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Long noncoding RNAs in bacterial infection

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Abstract Infectious and inflammatory diseases remain major causes of mortality and morbidity worldwide. To combat bacterial infections, the mammalian immune system employs a myriad of regulators, which secure the effective initiation of inflammatory responses while preventing pathologies due to overshooting immunity. Recently, the human genome has been shown to be pervasively transcribed and to generate thousands of still poorly characterized long noncoding RNAs (lncRNAs). A growing body of literature suggests that lncRNAs play important roles in the regulatory circuitries controlling innate and adaptive immune responses to bacterial pathogens. This review provides an overview of the roles of lncRNAs in the interaction of human and rodent host cells with bacterial pathogens. Further decoding of the lncRNA networks that underlie pathological inflammation and immune subversion could provide new insights into the host cell mechanisms and microbial strategies that determine the outcome of bacterial infections. This article is categorized under: RNA in Disease and Development > RNA in Disease RNA Interactions with Proteins and Other Molecules > Protein‐RNA Interactions: Functional Implications
LncRNAs in inflammatory pathway activation during bacterial infection. Upon innate detection of bacteria, such as L. monocytogenes, M. tuberculosis, P. aeruginosa or L. pneumophila, several lncRNAs are regulated, which impact on pro‐inflammatory and type I IFN gene expression. Through PRRs, lncRNAs AS‐IL1α and linc‐Cox2 are up‐, whereas lincRNA‐EPS is downregulated to promote NFκB pathway activation. Of note, linc‐Cox2 can also suppress the activation of a set of immune genes. LncRNA MEG3‐4 is a positive regulator of pro‐inflammatory cytokine IL1β expression and is downregulated upon detection of bacteria. NEAT1v2, which promotes immune gene expression, is upregulated in response to intracellular, replicating S. Typhimurium. MaIL1 is an lncRNA, which is upregulated through the MyD88‐NFκB pathway but interacts with components of the TRIF‐pathway to promote type I IFN expression and IFN‐dependent antimicrobial defense
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lncRNAs in IFNγ and autophagy dependent antibacterial defense. Lymphocytes, such as T or NK cells produce IFNγ in response to phagocyte signals, such as IL12. IFNγ production is promoted by lymphocyte lncRNAs such as IFNG‐AS1 or lnc‐CD244. Stimulation of infected cells with IFNγ promotes JAK–STAT dependent antibacterial defense via autophagy and nitric oxide production. iNOS production is positively regulated by linc‐Cox2. STAT activation is inhibited by Sros1, which is downregulated upon phagocyte activation. LncRNAs MEG3, PCED1B‐AS and lincRNA‐EPS, which inhibit autophagy, are also downregulated upon bacterial infection
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Major bacterial recognition pathways in the immune system. TLRs, such as TLR4 can activate NFκB and IRF3 dependent inflammatory mediator and type I IFN production through the MyD88 and TRIF pathway, respectively. NLRs can activate NFκB (e.g., NOD2) or inflammasome‐dependent cytokine maturation (e.g., NLRC4). RLRs, such as RigI promote type I IFN production through the MAVS pathway. Type I IFN stimulates STAT‐dependent interferon induced gene (ISG) expression via the IFNAR1/2 receptor
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LncRNAs linking bacterial infection to tumorigenesis. F. nucleatum is suspected to promote colorectal cancer and oral squamous cell carcinoma, among others by inducing the expression of the lncRNAs KRT4‐AS and MIR4435‐2HG. KRT7‐AS promotes KRT7‐dependent metastasis. MIR4435‐2HG promotes Akt2‐dependent cancer cell proliferation. H. pylori has been implicated in gastric cancer. Through suppression of the lncRNA lnc‐GNAT1 H. pylori activates the Wnt/β‐catenin pathway and cell proliferation. By inducing expression of the lncRNA SNHG17, H. pylori was suggested to impact on the activity of proteins associated with the DNA repair machinery, among others through a nuclear speckle protein NONO dependent mechanism
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RNA Interactions with Proteins and Other Molecules > Protein–RNA Interactions: Functional Implications
RNA in Disease and Development > RNA in Disease

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