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Pseudomonas Chemotaxis, Motility and Host-Pathogen Interactions MOJ Immunology Pseudomonas Chemotaxis, Motility and Host-Pathogen Interactions Abstract Mini Review Infection with the fluorescent pathogen Pseudomonas aeruginosa leads to Volume 5 Issue 5 - 2017 gastrointestinal infections, dermatitis, bacteremia and a variety of systemic infections. Thus, within a very complex chemosensory system this bacterium has requires an adaptive strategy to escape to the immune system. It chemosensory 1Department of Biology, University of Mustapha Stambouli, system has attracted a significant interest because of the very complex molecular Mascara, Algeria diversity of this one (> 20 chemotaxis (che) genes). With this diversified 2Department of Biology, University of Oran (Es-senia), Oran, chemotaxis system, this bacteria moves from cell to cell by a twitching motility Algeria and respond in a behavioral manner. For this, it can be viewed as an important prelude to infections and serious clinical challenge. *Corresponding author: Amina Meliani, Department of biology, University of Mustapha Stambouli, Mascara, Avenue Cheikh El Khaldi, Mascara 29000, Algeria, Tel: 002-135-518- Keywords: Pseudomonas Aeruginosa; Infections; Chemotaxis; Twitching 058-73; Email: Received: April 20, 2017 | Published: May 18, 2017 Introduction compromised individuals. In addition to these illnesses, P. aeruginosa lung infections are common in individuals with chronic Bacterial chemotaxis is a biased movement towards obstructive pulmonary disease (COPD), ventilator-associated higher concentrations of life-sustaining nutrients and lower concentrations of toxins. It involves sensing a gradient of chemicals as small as a few molecules [1]. Furthermore, this pneumoniaFurthermore, (VAP), the and outcome cystic fibrosis of infections (CF) [6]. and establishment of disease depends on both host defense and bacterial capacities. toward (positive chemotaxis) or away (negative chemotaxis) movement and under the influence of a chemical gradient, either and adapt to the environment, and the ability to sense, and their growth and survival [2]. Motile bacteria have the ability to communicateThe latter include with their its neighborsautonomic in theefficiency population to togrow, accomplish divide, sensefrom the changes gradient in the helps concentration bacteria to offind chemicals optimum in conditionsenvironments for and respond to them by altering their pattern of motility. This virulence factors [7]. Consequently, elucidating the motility and behavioral response is called chemotaxis. Chemotaxis signaling chemotacticcooperative activities,mechanisms e.g. for biofilm Pseudomonas formation and production of in many studies extending to bioremediation and host-pathogen interactions [8]. Low permeability of its spp.outer can membrane be beneficial by pathways control flagellar motility by regulating the frequency at which the flagellar motor changes its direction of rotation or the speed at which the flagellar motor rotates. This mode of toa complex become sethighly of efflux virulent pump and systems resistant and to secretion multiple of antibiotic alginate alsocontrol controls is conserved twitching, across the movement flagellated of bacteria,cells on moistregardless surfaces of agents.during biofilm Adding formation to these factors, are major other factors bacterial that allow exoproducts the pathogen such mediatedflagellar arrangement by type IV pili or (TFP), number but [1].Thus, the mechanisms chemotaxis involved signaling are as lipopolysaccharides and elastase induce harmful pathogenesis resulting in tissue destruction [9]. [3]. distinct from those controlling flagellum-dependent chemotaxis In recent years, chemotactic responses studies between The Pseudomonads also show chemotactic responses to bacteria and self have contributed to a more informed view various chemical compounds, including amino acids, organic acids, of the adaptative mechanisms used by P. aeruginosa. In this sugars, aromatic compounds and inorganic ions [4]. Thus, many bacterium, contact is mediated by several adhesins, particularly but many questions remain especially in the case of Pseudomonas aeruginosaaspects of chemotaxis. This bacterium are now can understood,modulate the at immuneleast superficially, response, type IV pili (TFP), long motorized fimbriae that also provide reminiscent of helminth parasites, and antibiotic resistance due attachment,cells with surface-specific and retraction twitching promote motility intimate and association are essential with to surfacesvirulence andand biofilmmotility formation along them. [11]. Because Successive TFP TFP dynamically extension, [5]. In humans, Pseudomonas aeruginosa infections tend to occur interact with the substrate, they mechanically couple cells with into associationthe production with ofepithelial extracellular cell damage enzymes to the(e.g. skin β-lactamase) or eye or surfaces. Consequently, although TFP have been viewed as medical devices such as catheters or ventilators or in immune- adhesion and motility structures, TFP could also potentially Submit Manuscript | http://medcraveonline.com MOJ Immunol 2017, 5(5): 00167 Copyright: Pseudomonas Chemotaxis, Motility and Host-Pathogen Interactions ©2017 Meliani et al. 2/6 function as mechanical sensors to rapidly signal surface contact aeruginosa encodes two intracellular adenylate cyclases (CyaA and [12]. This mini review provides some insight on the P. aeruginosa CyaB) responsible for cAMP synthesis [13]. Nevertheless, mutants chemotaxis and twitching motility. lacking both cyaA and cyaB exhibit reduced virulence factor expression and is severely attenuated in an adult mouse model Discussion of acute pneumonia [18]. In addition, whole-genome expression . mutants Pseudomonas Aeruginosa Virulence and Cyclic AMP P aeruginosa defective in cAMP synthesis or lacking vfr are nearly identical, Many virulence factors associated with P. aeruginosa infection suggestingprofiling revealed that Vfr that activity the transcriptomes is dependent of on cAMP availability [19]. It is also noteworthy, that Vfr is known to control twitching adenosine 3’, 5’-cyclic monophosphate (cAMP or cyclic AMP) [13]. motility in P. aeruginosa. Another regulator FimL has been In(figure the case 1) are of regulatedP. aeruginosa by ,the this small messenger molecule is believedsecond messenger to control gene expression through allosteric regulation of the transcription modulation of Vfr production. FimL affects the regulation of type factor Vfr (Virulence factor regulator), which is a member of the IVpilusidentified assembly that affects and function twitching rather motility than at production. least in part While through both cAMP receptor protein (CRP) family [14]. Thus, cyclic AMP and Vfr appear to be the central components controlling a global virulence gene response in P. aeruginosa through regulation of mutants-anfimL and vfr observation mutants show which reduced supports levels the of surface-assemblednotion that FimL multiple virulence systems including type IV pili (TFP) [13,15], mightpili compared also be controllingwith wild-type, additional the defect gene isproducts more severe necessary in fimL for the type II secretion (T2S) system and secreted toxins [14,15], functional type IV pili [4]. type III secretion (T3S) [13], quorum sensing (QS) [4] and Pseudomonas Aeruginosa Chemosensory System It is obvious that genetic organization and physiological flagellar biogenesis [16]. observations suggest that α proteobacteria and P. aeruginosa have different chemotaxis systems [20]. P. aeruginosa has a very complex chemosensory system with more than 20 chemotaxis (che mcp-like genes [21]. The Chp system was previously implicated in the production and )function genes in of five type distinct IV pili clusters (TFP)[22]. and 26The Che and the Che2 systems, both homologous to the E. coli Che chemotaxis system, while genes in Pil-Chp cluster and Wsp cluster are involved in have been implicated in flagella-mediated chemotaxis [20], respectively [23]. This bacterium also has multiple copies of E. colitype-like IV pilus chemotaxis synthesis, genes twitching arranged motility in and biofilm formation, che clusters, cluster I and cluster V, which encode homologues of the six che genes found in E. coli, have fivepreviously clusters been [21]. shown Two to be essential for chemotaxis by P. aeruginosa [24]. Cluster IV has been shown to be involved in twitching motility [25] (Figure 2). Furthermore, nine P. aeruginosa as for amino acids, inorganic phosphate, oxygen, ethylene and Figure 1: P. aeruginosa, volatile chlorinated aliphatic hydrocarbons, MCPs havewhereas been three identified MCPs a fundamental Biofilm role formation in P. aeruginosa and virulence are coupled in biosynthesis of type IV pilus [26]. The Chp system was previously Thesesince a threadvariety likeof components proteinaceous such organelles as flagellum display and type several IV pili modes play shownwere demonstrated to control TFP to production be involved and twitchingin biofilm motility, formation Fulcher, and biofilm formation and virulence. of motility such as swimming, swarming and twitching motility and et al. [21] analysis of TFP function also revealed that although may play important roles in host–pathogen interactions. Note that twitching motility is ultimately dependent on TFP biogenesis, the factor. Flagellin released from P. aeruginosa triggers airway epithelial Chp system exerts cAMP-independent regulatory control over TLR5 issignaling a sensor NF-kB,for monomeric and causing flagellin, production known
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