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PubMed1988

The biology of peritonitis and implications for treatment.

Peritonitis continues to be one of the major infectious problems confronting surgeons. Despite the many advances in antimicrobial agents and supportive care, mortality from diffuse suppurative peritonitis remains unacceptably high. The authors review the anatomy and defense capabilities of the peritoneal cavity and then focus on the polymicrobial nature of peritonitis and how, through microbial interactions with host defenses, there is either resolution or persistent infection. They also consider possible infection-potentiating agents in the peritoneal cavity and experimental modes of therapy.

Abdomen, Acute↗
PubMed2003

Calpain regulates enterocyte brush border actin assembly and pathogenic Escherichia coli-mediated effacement.

This study identifies calpain as being instrumental for brush border (BB) microvillus assembly during differentiation and effacement during bacterial pathogenesis. Calpain activity is decreased by 25-80% in Caco 2 lines stably overexpressing calpastatin, the physiological inhibitor of calpain, and the effect is proportional to the calpastatin/calpain ratio. These lines exhibit a 2.5-fold reduction in the rate of microvillus extension. Apical microvillus assembly is reduced by up to 50%, as measured by quantitative fluorometric microscopy (QFM) of ezrin, indicating that calpain recruits ezrin to BB microvilli. Calpain inhibitors ZLLYCHN2, MDL 28170, and PD 150606 block BB assembly and ezrin recruitment to the BB. The HIV protease inhibitor ritonavir, which inhibits calpain at clinically relevant concentrations, also blocks BB assembly, whereas cathepsin and proteasome inhibitors do not. Microvillus effacement is inhibited after exposure of calpastatin-overexpressing cells to enteropathogenic Escherichia coli. These results suggest that calpain regulates BB assembly as well as pathological effacement, and indicate that it is an important regulator involved in HIV protease inhibitor toxicity and host-microbial pathogen interactions.

Actins↗
PubMed2000

Hepatocyte toll-like receptor 2 expression in vivo and in vitro: role of cytokines in induction of rat TLR2 gene expression by lipopolysaccharide.

We and others have demonstrated previously that cytokines, including interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNFalpha), regulate LPS recognition proteins such as CD14 in the liver and on hepatocytes. Based on recent findings that the mammalian homologue of Drosophila Toll participates in LPS signaling, we examined the regulation of Toll-Like Receptor (TLR) gene expression by cytokines in vitro and its distribution in vivo with a focus on the liver as a site of host-microbe interaction. Our results show that IL-1beta and/or TNFalpha participate in the upregulation of TLR2 mRNA levels in hepatocytes. Rats treated concurrently with LPS and antagonists of the IL-1 or TNFalpha receptor demonstrated significantly reduced LPS-induced hepatic expression of TLR2 compared to animals treated with LPS alone. The increase in hepatic TLR2 mRNA expression was associated with enhanced transcription as determined by nuclear run-on analysis. LPS treatment in vivo caused a marked TLR2 mRNA up-regulation in all of the tissues examined, with liver showing the highest expression. The high level of TLR2 expression in the liver may have important implications for pathogen-host interactions or microbial signaling.

Animals↗
PubMed1996

Cellular events concurrent with Porphyromonas gingivalis invasion of oral epithelium in vitro.

The aim of the present study was to elucidate events related to receptor function, signal transmission and cytoskeletal rearrangements concurrent with Porphyromonas gingivalis invasion of oral epithelial cells in vitro. Porphyromonas gingivalis strain FDC 381 and the KB cell line (ATCC CCL 17) were used in a previously described antibiotic protection assay. The involvement of a receptor-mediated endocytosis pathway in the internalization process was demonstrated after treatment of the epithelial cells with monodansylcadaverine and ouabain, substances that inhibit formation of coated pits, resulting in reduction in the number of invading P. gingivalis: Treatment of the epithelial cells with the protein kinase (PK) inhibitor staurosporine and the tyrosine-specific PK inhibitor genistein was also found to significantly decrease the number of invading bacteria, suggesting involvement of tyrosine phosphorylation in signal transduction during invasion. This was further supported by the identification of a 43 kD protein acting as a substrate for tyrosine phosphorylation subsequent to the microbial-host cell interaction. Tyrosine phosphorylation of the 43 kD protein was strongly reduced by treatment with PK inhibitors. The decrease in invasion observed after treatment of epithelial cells with colchicine and nocodazole, inhibitors of microtubuli polymerization, suggested that the bacterial-receptor interaction and the phosphotyrosine-dependent intracellular signalling trigger an internalization process involving rearrangements of cytoskeletal microtubuli.

Cadaverine↗
PubMed2003

Intestinal microflora in early infancy: composition and development.

The neonatal intestinal microbiota is a complex ecosystem composed of numerous genera, species and strains of bacteria. This enormous cell mass performs a variety of unique activities that affect both the colonic and systemic physiology. Its primary activities include nutritive, metabolic, immunological and protective functions. Most studies of infants have been based on faecal samples using the classical plating techniques with culturing on specific media. The limitations of these methods must be taken into account when evaluating the varying results of the different studies. The establishment of the gut microbial population is not strictly a succession in the ecological sense; it is rather a complex process influenced by microbial and host interactions and by external and internal factors. The climax intestinal flora is attained in successive stages. The foetal intestine is sterile and bathed in swallowed amniotic fluid. Following delivery, multiple different antigens challenge the intestine of the newborn. The maternal intestinal flora is a source of bacteria for the neonatal gut. The bacterial flora is usually heterogeneous during the first few days of life, independently of feeding habits. After the first week of life, a stable bacterial flora is usually established. In full-term infants a diet of breast milk induces the development of a flora rich in Bifidobacterium spp. Other obligate anaerobes, such as Clostridium spp. and Bacteroides spp., are more rarely isolated and also enterobacteria and enterococci are relatively few. During the corresponding period, formula-fed babies are often colonized by other anaerobes in addition to bifidobacteria and by facultatively anaerobic bacteria; the development of a "bifidus flora" is unusual. In other studies the presence of a consistent number of bifidobacteria in infants delivered in large urban hospitals has not been demonstrated, whether the babies were bottle fed or exclusively breastfed. The predominant faecal bacteria were coliforms and bacteroides. According to these studies, environmental factors may be more important than breastfeeding in gut colonization after delivery. Environmental factors are indeed extremely important for the intestinal colonization of infants born by caesarean section. In these infants, the establishment of a stable flora characterized by a low incidence of Bacteroides spp. and by the isolation of few other bacteria is consistently delayed. In extremely low-birthweight infants, hospitalization in neonatal intensive care units, characterized by prolonged antibiotic therapy, parenteral nutrition, delayed oral feedings and intubation seems to affect the composition of the intestinal microbiota. The gut is colonized by a small number of bacterial species; Lactobacillus and Bifidobacteria spp. are seldom, if ever, identified. According to the few studies so far performed, the predominant species are Enterococcus faecalis, E. coli, Enterobacter cloacae, Klebsiella pneumoniae, Staphylococcus epidermidis and Staphylococcus haemolyticus. Hygienic conditions and antimicrobial procedures strongly influence the intestinal colonization pattern.

Anti-Bacterial Agents↗
PubMed2006

The type III pseudomonal exotoxin U activates the c-Jun NH2-terminal kinase pathway and increases human epithelial interleukin-8 production.

Microbial interactions with host cell signaling pathways are key determinants of the host cell response to infection. Many toxins secreted by bacterial type III secretion systems either stimulate or inhibit the host inflammatory response. We investigated the role of type III secreted toxins of the lung pathogen Pseudomonas aeruginosa in the inflammatory response of human respiratory epithelial cells to infection. Using bacteria with specific gene deletions, we found that interleukin-8 production by these cells was almost entirely dependent on bacterial type III secretion of exotoxin U (ExoU), a phospholipase, although other bacterial factors are involved. ExoU activated the c-Jun NH(2)-terminal kinase pathway, stimulating the phosphorylation and activation of mitogen-activated kinase kinase 4, c-Jun NH(2)-terminal kinase, and c-Jun. This in turn increased levels of transcriptionally competent activator protein-1. Although this pathway was dependent on the lipase activity of ExoU, it was independent of cell death. Activation of mitogen-activated kinase signaling by ExoU in this fashion is a novel mechanism by which a bacterial product can initiate a host inflammatory response, and it may result in increased epithelial permeability and bacterial spread.

Epithelial Cells↗
PubMed2026

Conserved protein folds underpin the diversification of secreted proteins in a fungal pathogen.

BACKGROUND: During host colonization, fungal plant pathogens secrete effector-like proteins that alter host cell physiology and target plant-associated microbes. However, rapid evolution and low sequence conservation hinder the study and characterization of these proteins. The fungus Zymoseptoria passerinii infects Hordeum spp. and includes lineages adapted to wild and domesticated barley. To date, the evolution of effector-like proteins in this species has not been addressed. RESULTS: We combined multiple structure-based and network analyses to unravel the secretome of Z. passerinii. We first compared AlphaFold2 and ESMFold predictions to establish the baseline for structural analyses. We identified 72 structural clusters in the secretome, revealing fold-level relationships across divergent sequences. We showed that effector-like proteins with predicted host immune-interfering functions evolved from a limited group of protein folds, whereas proteins with predicted antimicrobial properties were distributed across fold groups. Physicochemical comparisons indicate that putative antimicrobial effectors predominantly emerged through amino acid replacements on common effector-enriched scaffolds in Z. passerinii, reconfiguring surface charge and electrostatics. We analyzed intra- and interspecific variation in selected effector-enriched families by comparing Z. passerinii proteins and homologs across the genus Zymoseptoria. We describe constrained core folds, with local variation in loop and surface-exposed regions, consistent with fold stability while still enabling protein diversification. We further report that putative antimicrobial effector homologs are broadly distributed across the genus despite sequence divergence. CONCLUSIONS: The secretome of Z. passerinii is organized around common structural folds that support diverse biological roles, including host manipulation and host-associated microbial interactions. Conserved scaffolds combined with surface and physicochemical variation likely contribute to rapid adaptive evolution of effector-like proteins in Z. passerinii.

Fungal Proteins↗
PubMed1986

Effects of microbial and host variables on the interaction of rotavirus and Escherichia coli infections in gnotobiotic calves.

Naturally occurring mixed infections with Escherichia coli and rotavirus have been associated with fatal diarrhea of calves about 1 week old. Experiments were designed to reproduce this syndrome in gnotobiotic calves. Clinical, microbiological, and pathologic data were used to assess severity of disease and mechanisms of the interaction between the 2 infections. An initial study involved 5- to 8-day-old gnotobiotic calves inoculated with a strain of enterotoxigenic E coli (ETEC) and a strain of rotavirus. Calves were observed for 2 days after they were inoculated; fatal diarrhea was not produced. In later studies, variables were tested to identify those that might contribute to fatal diarrhea. Variables which did not result in fatal or severe diarrhea or which did not cause disease that was more severe in dually inoculated calves than that in monoinoculated calves were increasing feed to 2 times base line, increasing dose of ETEC to 10 times base line, inoculating calves when they were 2 days old, using a strain of E coli that causes colisepticemia, and using a different strain of rotavirus. When the observation period was extended from 2 days to 6 days after calves were inoculated, severe, watery, fatal diarrhea occurred in 6 of 12 calves by 32 to 72 hours after dual inoculation was given. Fatal diarrhea was associated with intensive colonization by the ETEC in the caudal half of the small intestine. Microscopic lesions were similar between dually inoculated and rotavirus-monoinoculated calves, except there was more severe atrophy of ileal villi of dually inoculated calves.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Microbial/host interactions: mechanisms involved in host responses to microbial antigens.

The indigenous oral microflora and the host are normally in a state of equilibrium; however, the introduction of a pathogen can result in innate and adaptive immune responses that either contribute to the development of the disease or lead to host immunity. The interactions between the microorganisms and the host are very dynamic, thus allowing the complex interplay between host molecules and bacterial antigens. In this article, we focus on the mechanisms involved in the pathogenesis of and host responses to two oral pathogens: the Gram-negative bacterium Porphyromonas gingivalis, implicated in the etiology of periodontal disease, and the Gram-positive Streptococcus mutans, a primary agent involved in dental caries formation. Furthermore, we address mechanisms involved in the ability of select adjuvants and delivery systems to potentiate mucosal and systemic immune responses to microbial vaccine antigens.

Animals↗
PubMed1980

[Interest in gnotoxenic systems for the study of host-microbial flora of the digestive tract].

It is necessary to use experimental models in all studies of interactions between a host, its digestive tract microbial flora and the environment because these interactions are complex. The gnotoxenic animal, reared in an isolator as the axenic animal and harbouring a known microbial flora, constitutes either an analytic or mimetic experimental model. The gnotoxenic animal may be considered as an analytic model when used to determine which biotic or abiotic environmental factor of the host-animal plays a role in the intestinal ecosystem. The potential metabolic or immunologic role of a given bacterial strain in the intestinal ecosystem may be determined when the axenic animal is associated with this strain. The variation of the expression of the potential role of this strain in relation to the environment can be ascertained by diversifying the diet of the host or by introducing other bacterial strains into the intestinal ecosystem. The role of an association of strains in host physiology and host protection against potentially pathogenic target strains can also be studied using this analytic model. An analytic model is created by associating either isolated strains of the holoxenic or heated or diluted suspensions of holoxenic digestive tract flora. Axenic mice associated with these simplified flora are called meroxenic. The gnotoxenic animal is considered to be a mimetic model when it harbours a microbial flora isolated from an animal of a different species. The advantage of the mimetic model is that it provides an easy-to-use biological tool, i.e. gnotoxenic mice, to first determine the potential role of these microbial strains. The validity of the mimetic model is then tested by comparing gnotoxenic mice and gnotoxenic piglets or chickens. When all the gnotoxenic animals are given the same diet, this comparison permits an estimation of the animal-host role in the expression of the potential activities of microbial strains. The mimetic model, composed of gnotoxenic animals harbouring microbial strains of human origin, is the only experimental model which can be used to study the role of microorganisms in the intestinal ecosystem of man.

Animals↗
PubMed2001

Host-pathogen interactions: the attributes of virulence.

Virulence is one of a number of possible outcomes of host-microbe interaction. As such, microbial virulence is dependent on host factors, as exemplified by the pathogenicity of avirulent microbes in immunocompromised hosts and the lack of pathogenicity of virulent pathogens in immune hosts. Pathogen-centered views of virulence assert that pathogens are distinguished from nonpathogens by their expression of virulence factors. Although this concept appears to apply to certain microbes that cause disease in normal hosts, it does not apply to most microbes that cause disease primarily in immunocompromised hosts. The study of virulence is fraught with the paradox that virulence, despite being a microbial characteristic, can only be expressed in a susceptible host. Thus, the question "What is a pathogen?" begs the question, "What is the outcome of the host-microbe interaction?" We propose that host damage provides a common denominator that translates into the different outcomes of host-microbe interaction.

Animals↗
PubMed2000

A fluorescence microscopy based genetic screen to identify mutants altered for interactions with host cells.

The study of microbial intracellular pathogenesis has benefited from the application of immunofluorescence microscopy to characterize interactions of the pathogen with host cells. Unfortunately, immunofluorescence microscopy is impractical for screening the large number of bacterial mutants necessary to represent the entire genome of the pathogen. Screening has been limited due to the lack of materials suitable for high-throughput processing (e.g. 96-well plates) that also possess the optical features needed for high resolution fluorescence microscopy. Recently marketed 96-well Special Optics (SO) plates provide both the 96-well template ideal for high-throughput analysis and optical features suitable for fluorescence microscopy. Until this work, mutants needed for the study of a fluorescence-based virulence phenotype could not be obtained by direct screening approaches. In this study, SO plates were used to examine 11520 individual Salmonella typhimurium MudJ mutants for the loss of the ability to disrupt host cell endocytic compartments. The direct application of the fluorescence phenotype for screening allowed us to obtain a set of mutants to characterize the formation of lysosomal membrane glycoprotein (lgp) containing tubules upon Salmonella infection of HeLa epithelial cells. This approach will facilitate the characterization of a wide range of microbial phenotypes detectable by fluorescence microscopy.

Antigens, CD↗
PubMed2005

Ligand specificity of human surfactant protein D: expression of a mutant trimeric collectin that shows enhanced interactions with influenza A virus.

Surfactant protein D is a pattern recognition molecule that plays diverse roles in immune regulation and anti-microbial host defense. Its interactions with known ligands are calcium-dependent and involve binding to the trimeric, C-type carbohydrate recognition domain. Surfactant protein D preferentially binds to glucose and related sugars. However, CL-43, a bovine serum lectin, which evolved through duplication of the surfactant protein D gene in ruminants, prefers mannose and mannose-rich polysaccharides. Surfactant protein D is characterized by two relatively conserved motifs at the binding face, along the edges of the shallow carbohydrate-binding groove. For CL-43, sequence alignments demonstrate a basic insertion, Arg-Ala-Lys (RAK), immediately N-terminal to the first motif. We hypothesized that this insertion contributes to the differences in saccharide selectivity and host defense function and compared the activities of recombinant trimeric neck + carbohydrate recognition domains of human surfactant protein D (NCRD) with CL-43 (RCL-43-NCRD) and selected NCRD mutants. Insertion of the CL-43 RAK sequence or a control Ala-Ala-Ala sequence (AAA) into the corresponding position in NCRD increased the efficiency of binding to mannan and changed the inhibitory potencies of competing saccharides to more closely resemble those of CL-43. In addition, RAK resembled CL-43 in its greater capacity to inhibit the infectivity of influenza A virus and to increase uptake of influenza by neutrophils.

Amino Acid Sequence↗
PubMed1990

Recent advances in rumen microbial ecology and metabolism: potential impact on nutrient output.

Feedstuffs consumed by ruminants are all initially exposed to fermentative activity in the rumen prior to gastric and intestinal digestion. The extent and type of transformation of feedstuffs thus determines the productive performance of the host. Research on rumen microbial ecology and metabolism is essentially a study of the interactions between the host, microorganisms present, substrates available, and end products of digestion. Furthermore, the interactions of the normal microbial flora with the host can be manipulated to improve the efficiency of nutrient utilization in ruminant animals. Three important areas of ruminal fermentation will be reviewed, N metabolism, fiber degradation, and biotransformation of toxic compounds. The extent of protein degradation and the rate of uptake of resultant peptides and ammonia are extremely important factors in determining the efficiency of N utilization by rumen bacteria and, therefore, the relative amounts of microbial or bypass protein available to the host. Strategies aimed at identifying and characterizing rate-limiting enzymes of cellulolytic bacteria are essential in elucidating mechanisms involved in ruminal fiber degradation. Results obtained with ruminococci will be described. The detoxification of phytotoxins by passage through the gastrointestinal tract of ruminants is a process deserving special attention and several examples will be presented. Opportunities for manipulation of rumen fermentation are good. However, successful manipulation and full exploitation depend on a through understanding of the mechanisms involved.

Animal Feed↗
PubMed2006

Effects of polymicrobial communities on host immunity and response.

Microorganisms grow as members of microbial communities in unique niches, such as the mucosal surfaces of the human body. These microbial communities, containing both commensals and opportunistic pathogens, serve to keep individual pathogens 'in check' through a variety of mechanisms and complex interactions, both between the microorganisms themselves and the microorganisms and the host. Recent studies shed new light on the diversity of microorganisms that form the human microbial communities and the interactions these microbial communities have with the host to stimulate immune responses. This occurs through their recognition by dendritic cells or their ability to induce differential cytokine and defensin profiles. The differential induction of defensins by commensals and pathogens and the ability of the induced defensins to interact with the antigens from these microorganisms may attenuate proinflammatory signaling and trigger adaptive immune responses to microbial antigens in a multistep process. Such an activity may be a mechanism that the host uses to sense what is on its mucosal surfaces, as well as to differentiate among commensals and pathogens.

Bacterial Infections↗
PubMed2002

Neutrophil-mediated host response to Porphyromonas gingivalis.

Periodontal diseases are infections initiated by specific species of microorganisms and are among the most common human infections. The pathogenesis of periodontitis is mediated by interactions between host and microbial factors, complicated by genetic and environmental risk factors. Periodontal disease also represents a unique model in which to study the roles of bacterial and host-related factors, a model in which patients do not suffer from life-threatening disease. The aim of this paper is to focus on recent findings relating to neutrophil-mediated host response mechanisms in Porphyromonas gingivalis-induced periodontal disease. Virulence factors of Porphyromonas gingivalis such as the gingipains, fimbrillin peptides, capsule polysaccharides, lipopolysaccharides, haemagglutinating and haemolysing activities, toxic products of metabolism, outer membrane vesicles, and other enzymes have important roles in eliciting host responses in various ways. These factors significantly affect epithelial/endothelial cells, but their major effect is observed on the modulation of neutrophil response. Periodontitis represents an important model for neutrophil-mediated host tissue injury. In this model, neutrophils, primed or stimulated by the presence or persistence of infection, express an elevated and excessive response. This, in turn, leads to tissue destruction mediated by neutrophil activity. It is essential to understand the mechanisms underlying the interactions between the neutrophils and the microbial virulence factors to be able to develop rational, novel treatment strategies.

Adhesins, Bacterial↗
PubMed2001

Microbes and microbial toxins: paradigms for microbial-mucosal interactions. VI. Entamoeba histolytica: parasite-host interactions.

The protozoan intestinal parasite Entamoeba histolytica remains a significant cause of morbidity and mortality worldwide. E. histolytica causes two major clinical syndromes, amebic colitis and amebic liver abscess. Recent advances in the development of in vitro and in vivo models of disease, new genetic approaches, the identification of key E. histolytica virulence factors, and the recognition of crucial elements of the host response to infection have led to significant insights into the pathogenesis of amebic infection. E. histolytica virulence factors include 1) a surface galactose binding lectin that mediates E. histolytica binding to host cells and may contribute to amebic resistance to complement, 2) amebapores, small peptides capable of lysing cells, which may play a role in killing intestinal epithelial cells, hepatocytes, and host defense cells, and 3) a family of secreted cysteine proteinases that play a key role in E. histolytica tissue invasion, evasion of host defenses, and parasite induction of gut inflammation. Amebae can both lyse host cells and induce their suicide through programmed cell death. The host response is also an important factor in the outcome of infection, and neutrophils may play a key role in contributing to the tissue damage seen in amebiasis and in controlling amebic infection.

Animals↗