Bacterial accumulation in intestinal folds induced by physical and biological factors.

BACKGROUND: The gut microbiota, vital for host health, influences metabolism, immune function, and development. Understanding the dynamic processes of bacterial accumulation within the gut is crucial, as it is closely related to immune responses, antibiotic resistance, and colorectal cancer. We investigated Escherichia coli behavior and distribution in zebrafish larval intestines, focusing on the gut microenvironment. RESULTS: We discovered that E. coli spread was considerably suppressed within the intestinal folds, leading to a strong physical accumulation in the folds. Moreover, a higher concentration of E. coli on the dorsal side than on the ventral side was observed. Our in vitro microfluidic experiments and theoretical analysis revealed that the overall distribution of E. coli in the intestines was established by a combination of physical factor and bacterial taxis. CONCLUSIONS: Our findings provide valuable insight into how the intestinal microenvironment affects bacterial motility and accumulation, enhancing our understanding of the behavioral and ecological dynamics of the intestinal microbiota.

Bacteria-surface interactions: role of impacting bacteria-laden droplets.

Understanding the interactions of pathogenic droplets with surfaces is crucial to biomedical applications. In this study, using E. coli as the model microbe, we investigate the impact of a bacteria-laden droplet on different substrates, both bare and antimicrobial. In doing so, we unveil the significance of kinetic energy and spreading parameters of the impacting droplet in determining the microbes' proliferation capabilities. Our results indicate an inverse relationship between the impact Weber number and the bacterial ability to proliferate. We reveal that the mechanical stress generated during impact impedes the capabilities of microbes present inside the droplet to create their progeny. Following an order analysis of the mechanical stress generated, we argue that the impact does not induce lysis-driven cell death of the bacteria; rather, it promotes a stress-driven transition of viable bacteria to a viable-but-non-culturable (VBNC) state. Furthermore, variations in the concentration of particles on the antimicrobial surfaces revealed the role of the post-impact spreading behaviour in dictating bacterial proliferation capabilities. Contrary to the conventional notion, we demonstrate that during the early stages of interaction, a bare substrate may outperform an antibacterial substrate in the inactivation of the bacterial load. Finally, we present an interaction map illustrating the complex relationship between bacterial colony-forming units, bactericide concentration on the surface, and the impact Weber number. We believe that the inferences of the study, highlighting the effect of mechanical stresses on the soft cell wall of microbes, could be a useful design consideration for the development of antimicrobial surfaces.

Biofilm exopolysaccharides alter sensory-neuron-mediated sickness during lung infection.

Infections of the lung cause observable sickness thought to be secondary to inflammation. Signs of sickness are crucial to alert others via behavioral-immune responses to limit contact with contagious individuals. Gram-negative bacteria produce exopolysaccharide (EPS) that provides microbial protection; however, the impact of EPS on sickness remains uncertain. Using genome-engineered Pseudomonas aeruginosa (P. aeruginosa) strains, we compared EPS-producers versus non-producers and a virulent Escherichia coli (E. coli) lung infection model in male and female mice. EPS-negative P. aeruginosa and virulent E. coli infection caused severe sickness, behavioral alterations, inflammation, and hypothermia mediated by TLR4 detection of the exposed lipopolysaccharide (LPS) in lung TRPV1+ sensory neurons. However, inflammation did not account for sickness. Stimulation of lung nociceptors induced acute stress responses in the paraventricular hypothalamic nuclei by activating corticotropin-releasing hormone neurons responsible for sickness behavior and hypothermia. Thus, EPS-producing biofilm pathogens evade initiating a lung-brain sensory neuronal response that results in sickness.

Interplay between environmental yielding and dynamic forcing modulates bacterial growth.

Many bacterial habitats-ranging from gels and tissues in the body to cell-secreted exopolysaccharides in biofilms-are rheologically complex, undergo dynamic external forcing, and have unevenly distributed nutrients. How do these features jointly influence how the resident cells grow and proliferate? Here, we address this question by studying the growth of Escherichia coli dispersed in granular hydrogel matrices with defined and highly tunable structural and rheological properties, under different amounts of external forcing imposed by mechanical shaking, and in both aerobic and anaerobic conditions. Our experiments establish a general principle: that the balance between the yield stress of the environment that the cells inhabit, σy, and the external stress imposed on the environment, σ, modulates bacterial growth by altering transport of essential nutrients to the cells. In particular, when σy<σ, the environment is easily fluidized and mixed over large scales, providing nutrients to the cells and sustaining complete cellular growth. By contrast, when σy>σ, the elasticity of the environment suppresses large-scale fluid mixing, limiting nutrient availability and arresting cellular growth. Our work thus reveals a new mechanism, beyond effects that change cellular behavior via local forcing, by which the rheology of the environment may modulate microbial physiology in diverse natural and industrial settings.

Enhanced cavitation dose and reactive oxygen species production in microbubble-mediated sonodynamic therapy for inhibition of Escherichia coli and biofilm.

Sonodynamic therapy (SDT) is an emerging antibacterial therapy. This work selected hematoporphyrin monomethyl ether (HMME) as the sonosensitizer, and studied the enhanced inhibition effect of Escherichia coli and biofilm by microbubble-mediated cavitation in SDT. Firstly, the influence of microbubble-mediated cavitation effect on different concentrations of HMME (10 µg/ml, 30 µg/ml, 50 µg/ml) was studied. Using 1,3-diphenylisobenzofuran (DPBF) as an indicator, the effect of microbubble-mediated cavitation on the production of reactive oxygen species (ROS) was studied by absorption spectroscopy. Secondly, using agar medium, laser confocal microscopy and scanning electron microscopy, the effect of microbubble-mediated cavitation on the activity and morphology of bacteria was studied. Finally, the inhibitory effect of cavitation combined with SDT on biofilm was evaluated by laser confocal microscopy. The research results indicate that: (1) Microbubble-mediated ultrasound cavitation can significantly increase cavitation intensity and production of ROS. (2) Microbubble-mediated acoustic cavitation can alter the morphological structure of bacteria. (3) It can significantly enhance the inhibition of SDT on the activity of Escherichia coli and its biofilm. Compared with the control group, the addition of microbubbles resulted in an increase in the number of dead bacteria by 61.7 %, 71.6 %, and 76.2 %, respectively. The fluorescence intensity of the biofilm decreased by 27.1 %, 80.3 %, and 98.2 %, respectively. On the basis of adding microbubbles to ensure antibacterial and biofilm inhibition effects, this work studied the influence of cavitation effect in SDT on bacterial structure, providing a foundation for further revealing the intrinsic mechanism of SDT.

Bacteriophage specificity is impacted by interactions between bacteria.

Predators play a central role in shaping community structure, function, and stability. The degree to which bacteriophage predators (viruses that infect bacteria) evolve to be specialists with a single bacterial prey species versus generalists able to consume multiple types of prey has implications for their effect on microbial communities. The presence and abundance of multiple bacterial prey types can alter selection for phage generalists, but less is known about how interactions between prey shape predator specificity in microbial systems. Using a phenomenological mathematical model of phage and bacterial populations, we find that the dominant phage strategy depends on prey ecology. Given a fitness cost for generalism, generalist predators maintain an advantage when prey species compete, while specialists dominate when prey are obligately engaged in cross-feeding interactions. We test these predictions in a synthetic microbial community with interacting strains of Escherichia coli and Salmonella enterica by competing a generalist T5-like phage able to infect both prey against P22vir, an S. enterica-specific phage. Our experimental data conform to our modeling expectations when prey species are competing or obligately mutualistic, although our results suggest that the in vitro cost of generalism is caused by a combination of biological mechanisms not anticipated in our model. Our work demonstrates that interactions between bacteria play a role in shaping ecological selection on predator specificity in obligately lytic bacteriophages and emphasizes the diversity of ways in which fitness trade-offs can manifest. IMPORTANCE: There is significant natural diversity in how many different types of bacteria a bacteriophage can infect, but the mechanisms driving this diversity are unclear. This study uses a combination of mathematical modeling and an in vitro system consisting of Escherichia coli, Salmonella enterica, a T5-like generalist phage, and the specialist phage P22vir to highlight the connection between bacteriophage specificity and interactions between their potential microbial prey. Mathematical modeling suggests that competing bacteria tend to favor generalist bacteriophage, while bacteria that benefit each other tend to favor specialist bacteriophage. Experimental results support this general finding. The experiments also show that the optimal phage strategy is impacted by phage degradation and bacterial physiology. These findings enhance our understanding of how complex microbial communities shape selection on bacteriophage specificity, which may improve our ability to use phage to manage antibiotic-resistant microbial infections.

Rediversification following ecotype isolation reveals hidden adaptive potential.

Microbial communities play a critical role in ecological processes, and their diversity is key to their functioning. However, little is known about whether communities can regenerate ecological diversity following ecotype removal or extinction and how the rediversified communities would compare to the original ones. Here, we show that simple two-ecotype communities from the E. coli long-term evolution experiment (LTEE) consistently rediversified into two ecotypes following the isolation of one of the ecotypes, coexisting via negative frequency-dependent selection. Communities separated by more than 30,000 generations of evolutionary time rediversify in similar ways. The rediversified ecotype appears to share a number of growth traits with the ecotype it replaces. However, the rediversified community is also different from the original community in ways relevant to the mechanism of ecotype coexistence-for example, in stationary phase response and survival. We found substantial variation in the transcriptional states between the two original ecotypes, whereas the differences within the rediversified community were comparatively smaller, although the rediversified community showed unique patterns of differential expression. Our results suggest that evolution may leave room for alternative diversification processes even in a maximally reduced community of only two strains. We hypothesize that the presence of alternative evolutionary pathways may be even more pronounced in communities of many species where there are even more potential niches, highlighting an important role for perturbations, such as species removal, in evolving ecological communities.

Klebsiella aerogenes ingestion elicits behavioral changes and innate immunity in the host, Caenorhabditis elegans.

Klebsiella aerogenes (previously known as Enterobacter aerogenes) is a common opportunistic pathogen that infect the respiratory tract and central nervous system. However, how it interferes the host regulatory mechanism has not been previously described. When C. elegans were exposed to K. aerogenes, they exhibited a shorter lifespan compared to those fed with E. coli OP50. The time required for 50 % of L4 hermaphrodite nematodes to die when exposed to K. aerogenes was approximately 9 days, whereas it was about 18 days when fed with E. coli OP50. The interaction with K. aerogenes also affected the physical activity of C. elegans. Parameters like pharyngeal pumping, head thrashing, body bending, and swimming showed a gradual decline during infection. The expression of serotonin-mediated axon regeneration K. aerogenes infection led to increased levels of reactive oxygen species (ROS) in C. elegans compared to E. coli OP50-fed worms. The nematodes activated antioxidant mechanisms, including the expression of SODs, to counteract elevated ROS levels. The interaction with K. aerogenes activated immune regulatory pathways in C. elegans, including the mTOR signaling pathway downstream player SGK-1. Lifespan regulatory pathways, such as pha-4 and pmk-1, were also affected, likely contributing to the nematode ability to survive in a pathogenic environment. K. aerogenes infection has a detrimental impact on the healthspan and lifespan of C. elegans, affecting physical activity, intestinal health, serotonin regulation, ROS levels, and immune responses. These findings provide insights into the complex interactions between K. aerogenes and host organisms.

Chemical basis of microbiome preference in the nematode C. elegans.

Animals are exposed to many microbes in their environment, some of which have been shown to colonize various tissues including the intestine. The composition of the intestinal microbiota affects many aspects of the host's physiology and health. Despite this, very little is known about whether host behavior contributes to the colonization. We approach this question in the nematode C. elegans, which feeds on bacteria and also harbors an intestinal microbiome. We examined the behavior of C. elegans towards CeMbio, a simplified microbiome consisting of twelve strains that represent the bacteria found in the animal's natural environment. We observed that C. elegans raised on E. coli shows a strong preference for three members of CeMbio (Lelliottia amnigena JUb66, Enterobacter hormaechei CEent1, and Pantoea nemavictus BIGb0393) compared to E. coli. Previously, these three bacterial strains have been shown to support faster C. elegans development time than E. coli OP50 and are low colonizers compared to eight other members of CeMbio. We then used gas chromatography coupled to mass spectrometry to identify that these three bacteria release isoamyl alcohol, a previously described C. elegans chemoattractant. We suggest that C. elegans seeks bacteria that release isoamyl alcohol and support faster growth.

Interfacial coupling of CuFe2O4 induced hotspots over self-assembled g-C3N4 nanosheets as an efficient photocatalytic bacterial disinfectant.

Most bacterial disinfectants contain high levels of extremely toxic and environmental hazardous chemicals, which pose a significant threat to the ecosystem. Semiconductor photocatalysis exhibits attractive prospects as an emerging greener technology for waste water disinfection. However, the fast recombination of charge carriers limits its practical application. Herein, self-assembled polymeric feather-like g-C3N4 (GCN) nanosheets modified with ferromagnetic CuFe2O4 (CFO) nanospheres were successfully applied as a reusable visible light photocatalytic disinfectant. As expected, the g-C3N4/CuFe2O4 (GCF) nanohybrid displayed superior photocatalytic inactivation efficiency of 0.157log within 120 min towards Escherichia coli DH5α (E. coli) compared with pristine GCN and CFO. The characterization results revealed the synergistic heterostructure interfaces, high surface area, and the transformative self-assembly of GCN to feather-like structure providing a rich active site for improved charge separation efficiency, and wide spectral response, therefore the superior performance of GCF. The radical trapping assay proclaimed that both O2•- and •OH radical played major role in the photocatalytic inactivation among the other reactive oxygen species (ROS). Furthermore, the chemical oxygen demand (COD), protein estimation, and DNA estimation assay results validated the cell damage caused by the photocatalyst. Besides that, GCN showed applicability in real-time wastewater samples with improved efficiency than in the saline solution. The excellent magnetic characteristics facilitated the recycling of the catalyst with insignificant leaching, magnetic induction, and distinguished separation. The results of this work signify the well-designed GCF as a high-performance and reusable photocatalyst for real-world pathogenic bacterial disinfection operations.

Comparative transcriptome analysis of E. coli & Staphylococcus aureus infected goat mammary epithelial cells reveals genes associated with infection.

Mastitis, an inflammatory disease of the mammary gland, imposes a significant financial burden on the dairy sector. However, the specific molecular mechanisms underlying their interactions with goat mammary epithelial cells (GMECs) remain poorly understood. This study aimed to investigate the transcriptomic response of GMECs during infection with E. coli and S. aureus, providing insights into the host-pathogen interactions. Differential expression of gene (DEGs) analysis was done to find genes and pathways dysregulated in the wake of infection. E. coli infection triggered a robust upregulation of immune response genes, including pro-inflammatory chemokines and cytokines as well as genes involved in tissue repair and remodeling. Conversely, S. aureus infection showed a more complex pattern, involving the activation of immune-related gene as well as those involved in autophagy, apoptosis and tissue remodeling. Furthermore, several key pathways, such as Toll-like receptor signaling and cytokine-cytokine receptor interaction, were differentially modulated in response to each pathogen. Understanding the specific responses of GMECs to these pathogens will provide a foundation for understanding the complex dynamics of infection and host response, offering potential avenues for the development of novel strategies to prevent and treat bacterial infections in both animals and humans.

Differential induction of NF-κB pathways by non-pathogenic and pathogenic bacteria in Helicoverpa armigera is critical for an efficient immune response and survival.

Following pathogen infection in a host, extensive changes occur in the host's gene expression pattern to suppress infection and increase the chance of host survival. Likewise, many pathogens have evolved to evade/suppress host immunity and increase their survival within the host. In this study, we assessed the NF-κB (Imd and Toll) essential gene expression response of Helicoverpa armigera to an entomopathogenic Serratia marcescens and non-pathogenic Escherichia coli. Bacterial cells of S. marcescens or E. coli were injected into the haemocoel of fifth-instar larvae of H. armigera, whereas distilled water was injected into control insects. Our results showed that the expression levels of the Imd and Toll pathway genes (i.e., Relish, imd, spätzle and dif) and the antimicrobial peptides (i.e., gloverin, transferin, gallerimycin, and galiomicin) were differentially expressed following the bacterial injections while control larvae showed no differences. The E. coli injection induced higher and longer-lasted gene expression than the S. marcescens injected larvae, in which the gene expressions were diminished from 24 h post injection. Transcript Knockdown of Relish increased the replication rates of S. marcescens and E. coli, and lowered the infected larvae survival rates. These results showed that H. armigera NF-κB immunity pathways (particularly Imd pathway) play a vital role in immunity against bacterial infections, and S. marcescens might modulate these pathways to survive and replicate in the host.

Flagellar motors of swimming bacteria contain an incomplete set of stator units to ensure robust motility.

Flagellated bacteria, like Escherichia coli, swim by rotating helical flagellar filaments powered by rotary flagellar motors at their base. Motor dynamics are sensitive to the load it drives. It was previously thought that motor load was high when driving filament rotation in free liquid environments. However, torque measurements from swimming bacteria revealed substantially lower values compared to single-motor studies. We addressed this inconsistency through motor resurrection experiments, abruptly attaching a 1-micrometer-diameter bead to the filament to ensure high load. Unexpectedly, we found that the motor works with only half the complement of stator units when driving filament rotation. This suggests that the motor is not under high load during bacterial swimming, which we confirmed by measuring the torque-speed relationship by varying media viscosity. Therefore, the motor operates in an intermediate-load region, adaptively regulating its stator number on the basis of external load conditions. This ensures the robustness of bacterial motility when swimming in diverse load conditions and varying flagella numbers.

Indole produced during dysbiosis mediates host-microorganism chemical communication.

An imbalance of the gut microbiota, termed dysbiosis, has a substantial impact on host physiology. However, the mechanism by which host deals with gut dysbiosis to maintain fitness remains largely unknown. In Caenorhabditis elegans, Escherichia coli, which is its bacterial diet, proliferates in its intestinal lumen during aging. Here, we demonstrate that progressive intestinal proliferation of E. coli activates the transcription factor DAF-16, which is required for maintenance of longevity and organismal fitness in worms with age. DAF-16 up-regulates two lysozymes lys-7 and lys-8, thus limiting the bacterial accumulation in the gut of worms during aging. During dysbiosis, the levels of indole produced by E. coli are increased in worms. Indole is involved in the activation of DAF-16 by TRPA-1 in neurons of worms. Our finding demonstrates that indole functions as a microbial signal of gut dysbiosis to promote fitness of the host.

Multiflagellarity leads to the size-independent swimming speed of peritrichous bacteria.

To swim through a viscous fluid, a flagellated bacterium must overcome the fluid drag on its body by rotating a flagellum or a bundle of multiple flagella. Because the drag increases with the size of bacteria, it is expected theoretically that the swimming speed of a bacterium inversely correlates with its body length. Nevertheless, despite extensive research, the fundamental size-speed relation of flagellated bacteria remains unclear with different experiments reporting conflicting results. Here, by critically reviewing the existing evidence and synergizing our own experiments of large sample sizes, hydrodynamic modeling, and simulations, we demonstrate that the average swimming speed of Escherichia coli, a premier model of peritrichous bacteria, is independent of their body length. Our quantitative analysis shows that such a counterintuitive relation is the consequence of the collective flagellar dynamics dictated by the linear correlation between the body length and the number of flagella of bacteria. Notably, our study reveals how bacteria utilize the increasing number of flagella to regulate the flagellar motor load. The collective load sharing among multiple flagella results in a lower load on each flagellar motor and therefore faster flagellar rotation, which compensates for the higher fluid drag on the longer bodies of bacteria. Without this balancing mechanism, the swimming speed of monotrichous bacteria generically decreases with increasing body length, a feature limiting the size variation of the bacteria. Altogether, our study resolves a long-standing controversy over the size-speed relation of flagellated bacteria and provides insights into the functional benefit of multiflagellarity in bacteria.

The efficacy of some probiotics and prebiotics on the prevalence of E. coli and the immune response of chickens.

The present study aimed to investigate the efficacy of probiotics and prebiotics in controlling Escherichia coli (E. coli) spp. isolated from chicken. A total of 230 birds representing 19 different commercial breeds were taken from various points. Birds were monitored for postmortem and clinical investigation. Aseptically collected liver samples, lungs, kidneys, hearts, and yolk sacs were then subjected to bacterial isolation and identification. E. coli were observed in 9 pooled samples from 120 examined with an incidence of 7.5%. Nine farms were E. coli-positive, with an incidence of farm infection of 47.3%. The 9 suspected isolates of E. coli were profiled by morphological and microbiological identification of the colony, motility, and gram reaction. The serogroup analysis showed 9 different E. coli for which 3 other groups were identified: 2 E. coli O78, 3 E. coli O111, and 4 untyped groups. Nine isolates of E. coli were subjected to PCR. Molecular detection of 9 strains was conducted to find the virulence genes of E. coli strains (8 STX1, 4 STX2, and 9 EAE). Probiotics and prebiotics significantly increased the total erythrocytic and leukocytic counts throughout the experiment. The phagocytic percentage's main values at 14 d were 47 and 30%, respectively. An increase in the humoral immunity against Newcastle disease (ND) was noticed after ND vaccination. The geometric mean (HI) was 5.9 and 4.2 for probiotic and prebiotic, respectively. It could be concluded that probiotics and prebiotics could stimulate a nonspecific immune response against experimental infection with a virulent strain of E. coli spp.

Molecular mechanism of Enteroaggregative Escherichia coli induced apoptosis in cultured human intestinal epithelial cells.

Background. Enteroaggregative Escherichia coli (EAEC) is an evolving etiological agent of acute and persistent diarrhoea worldwide. The previous study from our laboratory has reported the apoptosis-inducing activity of EAEC in human small intestinal and colonic epithelial cell lines. In the present investigation, we have explored the underlying mechanism of EAEC-induced apoptosis in human intestinal epithelial cell lines.Methods. INT-407 and HCT-15 cells were infected with EAEC-T8 and EAEC-pT8 (plasmid cured strain of EAEC-T8) separately. Cells cultured in the absence of bacteria served as a negative control in all the experiments. For the subsequent experiments, the molecular mechanism(s) of epithelial cell aposptosis was measured in EAEC infecting both the cell lines by flow cytometry, real-time PCR and Western blotting.Results and conclusions. EAEC was found to activate the intrinsic/mitochondrial apoptotic pathway in both the cell lines through upregulation of pro-apoptotic Bax and Bak, un-alteration/reduction in the level of anti-apoptotic Bcl-2 and Bcl-XL, decrease in mitochondrial transmembrane potential, accumulation of cytosolic cytochrome c leading to activation of procaspase-9 and procaspase-3, which ultimately resulted in DNA fragmentation and apoptosis. Further, an increased expression of Fas, activation of procaspase-8 and upregulation of pro-apoptotic Bid in the EAEC-infected cells indicated the involvement of extrinsic apoptotic pathway too in this process. Our finding has undoubtedly led to an increased understanding of EAEC pathogenesis, which may be helpful to develop an improved strategy to combat the infection.

Selective inhibition of the amyloid matrix of Escherichia coli biofilms by a bifunctional microbial metabolite.

The propensity of bacteria to grow collectively in communities known as biofilms and their ability to overcome clinical treatments in this condition has become a major medical problem, emphasizing the need for anti-biofilm strategies. Antagonistic microbial interactions have extensively served as searching platforms for antibiotics, but their potential as sources for anti-biofilm compounds has barely been exploited. By screening for microorganisms that in agar-set pairwise interactions could antagonize Escherichia coli's ability to form macrocolony biofilms, we found that the soil bacterium Bacillus subtilis strongly inhibits the synthesis of amyloid fibers -known as curli-, which are the primary extracellular matrix (ECM) components of E. coli biofilms. We identified bacillaene, a B. subtilis hybrid non-ribosomal peptide/polyketide metabolite, previously described as a bacteriostatic antibiotic, as the effector molecule. We found that bacillaene combines both antibiotic and anti-curli functions in a concentration-dependent order that potentiates the ecological competitiveness of B. subtilis, highlighting bacillaene as a metabolite naturally optimized for microbial inhibition. Our studies revealed that bacillaene inhibits curli by directly impeding the assembly of the CsgB and CsgA curli subunits into amyloid fibers. Moreover, we found that curli inhibition occurs despite E. coli attempts to reinforce its protective ECM by inducing curli genes via a RpoS-mediated competition sensing response trigged by the threatening presence of B. subtilis. Overall, our findings illustrate the relevance of exploring microbial interactions not only for finding compounds with unknown and unique activities, but for uncovering additional functions of compounds previously categorized as antibiotics.

Trade-offs between cost and information in cellular prediction.

Living cells can leverage correlations in environmental fluctuations to predict the future environment and mount a response ahead of time. To this end, cells need to encode the past signal into the output of the intracellular network from which the future input is predicted. Yet, storing information is costly while not all features of the past signal are equally informative on the future input signal. Here, we show for two classes of input signals that cellular networks can reach the fundamental bound on the predictive information as set by the information extracted from the past signal: Push-pull networks can reach this information bound for Markovian signals, while networks that take a temporal derivative can reach the bound for predicting the future derivative of non-Markovian signals. However, the bits of past information that are most informative about the future signal are also prohibitively costly. As a result, the optimal system that maximizes the predictive information for a given resource cost is, in general, not at the information bound. Applying our theory to the chemotaxis network of Escherichia coli reveals that its adaptive kernel is optimal for predicting future concentration changes over a broad range of background concentrations, and that the system has been tailored to predicting these changes in shallow gradients.