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Host Epigenetics in Intracellular Pathogen Infections

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Host Epigenetics in Intracellular Pathogen Infections International Journal of Molecular Sciences Review Host Epigenetics in Intracellular Pathogen Infections Marek Fol *, Marcin Włodarczyk and Magdalena Druszczy ´nska Division of Cellular Immunology, Department of Immunology and Infectious Biology, Faculty of Biology and Environmental Protection, University of Lodz, 90-237 Lodz, Poland; [email protected] (M.W.); [email protected] (M.D.) * Correspondence: [email protected]; Tel.: +48-42-635-44-72 Received: 27 May 2020; Accepted: 26 June 2020; Published: 27 June 2020 Abstract: Some intracellular pathogens are able to avoid the defense mechanisms contributing to host epigenetic modifications. These changes trigger alterations tothe chromatin structure and on the transcriptional level of genes involved in the pathogenesis of many bacterial diseases. In this way, pathogens manipulate the host cell for their own survival. The better understanding of epigenetic consequences in bacterial infection may open the door for designing new vaccine approaches and therapeutic implications. This article characterizes selected intracellular bacterial pathogens, including Mycobacterium spp., Listeria spp., Chlamydia spp., Mycoplasma spp., Rickettsia spp., Legionella spp. and Yersinia spp., which can modulate and reprogram of defense genes in host innate immune cells. Keywords: epigenetic modifications; intracellular pathogens; immune cells 1. Introduction Epigenetic regulation of the gene activity is a subject of deep and still-increasing interest. The appearance of an epigenetic trait defined as “a stably heritable phenotype resulting from changes in a chromosome without alterations in the DNA sequence” can be triggered by changes in the environment of the cell, precisely described and discussed by Berger et al. [1]. There is some evidence suggesting that certain microbial agents, e.g., Helicobacter pylori [2], Porphyromonas gingivalis, Fusobacterium nucleatum [3], Streptococcus bovis, Chlamydia pneumoniae, Campylobacter rectus, Epstein–Barr virus, hepatitis viruses, human papilloma virus, polyoma viruses, can contribute to the host epigenetic changes and are frequently associated with carcinogenesis [4]. In the context of host–pathogen interactions, microorganism trying to conquer the host would be regarded as co-called “epigenetor” (term proposed by Berger et al. [1])—a factor which descends from environment and triggers a cascade of events ultimately leading to the modulation of the host epigenome. The most common mechanisms by which epigenetics control changes in gene expression involve histone acetylation, histone deacetylation, histone methylation and DNA methylation [5–7]. However, these epigenetic modifications induced by the infectious agents in host cells are still not sufficiently explored. Possibly, these infectious agents have developed a wide variety of epigenetic regulatory mechanisms, through which they are able to effectively exploit the epigenome of the host for their own benefits (Figure1)[ 8]. In this review, the main interest is focused on certain intracellular bacterial pathogens: Mycobacterium tuberculosis—an obligatory, aerobic bacillus still remaining one of the major global health problems since it is estimated that one fourth of global human population is infected with that pathogen [9,10] and Listeria monocytogenes—mainly transmitted through the consumption of contaminated food, causing listeriosis, a disease whose importance is not sufficiently recognized [11]. We have also compiled selected information regarding another four obligatory or facultative intracellular widespread bacteria of the genera Chlamydia, Mycoplasma, Rickettsia, Yersinia and Legionella [12–14]. Their strategies to modulate the host epigenome in order to overcome the host defense for their persistence are reviewed in the present study. Int. J. Mol. Sci. 2020, 21, 4573; doi:10.3390/ijms21134573 www.mdpi.com/journal/ijms Int. J. Mol. Sci. 2020, 21, x FOR PEER REVIEW 2 of 15 strategies to modulate the host epigenome in order to overcome the host defense for their Int.persistence J. Mol. Sci. 2020 are, 21 reviewed, 4573 in the present study. 2 of 16 Figure 1. Strategies exploited by pathogens to modulate host epigenome. Figure 1. Strategies exploited by pathogens to modulate host epigenome. 2. Mycobacterium Tuberculosis 2. MycobacteriumMycobacterium tuberculosis Tuberculosis—the causative agent of tuberculosis (TB) in humans—is equipped with aMycobacterium broad spectrum tuberculosis of tools that—the allow causative it to surviveagent of and tuberculos avoid theis (TB) defense in humans—is mechanisms equipped of the hostwith [15 a– broad17]. Ofthe spectrum most of important tools that mycobacterialallow it to survive abilities and thatavoid enable the defense the eff mechanismsective conquering of the ofhost the[15–17]. host are Ofthe some most epifactors, important through mycobacterial which this abilities intracellular that enable pathogen the effective controls conquering the expression of the ofhost hostare genes some atepifactors, the chromatin through level which [18]. this Yaseen intracellula et al. [19r] pathogen described controls the mycobacterial the expression protein of host Rv1988 genes (methyltransferase)at the chromatin responsiblelevel [18]. forYaseen dimethylation et al. [1 of9] argininedescribed amino the acidmycobacterial present specifically protein atRv1988 the 42nd(methyltransferase) position within theresponsible core region for ofdimethylation histone H3 (H3R42me2)of arginine amino in the acid host present cell. This specifically modification at the alters42nd theposition expression within of the certain core host region genes, of histone whichbenefits H3 (H3R42 bacteriame2) and in the supports host cell. the developmentThis modification of infection.alters the It expression has been shown of certain that thishost secretorygenes, which protein benefits is a product bacteria of and only supports pathogenic the development mycobacteria of (M.infection. tuberculosis It has, M. been bovis shown), while that the this other secretory ones (M. pr smegmatisotein is a )product do not expressof only pathogenic Rv1988. Following mycobacteria the tubercle(M. tuberculosis bacilli entering, M. bovis the), while cell, released the other Rv1988 ones (M. localizes smegmatis with) do the not chromatin express Rv1988. in the host Following nucleus the afftubercleecting the bacilli expression entering of genes,the cell, which released are important Rv1988 localizes for host defense,with the e.g., chromatin NOX1, NOX4,in the host NOS2 nucleus and TRAF3affecting [18]. the The expression first three onesof genes, are an which important are impo sourcertant of reactivefor host oxygendefense, species e.g., NOX1, [20,21] NOX4, and the NOS2 last one,and together TRAF3 with[18]. TRAF2,The first plays three a ones pivotal are role an important in cell type—and source stimulus-specificof reactive oxygen production species [20,21] of type and I IFNthe [last22– one,24]. Interestingtogether with observations TRAF2, plays have a pivotal been made role in on cell another type—and secretory stimulus-specific mycobacterial production protein, namelyof type Rv2966c. I IFN [22–24]. This 5-methylcytosine-specific Interesting observations DNAhave methyltransferasebeen made on another released secretory by M. mycobacterial tuberculosis showsprotein, an abilitynamely to Rv2966c. localize toThis the 5-methylcytosine nucleus inside the-specific infected DNA mammalian methyltransferase cell. Rv2966c released binds by to M. specifictuberculosis DNA sequencesshows an andability causes to localize predominantly to the nucleus non-CpG inside methylation, the infected and mammalian its activity is cell. positively Rv2966c influencedbinds to specific by phosphorylation DNA sequences [25 ].and Similar causes to predominantly Rv1988, this proteinnon-CpG can methylation, also interact and with its histoneactivity is proteins,positively and influenced probably both by phosphoryl of them areation the key [25]. elements Similar ofto theRv1988, first impact this protein during can infection also interact hijacking with thehistone host defense proteins, control and probably center by both epigenetically of them are altering the key its elements action [18 of]. the As thefirst cytosine impact methylationduring infection is ratherhijacking commonly the host observed defense in control mammalian center cells by andepigenetically the Rv2966c altering shows its dual action nature [18]. characterized As the cytosine by themethylation ability to be is arather dcm/dam-like commonly prokaryotic observed in DNA mammalian methyltransferase cells and the which Rv2966c binds shows to specific dual DNA nature sequencescharacterized and by by the the ability ability to to methylate be a dcm/dam-like cytosines that prokaryotic are not canonical DNA methyltransferase dcm/dam sites, itwhich could binds be saidto thatspecific at some DNA level sequences tubercle and bacilli by hijackthe ability the epigenomic to methylate control cytosines center that of theare hostnot canonical cell. Furthermore, dcm/dam thissites, protein it could interacts be said with that histone at some H3 level and tubercle H4, and bacilli thus hijack acts similarly the epigenomic to DNMT3L—one control center of of the the mammalianhost cell. Furthermore, DNA methyltransferases this protein also interacts involved with in histone nuclear reprogrammingH3 and H4, and by thus binding acts tosimilarly histone to H3 and regulation of DNA methylation
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