scholarly journals Beyond arbitrium: identification of a second communication system in Bacillus phage phi3T that may regulate host defense mechanisms

2020 ◽  
Author(s):  
Charles Bernard ◽  
Yanyan Li ◽  
Philippe Lopez ◽  
Eric Bapteste
Keyword(s):  
Public Goods ◽  
Host Defense ◽  
Communication Systems ◽  
Defense Mechanisms ◽  
Evolutionary Stability ◽  
Lytic Cycle ◽  
Host Cells ◽  
The Public ◽  
Fitness Advantage ◽  
Bacillus Phage

Abstract The evolutionary stability of temperate bacteriophages at low abundance of susceptible bacterial hosts lies in the trade-off between the maximization of phage replication, performed by the host-destructive lytic cycle, and the protection of the phage-host collective, enacted by lysogeny. Upon Bacillus infection, Bacillus phages phi3T rely on the “arbitrium” quorum sensing (QS) system to communicate on their population density in order to orchestrate the lysis-to-lysogeny transition. At high phage densities, where there may be limited host cells to infect, lysogeny is induced to preserve chances of phage survival. Here, we report the presence of an additional, host-derived QS system in the phi3T genome, making it the first known virus with two communication systems. Specifically, this additional system, coined “Rapφ-Phrφ”, is predicted to downregulate host defense mechanisms during the viral infection, but only upon stress or high abundance of Bacillus cells and at low density of population of the phi3T phages. Post-lysogenization, Rapφ-Phrφ is also predicted to provide the lysogenized bacteria with an immediate fitness advantage: delaying the costly production of public goods while nonetheless benefiting from the public goods produced by other non-lysogenized Bacillus bacteria. The discovered “Rapφ-Phrφ” QS system hence provides novel mechanistic insights into how phage communication systems could contribute to the phage-host evolutionary stability.

scholarly journals Understanding policing as a mechanism of cheater control in cooperating bacteria

2018 ◽  
Author(s):  
Tobias Wechsler ◽  
Rolf Kümmerli ◽  
Akos Dobay
Keyword(s):  
Public Goods ◽  
Public Good ◽  
Parameter Space ◽  
Environmental Conditions ◽  
Genetic Linkage ◽  
Toxin Production ◽  
Evolutionary Stability ◽  
Conditional Strategy ◽  
The Public ◽  
Resistant Mutants

AbstractPolicing occurs in insect, animal and human societies, where it is used as a conditional strategy to prevent cheating and enforce cooperation. Recently, it has been suggested that policing might even be relevant in enforcing cooperation in much simpler organisms such as bacteria. Here, we used individual-based modelling to develop an evolutionary concept for policing in bacteria, and identify the conditions under which it can be adaptive. We modelled interactions between cooperators, producing a beneficial public good, cheaters exploiting the public good without contributing to it, and public good producing policers that secrete a toxin to selectively target cheaters. We found that toxin-mediated policing is favored when (i) toxins are potent and durable, (ii) cheap to produce, (iii) cell and public good diffusion is intermediate, and (iv) toxins diffuse farther than the public good. Overall, we show that toxin-mediated policing can enforce cooperation, but the parameter space where it is beneficial seems quite narrow. Moreover, we found that policing decays when the genetic linkage between public good and toxin production breaks. This is because policing is itself a public good, offering protection to toxin-resistant mutants that still produce public goods, yet no longer invest in toxins. Our work suggests that very specific environmental conditions are required for genetically fixed policing mechanisms to evolve in bacteria, and offers empirically testable predictions for their evolutionary stability.

scholarly journals The Phage Nucleus and PhuZ Spindle: Defining Features of the Subcellular Organization and Speciation of Nucleus-Forming Jumbo Phages

2021 ◽  
Vol 12 ◽  
Author(s):  
Vorrapon Chaikeeratisak ◽  
Erica A. Birkholz ◽  
Joe Pogliano
Keyword(s):  
Defense Mechanisms ◽  
Selective Advantage ◽  
Lytic Cycle ◽  
Host Cells ◽  
Nuclear Surface ◽  
Bacterial Host ◽  
Replication Factory ◽  
A Genome ◽  
Phage Dna ◽  
Subcellular Organization

Bacteriophages and their bacterial hosts are ancient organisms that have been co-evolving for billions of years. Some jumbo phages, those with a genome size larger than 200 kilobases, have recently been discovered to establish complex subcellular organization during replication. Here, we review our current understanding of jumbo phages that form a nucleus-like structure, or “Phage Nucleus,” during replication. The phage nucleus is made of a proteinaceous shell that surrounds replicating phage DNA and imparts a unique subcellular organization that is temporally and spatially controlled within bacterial host cells by a phage-encoded tubulin (PhuZ)-based spindle. This subcellular architecture serves as a replication factory for jumbo Pseudomonas phages and provides a selective advantage when these replicate in some host strains. Throughout the lytic cycle, the phage nucleus compartmentalizes proteins according to function and protects the phage genome from host defense mechanisms. Early during infection, the PhuZ spindle positions the newly formed phage nucleus at midcell and, later in the infection cycle, the spindle rotates the nucleus while delivering capsids and distributing them uniformly on the nuclear surface, where they dock for DNA packaging. During the co-infection of two different nucleus-forming jumbo phages in a bacterial cell, the phage nucleus establishes Subcellular Genetic Isolation that limits the potential for viral genetic exchange by physically separating co-infection genomes, and the PhuZ spindle causes Virogenesis Incompatibility, whereby interacting components from two diverging phages negatively affect phage reproduction. Thus, the phage nucleus and PhuZ spindle are defining cell biological structures that serve roles in both the life cycle of nucleus-forming jumbo phages and phage speciation.

scholarly journals Host-Bacteria Crosstalk at the Dentogingival Junction

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
M. T. Pöllänen ◽  
M. A. Laine ◽  
R. Ihalin ◽  
V.-J. Uitto
Keyword(s):  
Host Defense ◽  
Defense Mechanisms ◽  
Bacterial Flora ◽  
Oral Bacteria ◽  
Host Cells ◽  
Tooth Surface ◽  
Tissue Destruction ◽  
Remarkable Change ◽  
Bacterial Plaque

The dentogingival junction is of crucial importance in periodontal host defense both structurally and functionally. Oral bacteria exert a constant challenge to the host cells and tissues at the dentogingival junction. The host response is set up to eliminate the pathogens by the innate and adaptive defense mechanisms. In health, the commensal bacteria and the host defense mechanisms are in a dynamic steady state. During periodontal disease progression, the dental bacterial plaque, junctional epithelium (JE), inflammatory cells, connective tissue, and bone all go through a series of changes. The tissue homeostasis is turned into tissue destruction and progression of periodontitis. The classical study of Slots showed that in the bacterial plaque, the most remarkable change is the shift from gram-positive aerobic and facultatively anaerobic flora to a predominantly gram-negative and anaerobic flora. This has been later confirmed by several other studies. Furthermore, not only the shift of the bacterial flora to a more pathogenic one, but also bacterial growth as a biofilm on the tooth surface, allows the bacteria to communicate with each other and exert their virulence aimed at favoring their growth. This paper focuses on host-bacteria crosstalk at the dentogingival junction and the models studying itin vitro.

scholarly journals VAR2CSA-Mediated Host Defense Evasion of Plasmodium falciparum Infected Erythrocytes in Placental Malaria

2021 ◽  
Vol 11 ◽  
Author(s):  
Alice Tomlinson ◽  
Jean-Philippe Semblat ◽  
Benoît Gamain ◽  
Arnaud Chêne
Keyword(s):  
Plasmodium Falciparum ◽  
Immune System ◽  
Host Defense ◽  
Defense Mechanisms ◽  
Placental Malaria ◽  
Host Cells ◽  
Large Panel ◽  
Mother And Child ◽  
Malaria During Pregnancy ◽  
Massive Accumulation

Over 30 million women living in P. falciparum endemic areas are at risk of developing malaria during pregnancy every year. Placental malaria is characterized by massive accumulation of infected erythrocytes in the intervillous space of the placenta, accompanied by infiltration of immune cells, particularly monocytes. The consequent local inflammation and the obstruction of the maternofetal exchanges can lead to severe clinical outcomes for both mother and child. Even if protection against the disease can gradually be acquired following successive pregnancies, the malaria parasite has developed a large panel of evasion mechanisms to escape from host defense mechanisms and manipulate the immune system to its advantage. Infected erythrocytes isolated from placentas of women suffering from placental malaria present a unique phenotype and express the pregnancy-specific variant VAR2CSA of the Plasmodium falciparum Erythrocyte Membrane Protein (PfEMP1) family at their surface. The polymorphic VAR2CSA protein is able to mediate the interaction of infected erythrocytes with a variety of host cells including placental syncytiotrophoblasts and leukocytes but also with components of the immune system such as non-specific IgM. This review summarizes the described VAR2CSA-mediated host defense evasion mechanisms employed by the parasite during placental malaria to ensure its survival and persistence.

Effects of Anesthesia, Surgery and Inflammation Upon Host Defense Mechanisms

1975 ◽  
Vol 48 (5) ◽  
pp. 706-720 ◽  
Author(s):  
M. Schutte ◽  
R. DiCamelli ◽  
P. Murphy ◽  
M. Sadove ◽  
H. Gewurz
Keyword(s):  
Host Defense ◽  
Defense Mechanisms

scholarly journals The History and Mystery of Alveolar Epithelial Type II Cells: Focus on Their Physiologic and Pathologic Role in Lung

2021 ◽  
Vol 22 (5) ◽  
pp. 2566 ◽  
Author(s):  
Barbara Ruaro ◽  
Francesco Salton ◽  
Luca Braga ◽  
Barbara Wade ◽  
Paola Confalonieri ◽  
...  
Keyword(s):  
Host Defense ◽  
Defense Mechanisms ◽  
Work Of Breathing ◽  
Surfactant Proteins ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii ◽  
Lung Protection ◽  
Alveolar Epithelial ◽  
Distal Lung

Alveolar type II (ATII) cells are a key structure of the distal lung epithelium, where they exert their innate immune response and serve as progenitors of alveolar type I (ATI) cells, contributing to alveolar epithelial repair and regeneration. In the healthy lung, ATII cells coordinate the host defense mechanisms, not only generating a restrictive alveolar epithelial barrier, but also orchestrating host defense mechanisms and secreting surfactant proteins, which are important in lung protection against pathogen exposure. Moreover, surfactant proteins help to maintain homeostasis in the distal lung and reduce surface tension at the pulmonary air–liquid interface, thereby preventing atelectasis and reducing the work of breathing. ATII cells may also contribute to the fibroproliferative reaction by secreting growth factors and proinflammatory molecules after damage. Indeed, various acute and chronic diseases are associated with intensive inflammation. These include oedema, acute respiratory distress syndrome, fibrosis and numerous interstitial lung diseases, and are characterized by hyperplastic ATII cells which are considered an essential part of the epithelialization process and, consequently, wound healing. The aim of this review is that of revising the physiologic and pathologic role ATII cells play in pulmonary diseases, as, despite what has been learnt in the last few decades of research, the origin, phenotypic regulation and crosstalk of these cells still remain, in part, a mystery.

scholarly journals Punishment Strategies across Societies: Conventional Wisdoms Reconsidered

Games ◽  
2021 ◽  
Vol 12 (3) ◽  
pp. 63
Author(s):  
Ramzi Suleiman ◽  
Yuval Samid
Keyword(s):  
Public Goods ◽  
Strong Predictor ◽  
Social Environments ◽  
Public Goods Game ◽  
The Public ◽  
Free Riders ◽  
The World ◽  
Emergence Of Cooperation ◽  
Using Data ◽  
The Cost

Experiments using the public goods game have repeatedly shown that in cooperative social environments, punishment makes cooperation flourish, and withholding punishment makes cooperation collapse. In less cooperative social environments, where antisocial punishment has been detected, punishment was detrimental to cooperation. The success of punishment in enhancing cooperation was explained as deterrence of free riders by cooperative strong reciprocators, who were willing to pay the cost of punishing them, whereas in environments in which punishment diminished cooperation, antisocial punishment was explained as revenge by low cooperators against high cooperators suspected of punishing them in previous rounds. The present paper reconsiders the generality of both explanations. Using data from a public goods experiment with punishment, conducted by the authors on Israeli subjects (Study 1), and from a study published in Science using sixteen participant pools from cities around the world (Study 2), we found that: 1. The effect of punishment on the emergence of cooperation was mainly due to contributors increasing their cooperation, rather than from free riders being deterred. 2. Participants adhered to different contribution and punishment strategies. Some cooperated and did not punish (‘cooperators’); others cooperated and punished free riders (‘strong reciprocators’); a third subgroup punished upward and downward relative to their own contribution (‘norm-keepers’); and a small sub-group punished only cooperators (‘antisocial punishers’). 3. Clear societal differences emerged in the mix of the four participant types, with high-contributing pools characterized by higher ratios of ‘strong reciprocators’, and ‘cooperators’, and low-contributing pools characterized by a higher ratio of ‘norm keepers’. 4. The fraction of ‘strong reciprocators’ out of the total punishers emerged as a strong predictor of the groups’ level of cooperation and success in providing the public goods.

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