Chemoattractant Gradient Research Articles

Chemokines: A Potential Therapeutic Target to Suppress Autoimmune Arthritis.

Chemokines are a family of low molecular weight proteins that induce chemotaxis of inflammatory cells, which mainly depends on the recognition of a chemo-attractant gradient and interaction with the substratum. In Rheumatoid Arthritis (RA), abundant chemokines are expressed in synovial tissue, cause inflammatory cells migration into the inflamed joint that necessitates the formation of new blood vessels i.e. angiogenesis. Over the decades, studies showed that continuous inflammation may lead to the loss of tissue architecture and function, causing severe disability and cartilage destruction. In spite of the advancement of modern drug therapy, thousands of arthritic patients suffer mortality and morbidity globally. Thus, there is an urgent need for the development of novel therapeutic agents for the treatment of RA. This review is carried out throughout a non-systematic search of the accessible literature, will provide an overview of the current information of chemokine in RA and also exploring the future perspective of the vital role of targeting chemokine in RA treatment. Since, chemokines are associated with inflammatory cells/leucocyte migration at the site of inflammation in chronic inflammatory diseases and hence, blockade or interference with chemokines activity showing a potential approach for the development of new anti-inflammatory agents. Currently, results obtained from both preclinical and clinical studies showed significant improvement in arthritis. This review summarizes the role of chemokines and their receptors in the pathogenesis of RA and also indicates possible interactions of chemokines/receptors with various synthetic and natural compounds that may be used as a potential therapeutic target in the future for the treatment of RA.

The tetraspanin CD9 controls invasive migration and proliferation of parietal epithelial cells and glomerular disease progression

Introduction Crescentic glomerulonephritis (CGN) and focal segmental glomerulosclerosis (FSGS) are life-threatening diseases leading to irreversible renal failure. Increasing evidence supports the notion that glomerular parietal epithelial cells (PEC) are implicated in the formation of crescents in CGN and in glomerular scarring during FSGS. However, the mechanisms underlying the change in PEC phenotype remain unclear, as do those driving their oriented migration towards the glomerular tuft and their increased capacity to proliferate and form hypercellular and sclerotic lesions. Methodes Aiming to identify factors underlying PEC activation, we revealed increased expression of CD9 using comparative deep RNA sequencing of mouse and human normal and diseased glomeruli, confirmed expression by immunohistochemistry, and investigated roles of this tetraspanin in CGN and FSGS pathogeny. As CD9 de novo expression in glomeruli was observed in PEC in human CGN and FSGS and, given the recognized role of PEC in the progression of extracapillary lesions, we generated mice with a specific Cd9 deletion in PEC (iPec-Cd9lox/lox mice) that were challenged in experimental CGN and FSGS models. Cd9 gene knock-down were performed in a PEC line to evaluate its influence on migration, spreading and proliferation. Results During the CGN model, iPec-Cd9 wt/wt control mice showed a rapid increase in albuminuria, renal failure and severe glomerular crescentic lesions. Conversely, iPec-Cd9lox/lox mice displayed marked renal protection. We challenged iPec-Cd9lox/lox mice with the DOCA-salt and unilateral nephrectomy FSGS model. Glomerular ultrastructure and function was preserved in iPec-Cd9lox/lox DOCA mice, whereas iPec-Cd9 wt/wt DOCA mice exhibited flocculo-capsular synechiae and sclerosis. In vitro, we found that CD9 deficiency impairs the ability of PECs to proliferate and to migrate towards a steep gradient of chemoattractant in microfluidic channels. Conclusion These results indicate that de novo expression of CD9 in PECs participates in crescents in experimental CGN and is also critically involved in the development of glomerular lesions in FSGS.

A neutrophil-centric view of chemotaxis.

Neutrophils are key players of the innate immune system, that are involved in coordinating the initiation, propagation and resolution of inflammation. Accurate neutrophil migration (chemotaxis) to sites of inflammation in response to gradients of chemoattractants is pivotal to these roles. Binding of chemoattractants to dedicated G-protein-coupled receptors (GPCRs) initiates downstream signalling events that promote neutrophil polarisation, a prerequisite for directional migration. We provide a brief summary of some of the recent insights into signalling events and feedback loops that serve to initiate and maintain neutrophil polarisation. This is followed by a discussion of recent developments in the understanding of in vivo neutrophil chemotaxis, a process that is frequently referred to as 'recruitment' or 'trafficking'. Here, we summarise neutrophil mobilisation from and homing to the bone marrow, and briefly discuss the role of glucosaminoglycan-immobilised chemoattractants and their corresponding receptors in the regulation of neutrophil extravasation and neutrophil swarming. We furthermore touch on some of the most recent insights into the roles of atypical chemokine receptors (ACKRs) in neutrophil recruitment, and discuss neutrophil reverse (transendothelial) migration together with potential function(s) in the dissemination and/or resolution of inflammation.

Advanced 2D/3D cell migration assay for faster evaluation of chemotaxis of slow-moving cells.

Considering the essential role of chemotaxis of adherent, slow-moving cells in processes such as tumor metastasis or wound healing, a detailed understanding of the mechanisms and cues that direct migration of cells through tissues is highly desirable. The state-of-the-art chemotaxis instruments (e.g. microfluidic-based devices, bridge assays) can generate well-defined, long-term stable chemical gradients, crucial for quantitative investigation of chemotaxis in slow-moving cells. However, the majority of chemotaxis tools are designed for the purpose of an in-depth, but labor-intensive analysis of migratory behavior of single cells. This is rather inefficient for applications requiring higher experimental throughput, as it is the case of e.g. clinical examinations, chemoattractant screening or studies of the chemotaxis-related signaling pathways based on subcellular perturbations. Here, we present an advanced migration assay for accelerated and facilitated evaluation of the chemotactic response of slow-moving cells. The revised chemotaxis chamber contains a hydrogel microstructure–the migration arena, designed to enable identification of chemotactic behavior of a cell population in respect to the end-point of the experiment. At the same time, the assay in form of a microscopy slide enables direct visualization of the cells in either 2D or 3D environment, and provides a stable and linear gradient of chemoattractant. We demonstrate the correctness of the assay on the model study of HT-1080 chemotaxis in 3D and on 2D surface. Finally, we apply the migration arena chemotaxis assay to screen for a chemoattractant of primary keratinocytes, cells that play a major role in wound healing, being responsible for skin re-epithelialization and a successful wound closure. In direction of new therapeutic strategies to promote wound repair, we identified the chemotactic activity of the epithelial growth factor receptor (EGFR) ligands EGF and TGFα (transforming growth factor α).

Chemotaxis in shear flow: Similarity solutions of the steady‐state chemoattractant and bacterial distributions

AbstractWhen chemotactic bacteria are exposed to a concentration gradient of chemoattractant while flowing along a channel, the bacteria accumulate at the interface between the chemoattractant source and bacterial suspension. Assuming that the interface is no‐slip, we can apply the shear flow approximation near the no‐slip boundary and solve a steady‐state convection‐diffusion model for both chemoattractant and bacterial concentrations. We suggest similarity solutions for the two‐dimensional problem and identify a critical length scale ηc for bacteria chemotaxis in a given concentration gradient. The analysis identifies three dimensionless groups representing, respectively, chemotactic sensitivity, the chemotaxis receptor constant, and the bacteria diffusion coefficient, which typically show coupled effects in experimental systems. We study the effect of the dimensionless groups separately and provide understanding of the system involving shear flow and chemotaxis.

Molecular mechanisms of chemotropism and cell fusion in unicellular fungi.

In all eukaryotic phyla, cell fusion is important for many aspects of life, from sexual reproduction to tissue formation. Fungal cells fuse during mating to form the zygote, and during vegetative growth to connect mycelia. Prior to fusion, cells first detect gradients of pheromonal chemoattractants that are released by their partner and polarize growth in their direction. Upon pairing, cells digest their cell wall at the site of contact and merge their plasma membrane. In this Review, I discuss recent work on the chemotropic response of the yeast models Saccharomyces cerevisiae and Schizosaccharomyces pombe, which has led to a novel model of gradient sensing: the cell builds a motile cortical polarized patch, which acts as site of communication where pheromones are released and sensed. Initial patch dynamics serve to correct its position and align it with the gradient from the partner cell. Furthermore, I highlight the transition from cell wall expansion during growth to cell wall digestion, which is imposed by physical and signaling changes owing to hyperpolarization that is induced by cell proximity. To conclude, I discuss mechanisms of membrane fusion, whose characterization remains a major challenge for the future.

3D Analysis of Multi-cellular Responses to Chemoattractant Gradients

Various limitations of 2D cell culture systems have sparked interest in 3D cell culture and analysis platforms, which would better mimic the spatial and chemical complexity of living tissues and mimic in vivo tissue functions. Recent advances in microfabrication technologies have facilitated the development of 3D in vitro environments in which cells can be integrated into a well-defined extracellular matrix (ECM) and a defined set of soluble or matrix associated biomolecules. However, technological barriers have limited their widespread use in research laboratories. Here, we describe a method to construct simple devices for 3D culture and experimentation with cells and multicellular organoids in 3D microenvironments with a defined chemoattractant gradient. We illustrate the use of this platform for analysis of the response of epithelial cells and organoids to gradients of growth factors, such as epidermal growth factor (EGF). EGF gradients were stable in the devices for several days leading to directed branch formation in breast organoids. This analysis allowed us to conclude that collective gradient sensing by groups of cells is more sensitive vs. single cells. We also describe the fabrication method, which does not require photolithography facilities nor advanced soft lithography techniques. This method will be helpful to study 3D cellular behaviors in the context of the analysis of development and pathological states, including cancer.

3D Analysis of Multi-cellular Responses to Chemoattractant Gradients

3D Analysis of Multi-cellular Responses to Chemoattractant Gradients

Effects of Advective-Diffusive Transport of Multiple Chemoattractants on Motility of Engineered Chemosensory Particles in Fluidic Environments.

Motility behavior of an engineered chemosensory particle (ECP) in fluidic environments is driven by its responses to chemical stimuli. One of the challenges to understanding such behaviors lies in tracking changes in chemical signal gradients of chemoattractants and ECP-fluid dynamics as the fluid is continuously disturbed by ECP motion. To address this challenge, we introduce a new multiscale numerical model to simulate chemotactic swimming of an ECP in confined fluidic environments by accounting for motility-induced disturbances in spatiotemporal chemoattractant distributions. The model accommodates advective-diffusive transport of unmixed chemoattractants, ECP-fluid hydrodynamics at the ECP-fluid interface, and spatiotemporal disturbances in the chemoattractant concentrations due to particle motion. Demonstrative simulations are presented with an ECP, mimicking Escherichia coli (E. coli) chemotaxis, released into initially quiescent fluids with different source configurations of the chemoattractants N-methyl-L-aspartate and L-serine. Simulations demonstrate that initial distributions and temporal evolution of chemoattractants and their release modes (instantaneous vs. continuous, point source vs. distributed) dictate time histories of chemotactic motility of an ECP. Chemotactic motility is shown to be largely determined by spatiotemporal variation in chemoattractant concentration gradients due to transient disturbances imposed by ECP-fluid hydrodynamics, an observation not captured in previous numerical studies that relied on static chemoattractant concentration fields.

Ranking migration cue contributions to guiding individual fibroblasts faced with a directional decision in simple microfluidic bifurcations.

Directed cell migration in complex micro-environments, such as in vivo pores, is important for predicting locations of artificial tissue growth and optimizing scaffold architectures. Yet, the directional decisions of cells facing multiple physiochemical cues have not been characterized. Hence, we aim to provide a ranking of the relative importance of the following cues to the decision-making of individual fibroblast cells: chemoattractant concentration gradient, channel width, mitosis, and contact-guidance. In this study, bifurcated micro-channels with branches of different widths were created. Fibroblasts were then allowed to travel across these geometries by following a gradient of platelet-derived growth factor-BB (PDGF-BB) established inside the channels. Subsequently, a combination of statistical analysis and image-based diffusion modeling was used to report how the presence of multiple complex migration cues, including cell-cell influences, affect the fibroblast decision-making. It was found that the cells prefer wider channels over a higher chemoattractant gradient when choosing between asymmetric bifurcated branches. Only when the branches were symmetric in width did the gradient become predominant in directing which path the cell will take. Furthermore, when both the gradient and the channels were symmetric, contact guidance became important for guiding the cells in making directional choices. Based on these results we were able to rank these directional cues from most influential to the least as follows: mitosis > channel width asymmetry > chemoattractant gradient difference > and contact-guidance. It is expected that these results will benefit the fields of regenerative medicine, wound healing and developmental biology.

The Interplay Between Lymphatic Vessels and Chemokines.

Chemokines are a family of small protein cytokines that act as chemoattractants to migrating cells, in particular those of the immune system. They are categorized functionally as either homeostatic, constitutively produced by tissues for basal levels of cell migration, or inflammatory, where they are generated in association with a pathological inflammatory response. While the extravasation of leukocytes via blood vessels is a key step in cells entering the tissues, the lymphatic vessels also serve as a conduit for cells that are recruited and localized through chemoattractant gradients. Furthermore, the growth and remodeling of lymphatic vessels in pathologies is influenced by chemokines and their receptors expressed by lymphatic endothelial cells (LECs) in and around the pathological tissue. In this review we summarize the diverse role played by specific chemokines and their receptors in shaping the interaction of lymphatic vessels, immune cells, and other pathological cell types in physiology and disease.

Coherent directed movement toward food modeled in Trichoplax, a ciliated animal lacking a nervous system

Trichoplax adhaerens is a small, ciliated marine animal that glides on surfaces grazing upon algae, which it digests externally. It has no muscles or nervous system and only six cell types, all but two of which are embedded in its epithelium. The epithelial cells are joined by apical adherens junctions; neither tight junctions nor gap junctions are present. Monociliated epithelial cells on the lower surface propel gliding. The cilia beat regularly, but asynchronously, and transiently contact the substrate with each stroke. The animal moves in random directions in the absence of food. We show here that it exhibits chemotaxis, moving preferentially toward algae embedded in a disk of agar. We present a mathematical model to explain how coherent, directional movements could arise from the collective actions of a set of ciliated epithelial cells, each independently sensing and responding to a chemoattractant gradient. The model incorporates realistic values for viscoelastic properties of cells and produces coordinated movements and changes in body shape that resemble the actual movements of the animal. The model demonstrates that an animal can move coherently in search of food without any need for chemical signaling between cells and introduces a different approach to modeling behavior in primitive multicellular organisms.

A model of strongly biased chemotaxis reveals the trade-offs of different bacterial migration strategies.

Many bacteria actively bias their motility towards more favourable nutrient environments. In liquid, cells rotate their corkscrew-shaped flagella to swim, but in surface attached biofilms cells instead use grappling hook-like appendages called pili to pull themselves along. In both forms of motility, cells selectively alternate between relatively straight 'runs' and sharp reorientations to generate biased random walks up chemoattractant gradients. However, recent experiments suggest that swimming and biofilm cells employ fundamentally different strategies to generate chemotaxis: swimming cells typically suppress reorientations when moving up a chemoattractant gradient, whereas biofilm cells increase reorientations when moving down a chemoattractant gradient. The reason for this difference remains unknown. Here we develop a mathematical framework to understand how these different chemotactic strategies affect the distribution of cells at the population level. Current continuum models typically assume a weak bias in the reorientation rate and are not able to distinguish between these two strategies, so we derive a model for strong chemotaxis that resolves how both the drift and diffusive components depend on the underlying chemotactic strategy. We then test predictions from our continuum model against individual-based simulations and identify further refinements that allow our continuum model to resolve boundary effects. Our analyses reveal that the strategy employed by swimming cells yields a larger chemotactic drift, but the strategy used by biofilm cells allows them to more tightly aggregate where the chemoattractant is most abundant. This new modelling framework provides new quantitative insights into how the different chemical landscapes experienced by swimming and biofilm cells might select for divergent ways of generating chemotaxis.

Hybrid centralized/decentralized control of a network of bacteria-based bio-hybrid microrobots

Engineering microrobotic systems using a bio-hybrid approach that couples synthetic micro/nanoscale components with live cells is a powerful approach to address key shortcomings of micro/nanotechnology such as providing an on-board power source, communication, and decentralized control. In the last decade, a number of centralized control strategies based on native biological mechanisms have been demonstrated; however, decentralized cooperative control of a swarm of bio-hybrid microrobots has rarely been explored. In this work, we use our previously developed agent-based computational model to explore the utility of integrating synthetic biology with bio-hybrid microrobotics with the goal of developing strategies for robust decentralized control of bio-hybrid microrobotic systems. To this end, our Nanoscale Bacteria-Enabled Autonomous Delivery System (NanoBEADS), wherein each agent is comprised of an Escherichia coli bacterium conjugated with an ensemble of nanoparticles, was used as a model system. We imparted bacteria with engineered biological circuits to facilitate agent-agent communication and enable predictable and robust cooperative control of a network of NanoBEADS agents. We developed a hybrid control strategy wherein a centralized chemotaxis-based control scheme is used to direct migration, and a decentralized quorum sensing (QS)-based control scheme enables the agents to independently coordinate a cooperative behavior (fluorescent protein expression). We then computationally analyzed the role of bacterial subsystem properties and spatiotemporal changes in population organization in the emergent behavior (i.e., the activation time of the QS response) of the NanoBEADS. We show that the spatial changes in NanoBEADS agents’ distribution, in response to the centralized control input, and the mass transport boundary conditions are critical factors in determining the dynamics as well as the sensitivity and robustness of the QS response. We analyze the stark differences in feasible QS parameter domains under dissimilar chemoattractant gradients and show that the flow boundary conditions may greatly influence system function. Altogether, we show that a bacteria-based bio-hybrid system must be designed with careful consideration of growth rate, chemotaxis properties, QS properties, and the environment initial and boundary conditions in the context of its target application. This modeling framework can serve as an insightful tool for the predictive design of bio-hybrid microrobotic swarms with a tunable and robust response.

The Interplay of Tissue Landscape and Extracellular Signaling during Drosophila Oogenesis

Extracellular cues control developmental processes in a concentration‐dependent manner. Different amounts of morphogens elicit distinct cell fate decisions, and cells travel up chemoattractant gradients by assessing cue availability. Such signals must be tightly controlled to assure proper function. The concentration of signals in space and time depends on the parameters that govern the signal's release, diffusion, uptake, and decay rates. Chemical cues are often modeled as diffusing into open domains, but the structure of adjacent tissue could influence local signal availability, and thus cellular responses. The relatively simple tissue architecture of the Drosophila egg chamber, in which large germline cells are surrounded by a follicular epithelium, makes an ideal context to study how tissue contours influence extracellular signaling. In mid‐oogenesis, two anterior follicle cells secrete Unpaired (Upd) to activate the conserved factor Signal Transducer and Activator of Transcription (STAT) in nearby cells, and high STAT activity instructs a subset of those cells to become motile. Our genetic analysis identified specific vesicle trafficking components that modulate the secretion rate of Upd. While all cells near the source of Upd are responsive, we found that STAT activation and the resulting arrangements of motile cells often arose in unexpected, asymmetric patterns. We developed a mathematical model of the spatio‐temporal distribution of Upd in three‐dimensions to characterize signaling activity in the extracellular domain. Simulation results and genetic analysis of mutant phenotypes support the idea that irregular tissue domains result in asymmetric distributions of the Upd signal, consistent with outcomes in vivo. Additionally, modeling results suggest that the concentrations of chemoattractant signals that guide the motile cells can be spatially impacted by tissue structure. We conclude that the interstitial space generated by adjacent tissues creates complex distributions of signaling molecules, which impacts responding cells. This work illustrates novel aspects of how tissue topography alters signaling, and sheds light on cell motility during animal development.Support or Funding InformationNational Science Foundation IOS‐1656550This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Super-Low Dose Lipopolysaccharide Dysregulates Neutrophil Migratory Decision-Making.

Neutrophils are the first responders to infection and play a pivotal role in many inflammatory diseases, including sepsis. Recent studies have shown that lipopolysaccharide (LPS), a classical pattern recognition molecule, dynamically programs innate immune responses. In this study, we show that pre-treatment with super-low levels of LPS [1 ng/mL] significantly dysregulate neutrophil migratory phenotypes, including spontaneous migration and altering neutrophil decision-making. To quantify neutrophil migratory decision-making with single-cell resolution, we developed a novel microfluidic competitive chemotaxis-chip (μC3) that exposes cells in a central channel to competing chemoattractant gradients. In this reductionist approach, we use two chemoattractants: a pro-resolution (N-Formyl-Met-Leu-Phe, fMLP) and pro-inflammatory (Leukotriene B4, LTB4) chemoattractant to model how a neutrophil makes a decision to move toward an end target chemoattractant (e.g., bacterial infection) vs. an intermediary chemoattractant (e.g., inflammatory signal). We demonstrate that naïve neutrophils migrate toward the primary end target signal in higher percentages than toward the secondary intermediary signal. As expected, we found that training with high dose LPS [100 ng/mL] influences a higher percentage of neutrophils to migrate toward the end target signal, while reducing the percentage of neutrophils that migrate toward the intermediary signal. Surprisingly, super-low dose LPS [1 ng/mL] significantly changes the ratios of migrating cells and an increased percentage of cells migrate toward the intermediary signal. Significantly, there was also an increase in the numbers of spontaneously migrating neutrophils after treatment with super-low dose LPS. These results shed light onto the directional migratory decision-making of neutrophils exposed to inflammatory training signals. Understanding these mechanisms may lead to the development of pro-resolution therapies that correct the neutrophil compass and reduce off-target organ damage.

Escape band in Escherichia coli chemotaxis in opposing attractant and nutrient gradients

It is commonly believed that bacterial chemotaxis helps cells find food. However, not all attractants are nutrients, and not all nutrients are strong attractants. Here, by using microfluidic experiments, we studied Escherichia coli chemotaxis behavior in the presence of a strong chemoattractant (e.g., aspartate or methylaspartate) gradient and an opposing gradient of diluted tryptone broth (TB) growth medium. Our experiments showed that cells initially accumulate near the strong attractant source. However, after the peak cell density (h) reaches a critical value [Formula: see text], the cells form a "escape band" (EB) that moves toward the chemotactically weaker but metabolically richer nutrient source. By using various mutant strains and varying experimental conditions, we showed that the competition between Tap and Tar receptors is the key molecular mechanism underlying the formation of the escape band. A mathematical model combining chemotaxis signaling and cell growth was developed to explain the experiments quantitatively. The model also predicted that the width w and the peak position [Formula: see text] of EB satisfy two scaling relations: [Formula: see text] and [Formula: see text], where l is the channel length. Both scaling relations were verified by experiments. Our study shows that the combination of nutrient consumption, population growth, and chemotaxis with multiple receptors allows cells to search for optimal growth condition in complex environments with conflicting sources.

The Molecular Mechanisms of Gametic Incompatibility in Invertebrates.

Fertilization (gamete fusion followed by zygote formation) is a multistage process. Each stage is mediated by ligand-receptor recognition of gamete interaction molecules. This recognition includes the movement of sperm in the gradient of egg chemoattractants, destruction of the egg envelope by acrosomal proteins, etc. Gametic incompatibility is one of the mechanisms of reproductive isolation. It is based on species-specific molecular interactions that prevent heterospecific fertilization. Although gametic incompatibility may occur in any sexually reproducing organism, it has been studied only in a few model species. Gamete interactions in different taxa involve generally similar processes, but they often employ non-homologous molecules. Gamete recognition proteins evolve rapidly, like immunity proteins, and include many taxon-specific families. In fact, recently appeared proteins particularly contribute to reproductive isolation via gametic incompatibility. Thus, we can assume a multiple, independent origin of this type of reproductive isolation throughout animal evolution. Gametic incompatibility can be achieved at any fertilization stage and entails different consequences at different taxonomic levels and ranges, from complete incompatibility between closely related species to partial incompatibility between distantly related taxa.

Harnessing Motile Amoeboid Cells as Trucks for Microtransport and -Assembly.

Cell‐driven microtransport is one of the most prominent applications in the emerging field of biohybrid systems. While bacterial cells have been successfully employed to drive the swimming motion of micrometer‐sized cargo particles, the transport capacities of motile adherent cells remain largely unexplored. Here, it is demonstrated that motile amoeboid cells can act as efficient and versatile trucks to transport microcargo. When incubated together with microparticles, cells of the social amoeba Dictyostelium discoideum readily pick up and move the cargo particles. Relying on the unspecific adhesive properties of the amoeba, a wide range of different cargo materials can be used. The cell‐driven transport can be directionally guided based on the chemotactic responses of amoeba to chemoattractant gradients. On the one hand, the cargo can be assembled into clusters in a self‐organized fashion, relying on the developmentally induced chemotactic aggregation of cells. On the other hand, chemoattractant gradients can be externally imposed to guide the cellular microtrucks to a desired location. Finally, larger cargo particles of different shapes that exceed the size of a single cell by more than an order of magnitude, can also be transported by the collective effort of large numbers of motile cells.

Nonlinear concentration patterns and bands in autochemotactic suspensions

In suspensions of microorganisms, pattern formation can arise from the interplay of chemotaxis and the fluid flows collectively generated by the organisms themselves. Here we investigate the resulting pattern formation in square and elongated domains in the context of two distinct models of locomotion in which the chemoattractant dynamics is fully coupled to the fluid flows and swimmer motion. Analyses for both models reveal an aggregative instability due to chemotaxis, independent of swimmer shape and type, and a hydrodynamic instability for ``pusher'' swimmers. We discuss the similarities and differences between the models. Simulations reveal a critical length scale of the swimmer aggregates and this feature can be utilized to stabilize swimmer concentration patterns into quasi-one-dimensional bands by varying the domain size. These concentration bands transition to traveling pulses under an external chemoattractant gradient, as observed in experiments with chemotactic bacteria.