SEARCH · PubMed Health

Results for “Host Microbial Interactions”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 397 records · Page 22Linked to original sources

PubMed1995

Isolation and characterization of fibronectin-binding sites of Borrelia garinii N34.

Adherence of bacteria to host cell membranes is one of the initial steps of microbial pathogenicity. Numerous studies have suggested that fibronectin promotes this interaction in some bacterial species. In this study, we have examined the ability of Borrelia garinii to bind fibronectin. The binding of fibronectin to the spirochete was specific and saturable. Scatchard plot analysis of the binding data revealed two types of ligands on the spirochetal surface, one with high affinity and one with low affinity for fibronectin. The fibronectin-binding sites were solubilized from the surface of B. garinii N34 by lysozyme treatment. Fast protein liquid chromatography (FPLC) purification of the solubilized binding sites resulted in one band with a high fibronectin-binding activity and a molecular weight of ca. 147,000. FPLC-purified binding sites, fibronectin, and antibodies to fibronectin inhibited the adherence of the spirochete to epithelial cells competitively. These data provide strong support for the hypothesis that fibronectin-binding sites on the surface of B. garinii are involved in the adherence of the spirochete to their respective host cells.

Bacterial Adhesion↗

PubMed1997

Role of oxidants in microbial pathophysiology.

Reactive oxidant species (superoxide, hydrogen peroxide, hydroxyl radical, hypohalous acid, and nitric oxide) are involved in many of the complex interactions between the invading microorganism and its host. Regardless of the source of these compounds or whether they are produced under normal conditions or those of oxidative stress, these oxidants exhibit a broad range of toxic effects to biomolecules that are essential for cell survival. Production of these oxidants by microorganisms enables them to have a survival advantage in their environment. Host oxidant production, especially by phagocytes, is a counteractive mechanism aimed at microbial killing. However, this mechanism may be contribute to a deleterious consequence of oxidant exposure, i.e., inflammatory tissue injury. Both the host and the microorganism have evolved complex adaptive mechanisms to deflect oxidant-mediated damage, including enzymatic and nonenzymatic oxidant-scavenging systems. This review discusses the formation of reactive oxidant species in vivo and how they mediate many of the processes involved in the complex interplay between microbial invasion and host defense.

Animals↗

PubMed1996

Effects of ozone upon macrophage-interferon interactions.

Lung cell populations may be directly exposed to environmental airbone toxicants such as ozone (O3). Since pulmonary macrophages (M phi) play a pivotal role in host pulmonary immunocompetence, their function in this regard may be compromised by pollutant exposure thereby giving rise to an increased incidence of pulmonary disease. The current in vitro study was designed to provide some insight into possible mechanisms by which O3 induces decreased host pulmonary resistance against microbial pathogens. Specifically, this study investigated the impact of an acute O3 exposure upon the ability of a cultured mouse M phi cell line (WEHI-3) to interact with, and respond to, the major M phi-activating cytokine, interferon-gamma (IFN gamma). The results of this study indicate that WEHI-3 exposure to 1 ppm O3 for 4 h reduced both the binding of, and responsivity to, IFN gamma. Among the functional parameters affected by this inability to properly bind/respond to IFN gamma were: reactive oxygen intermediate production, phagocytic activity, and cellular calcium ion elevation; IFN gamma-enhanced expression of surface histocompatibility antigens was unaffected by O3 exposure. The reduced activity of any one of these critical M phi functions could provide a basis for previously-documented increases in microbial pathogen survival in the lungs, and overall compromise of host health following O3 exposure.

Animals↗

PubMed2025

In silico encounters: harnessing metabolic modelling to understand plant-microbe interactions.

Understanding plant-microbe interactions is vital for developing sustainable agricultural practices and mitigating the consequences of climate change on food security. Plant-microbe interactions can improve nutrient acquisition, reduce dependency on chemical fertilizers, affect plant health, growth, and yield, and impact plants' resistance to biotic and abiotic stresses. These interactions are largely driven by metabolic exchanges and can thus be understood through metabolic network modelling. Recent developments in genomics, metagenomics, phenotyping, and synthetic biology now enable researchers to harness the potential of metabolic modelling at the genome scale. Here, we review studies that utilize genome-scale metabolic modelling to study plant-microbe interactions in symbiotic, pathogenic, and microbial community systems. This review catalogues how metabolic modelling has advanced our understanding of the plant host and its associated microorganisms as a holobiont. We showcase how these models can contextualize heterogeneous datasets and serve as valuable tools to dissect and quantify underlying mechanisms. Finally, we consider studies that employ metabolic models as a testbed for in silico design of synthetic microbial communities with predefined traits. We conclude by discussing broader implications of the presented studies, future perspectives, and outstanding challenges.

Plants↗

PubMed2003

Identification of a Treponema pallidum laminin-binding protein.

Host extracellular matrix (ECM) components represent ideal microbial adhesion targets that many pathogens use for colonization of tissues and initiation of infection. This study investigated the interaction of the spirochete Treponema pallidum with the ECM component laminin. To identify candidate laminin-binding adhesins, the T. pallidum genome was analyzed to predict open reading frames that encode putative outer membrane proteins, as these proteins interact directly with host ECM components. Subsequent recombinant expression of these proteins and analysis of their laminin-binding potential identified one protein, Tp0751, that demonstrated specific attachment to laminin. Tp0751 attached to laminin in a dose-dependent, saturable manner but did not attach to the ECM component collagen type I or IV or to the negative control proteins fetuin or bovine serum albumin. Sodium metaperiodate treatment of laminin reduced the Tp0751-laminin interaction in a concentration-dependent manner, suggesting that oligosaccharides play a role in this interaction. In addition, Tp0751-specific antibodies were detected in serum samples collected from both experimental and natural syphilis infections, indicating that Tp0751 is expressed in vivo during the course of infection. Collectively, these experiments identified Tp0751 as a laminin-binding protein that is expressed during infection and may be involved in attachment of T. pallidum to host tissues.

Adhesins, Bacterial↗

PubMed2005

A lack of predatory interaction between rumen ciliate protozoa and Shiga-toxin producing Escherichia coli.

AIMS: To investigate interactions between rumen protozoa and Shiga toxin-producing Escherichia coli (STEC) and to ascertain whether it is likely that rumen protozoa act as ruminant hosts for STEC. METHODS AND RESULTS: The presence of stx genes in different microbial fractions recovered from cattle and sheep rumen contents and faeces was examined using PCR. In animals shedding faecal STEC, stx genes were not detected in the rumen bacterial or rumen protozoal fractions. Direct interactions between ruminal protozoa and STEC were investigated by in vitro co-incubation. Rumen protozoa did not appear to ingest STEC, a STEC lysogen or non-STEC E. coli populations when co-incubated. CONCLUSIONS: The ruminal environment is unlikely to be a preferred habitat for STEC. Bacterial grazing by rumen protozoa appears to have little, if any, effect on STEC populations. SIGNIFICANCE AND IMPACT OF THE STUDY: This study indicates that ruminal protozoa are unlikely to be a major factor in the survival of STEC in ruminants. They appear as neither a host that protects STEC from the ruminal environment nor a predator that might reduce STEC numbers.

Animals↗

PubMed2005

Innate immune responses to infection.

The human host survives many infectious challenges in the absence of preexisting specific (adaptive) immunity because of the existence of a separate set of protective mechanisms that do not depend on specific antigenic recognition. These antigen-independent mechanisms constitute innate immunity. Antimicrobial peptides are released at epithelial surfaces and disrupt the membranes of many microbial pathogens. Toll-like receptors on epithelial cells and leukocytes recognize a range of microbial molecular patterns and generate intracellular signals for activation of a range of host responses. Cytokines released from leukocytes and other cells exhibit a vast array of regulatory functions in both adaptive and innate immunity. Chemokines released from infected tissues recruit diverse populations of leukocytes that express distinct chemokine receptors. Natural killer cells recognize and bind virus-infected host cells and tumor cells and induce their apoptosis. Complement, through the alternative and mannose-binding lectin pathways, mediates antibody-independent opsonization, phagocyte recruitment, and microbial lysis. Phagocytes migrate from the microcirculation into infected tissue and ingest and kill invading microbes. These innate immune mechanisms and their interactions in defense against infection provide the host with the time needed to mobilize the more slowly developing mechanisms of adaptive immunity, which might protect against subsequent challenges.

Animals↗

PubMed2026

Functional analysis of Candida albicans protein kinases identifies Crk1 as a modulator of epithelial cell damage.

UNLABELLED: The commensal and pathogenic lifestyles of the opportunistic fungal pathogen Candida albicans require complex signaling networks regulated by protein kinases. To investigate the role of C. albicans protein kinases at the intestinal epithelial interface, we screened a comprehensive protein kinase deletion library for the capacity of the mutants to damage intestinal epithelial cells (IEC). Mutants showing altered IEC cytotoxicity relative to the wild type were further analyzed for their growth and morphology, focusing on hyper-damaging strains to identify kinases that rather prevent host cell damage. Deletion of CRK1 caused increased IEC-specific damage, despite slower growth, reduced hyphal length, and reduced adhesion as compared to wild-type cells. While tissue invasion levels and the formation of transcellular tunnels of the crk1Δ/Δ mutant were increased, the translocation capacity through the IEC barrier was reduced. Transcriptional and metabolic profiling suggested a role for Crk1 in metabolic adaptation to carbon and nitrogen sources, which was validated by showing that high glucose and amino acids are required for crk1Δ/Δ to cause increased IEC damage. Deletion of CRK1 rendered C. albicans more susceptible to cell wall and membrane stressors, but caused higher resistance to a catalase-specific and histidine biosynthesis inhibitor. This phenotypic pattern of medium- and epithelial cell type-specific cytotoxicity displayed by a C. albicans protein kinase mutant suggests that Crk1 regulates processes linked to carbon and amino acid metabolism that are relevant to interactions with intestinal epithelial cells. IMPORTANCE: Microbial signal transduction pathways regulate adaptation to changing environmental conditions and facilitate the success of many microbes during interactions with their hosts. The fungal pathobiont Candida albicans exists as a harmless commensal on mucosal surfaces of most humans but can also cause superficial and invasive infections under certain circumstances. Both lifestyles require complex signaling networks, predominantly regulated by protein kinases. The C. albicans genome was predicted to encode 108 protein kinases, yet nearly 50% remain uncharacterized. We aimed to dissect the role of C. albicans protein kinases during the transition from commensal to pathogen. We showed that multiple protein kinase genes are involved in epithelial cell damage. Particularly, the protein kinase gene Crk1 was of interest because deletion of CRK1 caused increased damage to intestinal epithelial cells under distinct conditions. Our study links Crk1 with regulation of metabolic processes relevant for commensalism and pathogenicity of C. albicans.

Candida albicans↗

PubMed2025

Synthetic community Hi-C benchmarking provides a baseline for virus-host inferences.

Microbiomes influence diverse ecosystems, and viruses increasingly appear to impose key constraints. While viromics has expanded genomic catalogs, host identification for these viruses remains challenging due to the limitations in scaling cultivation-based approaches and the uncertain reliability and relative low resolution of in silico predictions - particularly for understudied viral taxa. Towards this, Hi-C proximity ligation uses sequenced, cross-linked virus and host genomic fragments to infer virus-host linkages and has now been applied in at least ten studies. However, its accuracy remains unknown. Here we assess Hi-C performance in recovering virus-host interactions using synthetic communities (SynComs) composed of four marine bacterial strains and nine phages with known interactions and then apply optimized bioinformatic protocols to natural soil samples. In SynComs, standard Hi-C sample preparations and analyses showed poor normalized contact score performance (26% specificity, 100% sensitivity, incorrect matches up to class level) that could be dramatically improved by Z-score filtering (Z ≥ 0.5, 99% specificity), though at reduced sensitivity (62% down from 100%). Detection limits were established as reproducibility was poor below minimal phage abundances of 105 PFU/mL. Applying optimized bioinformatic protocols to natural soil samples, we compared virus-host linkages inferred from proximity-ligated Hi-C sequencing with predictions generated by in silico homology-based and machine learning-based bioinformatic approaches. Prior to Z-score thresholding, agreement was relatively high at the phylum to family levels (72%), but not at the genus (43%) or species (15%) levels. Z-score thresholding reduced sensitivity (only 34% of predictions were retained), with only modest improvements in congruence with bioinformatic methods (48% or 18% at genus or species levels, respectively). Regardless, this led to 79 genus-level-congruent virus-host linkages and 293 new ones revealed by Hi-C alone - i.e., providing many new virus-host interactions to explore in already well-studied climate-critical soils. Overall, these findings provide empirical benchmarks and methodological guidelines to improve the accuracy and reliability of Hi-C for virus-host linkage studies in complex microbial communities.

Genomics↗

PubMed2006

A reappraisal of humoral immunity based on mechanisms of antibody-mediated protection against intracellular pathogens.

Sometime in the mid to late twentieth century the study of antibody-mediated immunity (AMI) entered the doldrums, as many immunologists believed that the function of AMI was well understood, and was no longer deserving of intensive investigation. However, beginning in the 1990s studies using monoclonal antibodies (mAbs) revealed new functions for antibodies, including direct antimicrobial effects and their ability to modify host inflammatory and cellular responses. Furthermore, the demonstration that mAbs to several intracellular bacterial and fungal pathogens were protective issued a serious challenge to the paradigm that host defense against such microbes was strictly governed by cell-mediated immunity (CMI). Hence, a new view of AMI is emerging. This view is based on the concept that a major function of antibody (Ab) is to amplify or subdue the inflammatory response to a microbe. In this regard, the "damage-response framework" of microbial pathogenesis provides a new conceptual viewpoint for understanding mechanisms of AMI. According to this view, the ability of an Ab to affect the outcome of a host-microbe interaction is a function of its capacity to modify the damage ensuing from such an interaction. In fact, it is increasingly apparent that the efficacy of an Ab cannot be defined either by immunoglobulin or epitope characteristics alone, but rather by a complex function of Ab variables, such as specificity, isotype, and amount, host variables, such as genetic background and immune status, and microbial variables, such as inoculum, mechanisms of avoiding host immune surveillance and pathogenic strategy. Consequently, far from being understood, recent findings in AMI imply a system with unfathomable complexity and the field is poised for a long overdue renaissance.

Animals↗

PubMed2006

Microbial ecology of drinking water distribution systems.

The supply of clean drinking water is a major, and relatively recent, public health milestone. Control of microbial growth in drinking water distribution systems, often achieved through the addition of disinfectants, is essential to limiting waterborne illness, particularly in immunocompromised subpopulations. Recent inquiries into the microbial ecology of distribution systems have found that pathogen resistance to chlorination is affected by microbial community diversity and interspecies relationships. Research indicates that multispecies biofilms are generally more resistant to disinfection than single-species biofilms. Other recent findings are the increased survival of the bacterial pathogen Legionella pneumophila when present inside its protozoan host Hartmannella vermiformis and the depletion of chloramine disinfectant residuals by nitrifying bacteria, leading to increased overall microbial growth. Interactions such as these are unaccounted for in current disinfection models. An understanding of the microbial ecology of distribution systems is necessary to design innovative and effective control strategies that will ensure safe and high-quality drinking water.

Animals↗

PubMed2000

Mechanisms of attachment and internalization of Cryptosporidium parvum to biliary and intestinal epithelial cells.

BACKGROUND & AIMS: Although infection of the intestinal and biliary tracts by Cryptosporidium parvum is a major problem in patients with the acquired immunodeficiency syndrome, the specific microbial and host molecules involved in C. parvum infection are unknown. We tested the hypothesis that lectin-carbohydrate interactions and cytoskeleton reorganization are involved in the infection of biliary and intestinal epithelia by C. parvum. METHODS: In vitro models of cryptosporidial infection using human biliary and intestinal epithelial cell lines were used to assay C. parvum attachment and invasion. RESULTS: Exposure of C. parvum sporozoites to the sugar, galactose-N-acetylgalactosamine (Gal/GalNAc), and to bovine mucin reduced C. parvum attachment to biliary and intestinal epithelia up to 70%. Preincubation of cell monolayers with either lectins specific to Gal/GalNAc, or glycosidases that specifically release Gal/GalNAc oligosaccharides from glycoproteins, decreased attachment up to 80%. Cytochalasin B and cytochalasin D, but not nocodazole, decreased invasion of cells by C. parvum up to 70% without affecting attachment. During cell invasion (but not attachment), confocal microscopy showed recruitment of actin (but not tubulin) in biliary and intestinal epithelia directly adjacent to C. parvum. CONCLUSIONS: Gal/GalNAc epitopes of glycoproteins on the epithelial apical membrane and Gal/GalNAc-specific sporozoite surface lectins are involved in the mechanism(s) of C. parvum attachment to intestinal and biliary epithelial cells, and actin remodeling in host cells is required for C. parvum invasion.

Animals↗

PubMed2006

Improvement of bioprocess monitoring: development of novel concepts.

The advancement of bioprocess monitoring will play a crucial role to meet the future requirements of bioprocess technology. Major issues are the acceleration of process development to reduce the time to the market and to ensure optimal exploitation of the cell factory and further to cope with the requirements of the Process Analytical Technology initiative. Due to the enormous complexity of cellular systems and lack of appropriate sensor systems microbial production processes are still poorly understood. This holds generally true for the most microbial production processes, in particular for the recombinant protein production due to strong interaction between recombinant gene expression and host cell metabolism. Therefore, it is necessary to scrutinise the role of the different cellular compartments in the biosynthesis process in order to develop comprehensive process monitoring concepts by involving the most significant process variables and their interconnections. Although research for the development of novel sensor systems is progressing their applicability in bioprocessing is very limited with respect to on-line and in-situ measurement due to specific requirements of aseptic conditions, high number of analytes, drift, and often rather low physiological relevance. A comprehensive survey of the state of the art of bioprocess monitoring reveals that only a limited number of metabolic variables show a close correlation to the currently explored chemical/physical principles. In order to circumvent this unsatisfying situation mathematical methods are applied to uncover "hidden" information contained in the on-line data and thereby creating correlations to the multitude of highly specific biochemical off-line data. Modelling enables the continuous prediction of otherwise discrete off-line data whereby critical process states can be more easily detected. The challenging issue of this concept is to establish significant on-line and off-line data sets. In this context, online sensor systems are reviewed with respect to commercial availability in combination with the suitability of offline analytical measurement methods. In a case study, the aptitude of the concept to exploit easily available online data for prediction of complex process variables in a recombinant E. coli fed-batch cultivation aiming at the improvement of monitoring capabilities is demonstrated. In addition, the perspectives for model-based process supervision and process control are outlined.

Journal Article↗

PubMedDate not supplied

[Characteristics of the immune response in protozoan infections].

INTRODUCTION: When protozoa enter the blood stream or tissues they can often survive and replicate because they adapt to the resisting natural host defenses. The interaction of immune system with infectious organisms is a dynamic interplay of host mechanisms aimed at eliminating infections and microbial strategies designed to permit survival in the face of powerful effector mechanisms. Protozoa cause chronic and persistent infections, because natural immunity against them is weak and because protozoa have evolved multiple mechanisms for evading and resisting specific immunity. NATURAL AND SPECIFIC IMMUNE RESPONSE TO PROTOZOA: Different protozoa vary greatly in their structural and biochemical properties and stimulate distinct patterns of immune responses and have evolved unique mechanisms for evading specific immunity. Protozoa activate quite distinct specific immune responses, which are different from the responses to fungi, bacteria and viruses. Protozoa may be phagocytozed by macrophages, but many are resistant to phagocytic killing and may even replicate within macrophages. T. brucei gambiense is the best example of protozoa which can induce humoral immune response because of its extra-cellular location. In Leishmania sp. infections, cellular defense mechanisms depend upon CD4+ T-lymphocytes and activate macrophages as effector cells that are regulated by cytokines of Th1 subset. Plasmodium sp. is a protozoa which show the diversity of defence mechanisms which can be cellular or humoral, depending on Ag and protozoa's location. IMMUNE EVASION MECHANISMS OF PROTOZOA: Different protozoa have developed remarkably effective ways of resisting specific immunity: a) anatomic sequestration is commonly observed with protozoa Plasmodium and T. gondii; b) some protozoa can become resistant to immune effector mechanisms: Trypanosoma, Leishmania and T. gondii; c) some protozoa have developed effective mechanisms for varying their surface antigens: Plasmodium and Trypanosoma; d) some protozoa shed their antigen coats, either spontaneously or after binding with specific antibodies: E. histolytica; e) some protozoa alter host immune response by nonspecific and generalized immunosuppression (abnormalities in cytokine production, deficient T cell activation): Trypanosoma, Leishmania, Toxoplasma, Entamoeba. CONCLUSION: Protozoa activate numerous, different immune mechanisms in human body. Evolution, progression and outcome of diseases depend upon these mechanisms. Resent progresses in research have defined and selected Ag as candidates for new vaccines. Better definitions regarding the role of cytokines in protozoan infections will facilitate rational development of cytokines and cytokine antagonists and their use as immunotherapeutic agents.

Animals↗

PubMed2005

Conserved virulence factors of Pseudomonas aeruginosa are required for killing Bacillus subtilis.

The multi-host pathogen, Pseudomonas aeruginosa, possesses an extraordinary versatility which makes it capable of surviving the adverse conditions provided by environmental, host, and, presumably, competing microbial factors in its natural habitats. Here, we investigated the P. aeruginosa-Bacillus subtilis interaction in laboratory conditions and found that some P. aeruginosa strains can outcompete B. subtilis in mixed planktonic cultures. This is accompanied by the loss of B. subtilis viability. The bactericidal activity of P. aeruginosa is measured on B. subtilis plate cultures. The bactericidal activity is attenuated in pqsA, mvfR, lasR, pilB, gacA, dsbA, rpoS, and phnAB mutants. These results suggest that P. aeruginosa utilizes a subset of conserved virulence pathways in order to survive the conditions provided by its bacterial neighbors.

Antibiosis↗

PubMed2001

Molecular analysis of commensal host-microbial relationships in the intestine.

Human beings contain complex societies of indigenous microbes, yet little is known about how resident bacteria shape our physiology. We colonized germ-free mice with Bacteroides thetaiotaomicron, a prominent component of the normal mouse and human intestinal microflora. Global intestinal transcriptional responses to colonization were observed with DNA microarrays, and the cellular origins of selected responses were established by laser-capture microdissection. The results reveal that this commensal bacterium modulates expression of genes involved in several important intestinal functions, including nutrient absorption, mucosal barrier fortification, xenobiotic metabolism, angiogenesis, and postnatal intestinal maturation. These findings provide perspectives about the essential nature of the interactions between resident microorganisms and their hosts.

Animals↗

PubMed2026

Symbiotic interactions and climate change implications of the octocoral microbiome.

Octocorals are vital components of tropical, temperate, and cold-water benthic marine ecosystems. Their associated microbiomes, comprising microeukaryotes, prokaryotes, and viruses, are increasingly recognised as central to host health, nutrient cycling, and chemical defence. Metagenomics and amplicon sequencing have uncovered taxonomic and functional complexity within these microbial communities, revealing patterns of host specificity and health status, along with seasonality and geographic structuring. However, anthropogenic stressors, particularly those associated with global climate change, exert intense pressure on coral-dominated ecosystems, leading to complex and poorly understood local and regional patterns of octocoral expansion and mortality. Microbial interactions may be a main driver of these contrasting outcomes by mediating the ecological resilience of octocorals to environmental stress. We synthesise the current state of research on the diversity, organisation, and function of the octocoral microbiome, and identify critical knowledge gaps on octocoral holobionts relative to scleractinian corals. Our meta-analysis of 79 publicly available bacterial genomes from octocorals reveals group-specific specialisation in denitrification and nitrate assimilation, along with widespread capacities for essential amino acid, cofactor, and vitamin production, suggesting important contributions to nutrient cycling in the holobiont. While sampling efforts between cultured and uncultured lineages are even, our genomic survey reveals strong sampling bias toward the Atlantic Ocean, temperate gorgonians, and healthy host states, whereas bacterial genomes representing the pathobiome, tropical and/or deep-sea regions, and other octocoral taxa remain underrepresented. Accordingly, we propose future research directions to advance understanding of octocoral microbiome ecology and its role in the resilience of tropical, temperate and cold-water coral reefs.

Endozoicomonadaceae↗

PubMed2005

Lactoferrin: an important host defence against microbial and viral attack.

The first function attributed to lactoferrin (Lf), an iron binding protein belonging to the non-immune natural defences, was antimicrobial activity that depended on its capacity to sequester iron. Iron-independent microbicidal activities, requiring direct interaction between this cationic protein and microbial surface components, were later demonstrated. Many other anti-microbial and anti-viral functions have since been ascribed to Lf. In mucosal secretions, iron and Lf modulate the motility and aggregation of pathogenic bacteria. Lf inhibits bacterial adhesion on abiotic surfaces through ionic binding to biomaterials, or specific binding to bacterial structures or both. Lf inhibition of bacterial adhesion to host cells requires Lf binding to bacteria and/or host cells. Lf hinders microbial internalization by binding to both glycosaminoglycans and bacterial proteins which can be degraded by Lf-mediated proteolysis. Moreover, Lf internalisation and localisation to the host cell nuclei could modulate bacterial entry into cells through gene regulation. Finally, the capability of Lf to exert antiviral activity, through its binding to host cells and/or viral particles, strengthens the idea that it is an important brick in the mucosal wall, effective against both microbial and viral attacks.

Animals↗