frequently found in cultured cells that have not been adequately…”

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confidence: 99%

The Lipocalin2 Gene is Regulated in Mammary Epithelial Cells by NFκB and C/EBP In Response to Mycoplasma

Zhao

Bendickson

Nilsen-Hamilton

2020

Sci Rep

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Lcn2 gene expression increases in response to cell stress signals, particularly in cells involved in the innate immune response. Human Lcn2 (NGAL) is increased in the blood and tissues in response to many stressors including microbial infection and in response to LPS in myeloid and epithelial cells. Here we extend the microbial activators of Lcn2 to mycoplasma and describe studies in which the mechanism of Lcn2 gene regulation by MALP-2 and mycoplasma infection was investigated in mouse mammary epithelial cells. As for the LPS response of myeloid cells, Lcn2 expression in epithelial cells is preceded by increased TNFα, IL-6 and IκBζ expression and selective reduction of IκBζ reduces Lcn2 promoter activity. Lcn2 promoter activation remains elevated well beyond the period of exposure to MALP-2 and is persistently elevated in mycoplasma infected cells. Activation of either the human or the mouse Lcn2 promoter requires both NFκB and C/EBP for activation. Thus, Lcn2 is strongly and enduringly activated by mycoplasma components that stimulate the innate immune response with the same basic regulatory mechanism for the human and mouse genes.

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Effects of mycoplasma infection on the host organism response via p53/NF‐κB signaling

Cited by 17 publications

References 100 publications

Genetic Variants of Matrix Metalloproteinase and Sepsis: The Need Speed Study

Genetic Variants of Matrix Metalloproteinase and Sepsis: The Need Speed Study

Mycoplasmas–Host Interaction: Mechanisms of Inflammation and Association with Cellular Transformation

The Lipocalin2 Gene is Regulated in Mammary Epithelial Cells by NFκB and C/EBP In Response to Mycoplasma

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