Host Tissue Research Articles

Plant cell wall structure and dynamics in plant-pathogen interactions and pathogen defence.

Plant cell walls delimit plant cells from their environment and provide mechanical stability to withstand internal turgor pressure as well as external influences. Environmental factors can be beneficial or harmful for the plants and vary substantially depending on prevailing combinations of climate conditions and stress exposure. Consequently, the physicochemical properties of plant cell walls need to be adaptive, and their functional integrity needs to be monitored by the plant. One major threat to plants is posed by phytopathogens, which employ a diversity of infection strategies and lifestyles to colonise host tissues. During these interactions, the plant cell wall represents a barrier that impedes the colonisation of host tissues and pathogen spread. In a tussle over maintenance and breakdown, plant cell walls can be rapidly and efficiently remodelled by enzymatic activities of plant and pathogen origin, heavily influencing the outcome of plant-pathogen interactions. We review the role of locally and systemically induced cell wall remodelling and the importance of tissue-dependent cell wall properties for the interaction with pathogens. Furthermore, we discuss the importance of cell wall-dependent signalling for defence response induction and the influence of abiotic factors on cell wall integrity and cell wall-associated pathogen resistance mechanisms.

Root-filling materials for endodontic surgery: biological and clinical aspects

The placement of root filling materials aims to prevent the occurrence of post-treatment apical periodontitis following completion of endodontic treatment. Materials should possess properties that will not permit bacterial invasion and infection, namely excellent sealing ability and/or antibacterial properties. In root-end filling procedures or repair of root perforations, the root filling materials are placed in a particularly challenging clinical environment, as they interface with a relatively large area with the periradicular tissues. The biological properties of these materials are therefore of significant importance. The current review discusses the most widely used materials for endodontic surgery (i.e., root-end filling and perforation repair), with particular focus on their biological characteristics, namely antibacterial properties and interactions with host tissue cells, together with clinical studies. Properties of amalgam, glass ionomer cements (GICs), resin systems, zinc oxide eugenol-based cements and hydraulic calcium silicate cements (HCSCs), together with representative and well-researched commercial materials in the context of their use in endodontic surgery are presented. While the use of HCSCs seems to offer several biological advantages, together with addressing issues with the initial formulation in the most recent versions, materials with different chemical compositions, such as zinc oxide eugenol-based cements, are still in use and appear to provide similar clinical success rates to HCSCs. Thus, the significance of the currently available materials on clinical outcomes remains unclear.

Complement Evasion Protects FCoV from Virus Clearance Within Prototypic FIP Lesions

Feline infectious peritonitis (FIP) is a fatal disease in cats caused by infection with feline coronavirus (FCoV). Despite severe inflammatory changes, defense mechanisms fail to achieve virus clearance. Some studies focused on various immune evasion mechanisms, but none of these studies elucidated the inefficacy of the complement system, which is one major player in FIP-associated immune pathogenesis. This study aimed to investigate the involvement of complement-regulating factors (CRFs). CRFs help modulate the immune response and prevent host tissue damage. Archived tissue samples from 31 deceased, FIP-affected cats were evaluated using multiplex immunohistochemistry for the spatial expression of the complement-regulating factors CD46 and CD59 in association with FIP lesions and their colocalization with complement-activating factor C1q and membrane attack complex C9 in relation to the presence and proximity of FCoV-infected cells. The FIP lesions of all 31 cats exhibited marked expression of both complement-regulating factors in proximity to FCoV-infected macrophages. Moreover, their expression in all 31 animals was significantly lower than the expression of the complement-activating factors C1q and C9 compared to areas farther distal to FCoV-infected cells. In conclusion, FCoV-infected macrophages in cats with FIP appear to use autocrine and paracrine expression of complement-regulating factors in their immediate environment to shield themselves from destruction by the complement system.

A UTILIZAÇÃO DE BIOMATERIAIS EM PROCEDIMENTOS CIRÚRGICOS ODONTOLÓGICOS

Sustainable practices are necessary in all areas, and in dentistry, this need is becoming increasingly present. Thus, new materials and materials become important in this process. Among these materials, biomaterials stand out. Biomaterials are natural or synthetic materials used in contact with biological systems whose purpose is to repair or replace tissues, organs or functions of the organism, with the aim of maintaining or improving the patient's quality of life. This literature review aims to examine and demonstrate the application of biomaterials, highlighting them as a viable option in dentistry. Currently, in dentistry, three categories of biomaterials stand out: metals, polymers and ceramics, with the use of Nile tilapia skin in dentistry being considered an innovation. Biomaterials must present physical and biological properties compatible with the host's biological tissues, in order to stimulate an adequate response from them. As demonstrated, the use of biomaterials in surgical procedures becomes necessary. Biomaterials, their use and innovations, as highlighted throughout this literature review, emerge as a fundamental tool in promoting quality, efficiency and sustainability in oral health services.

Epigenetic modulation of fungal pathogens: a focus on Magnaporthe oryzae

Epigenetics has emerged as a potent field of study for understanding the factors influencing the effectiveness of human disease treatments and for identifying alternations induced by pathogens in host plants. However, there has been a paucity of research on the epigenetic control of the proliferation and pathogenicity of fungal plant pathogens. Fungal plant pathogens such as Magnaporthe oryzae, a significant threat to global rice production, provide an important model for exploring how epigenetic mechanisms govern fungal proliferation and virulence. In M. oryzae, epigenetic alterations, such as DNA methylation, histone modification, and non-coding RNAs, regulate gene expression patterns that influence the pathogen’s ability to infect its host. These modifications can enhance fungal adaptability, allowing the pathogen to survive in diverse environments and evade host immune responses. Our primary objective is to provide a comprehensive review of the existing epigenetic research on M. oryzae and shed light on how these changes influence the pathogen’s lifecycle, its ability to invade host tissues, and the overall severity of the disease. We begin by examining the epigenetic alterations occurring in M. oryzae and their contributions to the virulence and proliferation of the fungus. To advance our understanding of epigenetic mechanisms in M. oryzae and similar plant diseases, we emphasize the need to address unanswered questions and explore future research directions. This information is crucial for developing new antifungal treatments that target epigenetic pathways, which could lead to improved disease management.

Exploration of the Sclerotinia sclerotiorum-Brassica pathosystem: advances and perspectives in omics studies.

The polyphagous phytopathogen Sclerotinia sclerotiorum causing Stem rot disease is a major biotic stress in Brassica, and affects the yield and quality in various crops of agricultural significance. It affects the crop at pre-maturity which causes a reduction in the seed yield and deteriorates the oil quality in rapeseeds and Indian mustard globally. The hemibiotrophic nature and long persistence in the soil as sclerotia have made this pathogen difficult to manage through conventional agronomical practices. Hence, for alternative strategies, it is important to understand the basic aspects of the pathogen and the pathogenesis processes in the host. The current developments in technologies for omics studies including whole-genomes, transcriptomes, proteomes, and metabolomes have deciphered various genes, transcription factors, effectors and their target molecules involved in interaction, disease establishment and pathogen progress in the host tissues. The current review encompasses the studies that were conducted to decipher the Brassica-S. sclerotiorum pathosystem and the molecular factors identified through multi-omics studies for their application in building resistance to Sclerotinia stem rot disease in the susceptible cultivars of oilseed Brassica.

Functional Characterization of the Sterol-Synthesis-Related Gene CgCYP51 in the Poplar Anthracnose-Causing Fungus Colletotrichum gloeosporioides

Poplar is an economically and ecologically valuable tree species. Anthracnose, which severely affects poplar tree growth, is mainly caused by Colletotrichum gloeosporioides. In the infestation cycle of poplar anthracnose, the entry of C. gloeosporioides into the host tissue depends on the formation of an appressorium. The subsequent development of the appressorium determines the pathogenesis of poplar anthracnose and the degree of damage. Previous studies have found that the transcription factor CgSte12 affects appressorium formation and development by regulating the expression of a series of genes, including the sterol-synthesis-related gene CgCYP51, which influences appressorium formation and development. In this study, knockout and functional analyses of CgCYP51 revealed decreases in differentiation, darkening rate, and turgor pressure of appressoria in mutants. Additionally, compared with the wild-type appressorium, mutant appressoria secreted less mucus and exhibited abnormal penetration pore formation, ultimately leading to decreased pathogenicity. Moreover, CgCyp51 affected the sensitivity of C. gloeosporioides to sterol biosynthesis inhibitors. Considered together, the study findings indicate CgCYP51 is a key CgSte12-regulated gene that affects C. gloeosporioides appressorium formation and development. Furthermore, the study data provide new insights into the molecular basis of C. gloeosporioides appressorium formation and development.

Establishment of Animal Infection Model of Spirometra Mansoni and Identification of Spirometra Mansoni by Enzyme-Linked Immunosorbent Assay.

Objective: Spirometra mansoni is a crucial zoonotic parasite. Its larvae are more harmful than adult worms due to their ability to migrate through the host's tissues and organs. Therefore, it is necessary to establish an animal model of spargana for observing pathological changes and exploring diagnostic techniques. Methods: In this study, we infected Kunming mice and cats without any pathogens by feeding sparganum (with the scolex and neck) in order to understand the infection cycle of S. mansoni and explore the preservation host of sparganosis. The infection of S. mansoni was determined by fecal detection and enzyme-linked immunosorbent assay (ELISA). Results: In the model of cats, the eggs of S. mansoni were found in the feces ten days after the infection. The serum-specific IgG antibodies against S. mansoni were positive in experimental groups (mice and cats), and after sixty days, the S. mansoni worms isolated from experimental groups were collected. Conclusion: In conclusion, the experimental results show that mice and cats can be stably infected with S. mansoni through feeding sparganum (with the scolex and neck). The infection method of this study has the potential to establish a practical model for investigating the diagnostic process of S. mansoni, laying the groundwork for application and development. ELISA was used to diagnose mice and cats infected with sparganosis mansoni, providing a case for non-invasive identification of animal sparganosis.

LC3-associated phagocytosis and human diseases: Insights from mechanisms to therapeutic potential.

LC3-associated phagocytosis (LAP) is a distinct type of autophagy that involves the sequestration of extracellular material by phagocytes. Beyond the removal of dead cells and cellular debris from eukaryotic cells, LAP is also involved in the removal of a variety of pathogens, including bacteria, fungi, and viruses. These events are integral to multiple physiological and pathological processes, such as host defense, inflammation, and tissue homeostasis. Dysregulation of LAP has been associated with the pathogenesis of several human diseases, including infectious diseases, autoimmune diseases, and neurodegenerative diseases. Thus, understanding the molecular mechanisms underlying LAP and its involvement in human diseases may provide new insights into the development of novel therapeutic strategies for these conditions. In this review, we summarize and highlight the current consensus on the role of LAP and its biological functions in disease progression to propose new therapeutic strategies. Further studies are needed to illustrate the precise role of LAP in human disease and to determine new therapeutic targets for LAP-associated pathologies.

Delving the depths of 'terra incognita' in the human intestine - the small intestinal microbiota.

The small intestinal microbiota has a crucial role in gastrointestinal health, affecting digestion, immune function, bile acid homeostasis and nutrient metabolism. The challenges of accessibility at this site mean that our knowledge of the small intestinal microbiota is less developed than of the colonic or faecal microbiota. Here, we summarize the features and fluctuations of the microbiota along the small intestinal tract, focusing on humans, and discuss physicochemical factors and assessment methods, including the technical challenges of investigating the low microbial biomass of the proximal small bowel. We highlight the essential protective mechanisms of the small intestine, including motility, the paracellular barrier and mucus, and secretory immunity, to show their roles in limiting excessive exposure of host tissues to microbial metabolites. We address current knowledge gaps, particularly the variability among individuals, the effects of dysbiosis of the small intestinal microbiota on health and how different taxa in small intestinal microbiota could compensate for each other functionally.

Specificity determinants of pathogens in forest

Abstract Host‐specific pathogens have long been suggested to act as a major driver of species diversity in tropical forests. However, determining the degree of host specificity of potential pathogens coupled to key cellular characteristics of infection is difficult and time‐consuming. These challenges have delayed progress in relating the functional specificity of pathogenic fungi to ecological consequences. We tested the pathogenicity of 27 (of 215) fungi that were isolated from surface sterilized roots of seedlings from four common tree species in a diverse subtropical forest. Inoculation experiments showed that six fungi exhibited strong pathogenicity on the host seedlings. Five of these only infected their specific hosts (i.e. host‐specific pathogen species). Green fluorescent protein labelling revealed that in three host‐specific pathogens fungal hyphae were able to grow into the vascular tissues only in their specific host plant, in contrast to other fungal‐host combinations that exhibit non‐pathogenic interactions. This fluorescent labelling technique allows direct tracking of the progress of fungal infection in different host tissues. Synthesis. By coupling the green fluorescent protein technique with standard host inoculation experiments, we determined the developmental differences between infections by pathogenic and non‐pathogenic fungi in a relatively simple and straightforward way. Our work provides a useful tool for rapidly screening and categorizing host–fungal interactions, reflecting the functional basis of host specificity of pathogenic fungi. More broadly, this technique can contribute to understanding the roles of pathogens in species coexistence and biodiversity maintenance in forest communities.

Biothermodynamic analysis of the Dengue virus: Empirical formulas, biosynthesis reactions and thermodynamic properties of antigen-receptor binding and biosynthesis

After the experience with the COVID-19 pandemic, WHO has issued a warning about the possible causes of future pandemics. One such causative agent is the Dengue virus. Until now, we have had information mostly on biological properties of the Dengue virus and very little information about its chemical and thermodynamic properties. To be better prepared for a potential Dengue pandemic, the goal of this paper is to chemically and thermodynamically characterize the Dengue virus, as well as to describe the biophysical basis of the virus-host interactions of the Dengue virus. To that goal, the empirical formula was determined, as well as biosynthesis reactions and thermodynamic properties of antigen-receptor binding and thermodynamic properties of biosynthesis and multiplication of the Dengue virus. A model was developed of virus-host interactions between the Dengue virus and its host tissues, based on nonequilibrium thermodynamics.

Geophysics-Inspired Nonlinear Stress-Strain Law for Biological Tissues and Its Applications in Compression Optical Coherence Elastography.

We propose a nonlinear stress-strain law to describe nonlinear elastic properties of biological tissues using an analogy with the derivation of nonlinear constitutive laws for cracked rocks. The derivation of such a constitutive equation has been stimulated by the recently developed experimental technique-quasistatic Compression Optical Coherence Elastography (C-OCE). C-OCE enables obtaining nonlinear stress-strain dependences relating the applied uniaxial compressive stress and the axial component of the resultant strain in the tissue. To adequately describe nonlinear stress-strain dependences obtained with C-OCE for various tissues, the central idea is that, by analogy with geophysics, nonlinear elastic response of tissues is mostly determined by the histologically confirmed presence of interstitial gaps/pores resembling cracks in rocks. For the latter, the nonlinear elastic response is mostly determined by elastic properties of narrow cracks that are highly compliant and can easily be closed by applied compressing stress. The smaller the aspect ratio of such a gap/crack, the smaller the stress required to close it. Upon reaching sufficiently high compressive stress, almost all such gaps become closed, so that with further increase in the compressive stress, the elastic response of the tissue becomes nearly linear and is determined by the Young's modulus of the host tissue. The form of such a nonlinear dependence is determined by the distribution of the cracks/gaps over closing pressures; for describing this process, an analogy with geophysics is also used. After presenting the derivation of the proposed nonlinear law, we demonstrate that it enables surprisingly good fitting of experimental stress-strain curves obtained with C-OCE for a broad range of various tissues. Unlike empirical fitting, each of the fitting parameters in the proposed law has a clear physical meaning. The linear and nonlinear elastic parameters extracted using this law have already demonstrated high diagnostic value, e.g., for differentiating various types of cancerous and noncancerous tissues.

Differential transcriptomic host responses in the early phase of viral and bacterial infections in human lung tissue explants ex vivo

BackgroundThe first 24 h of infection represent a critical time window in interactions between pathogens and host tissue. However, it is not possible to study such early events in human lung during natural infection due to lack of clinical access to tissue this early in infection. We, therefore, applied RNA sequencing to ex vivo cultured human lung tissue explants (HLTE) from patients with emphysema to study global changes in small noncoding RNA, mRNA, and long noncoding RNA (lncRNA, lincRNA) populations during the first 24 h of infection with influenza A virus (IAV), Mycobacterium bovis Bacille Calmette-Guerin (BCG), and Pseudomonas aeruginosa.ResultsPseudomonas aeruginosa caused the strongest expression changes and was the only pathogen that notably affected expression of microRNA and PIWI-associated RNA. The major classes of long RNAs (> 100 nt) were represented similarly among the RNAs that were differentially expressed upon infection with the three pathogens (mRNA 77–82%; lncRNA 15–17%; pseudogenes 4–5%), but lnc-DDX60-1, RP11-202G18.1, and lnc-THOC3-2 were part of an RNA signature (additionally containing SNX10 and SLC8A1) specifically associated with IAV infection. IAV infection induced brisk interferon responses, CCL8 being the most strongly upregulated mRNA. Single-cell RNA sequencing identified airway epithelial cells and macrophages as the predominant IAV host cells, but inflammatory responses were also detected in cell types expressing few or no IAV transcripts. Combined analysis of bulk and single-cell RNAseq data identified a set of 6 mRNAs (IFI6, IFI44L, IRF7, ISG15, MX1, MX2) as the core transcriptomic response to IAV infection. The two bacterial pathogens induced qualitatively very similar changes in mRNA expression and predicted signaling pathways, but the magnitude of change was greater in P. aeruginosa infection. Upregulation of GJB2, VNN1, DUSP4, SerpinB7, and IL10, and downregulation of PKMYT1, S100A4, GGTA1P, and SLC22A31 were most strongly associated with bacterial infection.ConclusionsHuman lung tissue mounted substantially different transcriptomic responses to infection by IAV than by BCG and P. aeruginosa, whereas responses to these two divergent bacterial pathogens were surprisingly similar. This HLTE model should prove useful for RNA-directed pathogenesis research and tissue biomarker discovery during the early phase of infections, both at the tissue and single-cell level.

Unveiling the impact of Leptospira TolC efflux protein on host tissue adherence, complement evasion, and diagnostic potential.

The TolC family protein of Leptospira is a type I outer membrane efflux protein. Phylogenetic analysis revealed significant sequence conservation among pathogenic Leptospira species (83%-98% identity) compared with intermediate and saprophytic species. Structural modeling indicated a composition of six β-strands and 10 α-helices arranged in two repeats, resembling bacterial outer membrane efflux proteins. Recombinant TolC (rTolC), expressed in a heterologous host and purified via Ni-NTA chromatography, maintained its secondary structural integrity, as verified by circular dichroism spectroscopy. Polyclonal antibodies against rTolC detected native TolC expression in pathogenic Leptospira but not in nonpathogenic ones. Immunoassays and detergent fractionation assays indicated surface localization of TolC. The rTolC's recognition by sera from leptospirosis-infected hosts across species suggests its utility as a diagnostic marker. Notably, rTolC demonstrated binding affinity for various extracellular matrix components, including collagen and chondroitin sulfate A, as well as plasma proteins such as factor H, C3b, and plasminogen, indicating potential roles in tissue adhesion and immune evasion. Functional assays demonstrated that rTolC-bound FH retained cofactor activity for C3b cleavage, highlighting TolC's role in complement regulation. The rTolC protein inhibited both the alternative and the classical pathway-mediated membrane attack complex (MAC) deposition in vitro. Blocking surface-expressed TolC on leptospires using specific antibodies reduced FH acquisition by Leptospira and increased MAC deposition on the spirochete. These findings indicate that TolC contributes to leptospiral virulence by promoting host tissue colonization and evading the immune response, presenting it as a potential target for diagnostic and therapeutic strategies.

Differential requirement of formyl peptide receptor 1 in macrophages and neutrophils in the host defense against Mycobacterium tuberculosis Infection

Formyl peptide receptors (FPR), part of the G-protein coupled receptor superfamily, are pivotal in directing phagocyte migration towards chemotactic signals from bacteria and host tissues. Although their roles in acute bacterial infections are well-documented, their involvement in immunity against tuberculosis (TB) remains unexplored. Here, we investigate the functions of Fpr1 and Fpr2 in defense against Mycobacterium tuberculosis (Mtb), the causative agent of TB. Elevated levels of Fpr1 and Fpr2 were found in the lungs of mice, rabbits and peripheral blood of humans infected with Mtb, suggesting a crucial role in the immune response. The effects of Fpr1 and Fpr2 deletion on bacterial load, lung damage, and cellular inflammation were assessed in a murine TB model utilizing hypervirulent strain of Mtb from the W-Beijing lineage. While Fpr2 deletion had no impact on disease outcome, Fpr1-deficient mice demonstrated improved bacterial control, especially by macrophages. Bone marrow-derived macrophages from these Fpr1−/− mice exhibited an enhanced ability to contain bacterial growth over time. Contrarily, treating genetically susceptible mice with Fpr1-specific inhibitors caused impaired early bacterial control, corresponding with increased Mtb persistence in necrotic neutrophils. Furthermore, ex vivo assays revealed that Fpr1−/− neutrophils were unable to restrain Mtb growth, indicating a differential function of Fpr1 among myeloid cells. These findings highlight the distinct and complex roles of Fpr1 in myeloid cell-mediated immunity against Mtb infection, underscoring the need for further research into these mechanisms for a better understanding of TB immunity.

Magnetically Driven Hydrogel Surfaces for Modulating Macrophage Behavior.

During the host response toward implanted biomaterials, macrophages can shift phenotypes rapidly upon changes in their microenvironment within the host tissue. Exploration of this phenomenon can benefit significantly from the development of adequate tools. Creating cell microenvironment alterations on classical hydrogel substrates presents challenges, particularly when integrating them with cell cultivation and monitoring processes. However, having the capability to dynamically manipulate the cell microenvironment on biomaterial surfaces holds significant potential. We introduce magnetically actuated hydrogels (MadSurface) tailored to induce reversible stiffness changes on polyacrylamide hydrogel substrates with embedded magnetic microparticles in a time-controllable manner. Our investigation focused on exploring the potential of magnetic fields and MadSurfaces in dynamically modulating macrophage behavior in a programmable manner. We achieved a consistent modulation by subjecting the MadSurface to a pulsed magnetic field with a frequency of 0.1 Hz and a magnetic field flux density of 50 mT and analyzed exposed cells using flow cytometry and ELISA. At the single-cell level, we identified a subpopulation for which the dynamic stiffness conditions in conjunction with the pulsed magnetic field increased the expression of CD206 in M1-activated THP-1 cells, indicating a consistent shift toward the M2 anti-inflammatory phenotype on MadSurface. At the population level, this effect was mostly hindered in the culture period utilized in this work. The MadSurface approach advances our understanding of the interplay between magnetic field, cell microenvironment alterations, and macrophage behavior.

Self-Assembly Behavior of Collagen and Its Composite Materials: Preparation, Characterizations, and Biomedical Engineering and Allied Applications.

Collagen is the oldest and most abundant extracellular matrix protein and has many applications in biomedical, food, cosmetic, and other industries. Previous reviews have already introduced collagen's sources, structures, and biosynthesis. The biological and mechanical properties of collagen-based composite materials, their modification and application forms, and their interactions with host tissues are pinpointed. It is worth noting that self-assembly behavior is the main characteristic of collagen molecules. However, there is currently relatively little review on collagen-based composite materials based on self-assembly. Herein, we briefly reviewed the biosynthesis, extraction, structure, and properties of collagen, systematically presented an overview of the various factors and corresponding characterization techniques that affect the collagen self-assembly process, and summarize and discuss the preparation methods and application progress of collagen-based composite materials in different fields. By combining the self-assembly behavior of collagen with preparation methods of collagen-based composite materials, collagen-based composite materials with various functional reactions can be selectively prepared, and these experiences and outcomes can provide inspiration and practical techniques for the future development directions and challenges of collagen-based composite biomaterials in related applications fields.

Comparative In Vivo Biocompatibility of Cellulose-Derived and Synthetic Meshes in Subcutaneous Transplantation Models.

Despite the increasing interest in cellulose-derived materials in biomedical research, there remains a significant gap in comprehensive in vivo analyses of cellulosic materials obtained from various sources and processing methods. To explore durable alternatives to synthetic medical meshes, we evaluated the in vivo biocompatibility of bacterial nanocellulose, regenerated cellulose, and cellulose nanofibrils in a subcutaneous transplantation model, alongside incumbent polypropylene and polydioxanone. Notably, this study demonstrates the in vivo biocompatibility of regenerated cellulose obtained through alkali dissolution and subsequent regeneration. All cellulose-derived implants triggered the expected foreign body response in the host tissue, characterized predominantly by macrophages and foreign body giant cells. Porous materials promoted cell ingrowth and biointegration. Our results highlight the potential of bacterial nanocellulose and regenerated cellulose as safe alternatives to commercial polypropylene meshes. However, the in vivo fragmentation observed for cellulose nanofibril meshes suggests the need for measures to optimize their processing and preparation.

Senescent cell transplantation into the skin induces age-related peripheral dysfunction and cognitive decline.

Cellular senescence is an established cause of cell and tissue aging. Senescent cells have been shown to increase in multiple organs during aging, including the skin. Here we hypothesized that senescent cells residing in the skin can spread senescence to distant organs, thereby accelerating systemic aging processes. To explore this hypothesis, we initially observed an increase in several markers of senescence in the skin of aging mice. Subsequently, we conducted experiments wherein senescent fibroblasts were transplanted into the dermis of young mice and assessed various age-associated parameters. Our findings reveal that the presence of senescent cells in the dermal layer of young mice leads to increased senescence in both proximal and distal host tissues, alongside increased frailty, and impaired musculoskeletal function. Additionally, there was a significant decline in cognitive function, concomitant with increased expression of senescence-associated markers within the hippocampus brain area. These results support the concept that the accumulation of senescent cells in the skin can exert remote effects on other organs including the brain, potentially explaining links between skin and brain disorders and diseases and, contributing to physical and cognitive decline associated with aging.