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PubMed2003

The 10(5) bacterial growth guideline: reassessing its clinical relevance in wound healing.

The microbiology of wounds is a key determinant in healing and clinicians generally accept that a level of microbial (ie, bacterial) growth greater than 100,000 viable organisms per gram of tissue can be used to diagnose infection. Although other factors that predispose a wound to infection are widely recognized, today's wound care practitioners are influenced primarily by the 10 5 guideline, with treatment being based on the microbial count in deep or superficial tissue. However, to appropriately manage microbially challenged wounds (eg, heavily colonized and clinically infected), a more balanced awareness of the broader issues relating to micro-organisms and wounds is needed. The types of micro-organisms, their interactions with each other and with the wound environment, the local conditions, and host resistance are all key factors that collectively influence healing. From a microbiological perspective, successful wound healing is dependent on maintaining a host-manageable bioburden. If local conditions favor microbial growth, a wound may fail to heal and become infected, requiring topical antiseptics or antibiotics to supplement the host inflammatory response and restore balance in favor of the host. This paper provides a critical examination of the 10 5 guideline to enhance clinician understanding and utilization of a commonly applied diagnostic consideration.

Colony Count, Microbial↗
PubMed1991

T lymphocyte-stimulating microbial toxins as "superantigens".

Infectious pathogens generally have to cope with the host's adaptive immune system, i.e., T and B lymphocytes. Common evasion mechanisms in this complex interaction are antigenic variations, the escape to immunologically priviledged sites or the use of immunosuppressive mechanisms. Many bacteria and other microorganisms eleborate soluble factors or toxins that act suppressively on cells of the immune system, such as pore-forming molecules or proteins that interfere with the function of G proteins. Gram-positive cocci and a mycoplasma have developed an extremely potent mechanism of T cell stimulation by closely mimicking recognition of specific antigen. From the functional similarity to antigen recognition and the multiclonal activation of T cells the designation "superantigens" has been suggested for these molecules.

Animals↗
PubMed2003

Intestinal microflora and homeostasis of the mucosal immune response: implications for probiotic bacteria?

The intestinal microflora can be considered a postnatally acquired organ that is composed of a large diversity of bacteria that perform important functions for the host and can be modulated by environmental factors, such as nutrition. Specific components of the intestinal microflora, including lactobacilli and bifidobacteria, have been associated with beneficial effects on the host, such as promotion of gut maturation and integrity, antagonisms against pathogens and immune modulation. Beyond this, the microflora seems to play a significant role in the maintenance of intestinal immune homeostasis and prevention of inflammation. The contribution of the intestinal epithelial cell in the first line of defense against pathogenic bacteria and microbial antigens has been recognized. However, the interactions of intestinal epithelial cells with indigenous bacteria are less well understood. This review will summarize the increasing scientific attention to mechanisms of the innate immune response of the host towards different components of the microflora, and suggest a potential role for selected probiotic bacteria in the regulation of intestinal inflammation.

Animals↗
PubMed2005

Disruption of protein-protein interactions: towards new targets for chemotherapy.

Protein-protein interactions play a key role in various mechanisms of cellular growth and differentiation, and in the replication of pathogen organisms in host cells. Thus, inhibition of these interactions is a promising novel approach for rational drug design against a wide number of cellular and microbial targets. In the past few years, attempts to inhibit protein-protein interactions using antibodies, peptides, and synthetic or natural small molecules have met with varying degrees of success, and these will be the focus of this review.

Animals↗
PubMed1999

Mechanisms and assessment of lectin-mediated mitogenesis.

The discovery of lectin-mediated mitogenesis by Nowell in 1960 stimulated interest in the properties of lectins while advancing knowledge of immunology. Although some lectins are polyclonal activators both in vitro and in vivo, others may display a broad range of activities toward human lymphocytes. Indeed, the same lectin (e.g., wheat germ agglutinin or Datura lectin) may be mitogenic, comitogenic, or antimitogenic, depending on the experimental conditions. An individual lectin may bind to several glycoproteins on the lymphocyte surface, resulting in interactions that may or may not be functionally relevant, and that may have opposing effects. Studies with lectins and with monoclonal antibodies (MAbs) have established that a surprisingly large variety of cell-surface molecules can influence the initiation and regulation of lymphocyte activation and proliferation. Interactions between lymphocytes and accessory cells are crucial; some signals are cell-mediated, but others depend on soluble cytokines. Mitogenic lectins presumably bind to the T-cell receptor complex and also promote a positive costimulatory signal leading to the synthesis of interleukin 2 and interleukin 2 receptors (IL-2R). Nonmitogenic, comitogenic, and antimitogenic lectin activities also probably act via accessory molecules involved in costimulation. Plant lectin-animal lymphocyte interactions presumably have no physiological significance, but it is suggested that the former mimics microbial superantigens, which may function in the colonization of host cells. Mitogenic stimulation of lymphocytes can be assessed in several ways. The standard technique measures [3H]-thymidine incorporation into DNA, but nonradioactive procedures are also available.

Animals↗
PubMed1992

Changes of expression of endogenous sugar receptors by polymorphonuclear leukocytes after prolonged anaesthesia and surgery.

Anaesthesia and surgery are known to depress granulocyte function in the early postoperative period, leading to deterioration of the immune defence against infection. Carbohydrate-lectin interactions may play an important role in the activities of phagocytic cells in that they facilitate initial host defence in the event of microbial antigenic challenge. A panel of biotinylated (neo)glycoproteins (chemically glycosilated carrier proteins) was used to detect endogenous carbohydrate-binding receptors /lectins/, on peripheral blood polymorphonuclear leukocytes of patients undergoing prolonged anaesthesia for replantation surgery. Four hours after induction of anaesthesia, a progressive decline of expression of endogenous sugar receptors on granulocytes was detected using the labelled (neo)glycoproteins lactose-BSA, N-acetyl-D-glucosamine-BSA, D-mannose-BSA, sialic-acid-BSA and D-xylose-BSA. Concomitant changes in peripheral white blood cell counts and the lack of depression in the absence of general anaesthetic agents suggested the existence of a possible relationship between reduced expression of (neo)glycoprotein receptors to impaired granulocyte function and anaesthetic-induced immunodepression.

Acetylglucosamine↗
PubMed2005

Salmonella flagellin, a microbial target of the innate and adaptive immune system.

Bacterial flagellins are important components of the motility apparatus used by many microbial pathogens. These proteins are also targets of the innate and adaptive immune response of the host during infection and autoimmune disease. Flagellin interacts with TLR-5 and leads to the generation of a pro-inflammatory response and activation of host dendritic cells in vivo. Furthermore, flagellin is recognized by antibody and CD4 T cells responses during Salmonella infection. Here, we review recent developments in the understanding of flagellin interactions with the host immune system.

Animals↗
PubMed1999

Microbial fusion.

Explore the source record for details and available documents.

Bacterial Adhesion↗
PubMed2003

Death by a B cell superantigen: In vivo VH-targeted apoptotic supraclonal B cell deletion by a Staphylococcal Toxin.

Amongst the many ploys used by microbial pathogens to interfere with host immune responses is the production of proteins with the properties of superantigens. These properties enable superantigens to interact with conserved variable region framework subdomains of the antigen receptors of lymphocytes rather than the complementarity determining region involved in the binding of conventional antigens. To understand how a B cell superantigen affects the host immune system, we infused protein A of Staphylococcus aureus (SpA) and followed the fate of peripheral B cells expressing B cell receptors (BCRs) with VH regions capable of binding SpA. Within hours, a sequence of events was initiated in SpA-binding splenic B cells, with rapid down-regulation of BCRs and coreceptors, CD19 and CD21, the induction of an activation phenotype, and limited rounds of proliferation. Apoptosis followed through a process heralded by the dissipation of mitochondrial membrane potential, the induction of the caspase pathway, and DNA fragmentation. After exposure, B cell apoptotic bodies were deposited in the spleen, lymph nodes, and Peyer's patches. Although in vivo apoptosis did not require the Fas death receptor, B cells were protected by interleukin (IL)-4 or CD40L, or overexpression of Bcl-2. These studies define a pathway for BCR-mediated programmed cell death that is VH region targeted by a superantigen.

Animals↗
PubMed2004

Bacterial inhibition of eukaryotic pro-inflammatory pathways.

Eukaryotic cells perceive and respond to microbes, both pathogenic and commensal, by activation of signaling cascades such as the NF-kappaB pathway. Induction of such pathways leads to the upregulation of a program of gene expression that mediates pro-inflammatory and anti-apoptotic effector proteins. This host response is usually effective in clearing or controlling an infection. For pathogens (and potentially, symbionts) to continue their lifecycle, it is necessary to evade or repress these cellular responses. There has been recent interest in bacteria that can inhibit pro-inflammatory pathways, in some cases by the actions of soluble effector proteins secreted via a Type III secretion system. Certain effector proteins with this function possess enzymatic activity toward ubiquitin and related molecules. Ubiquitination is an increasingly recognized regulatory modification in eukaryotic cells, and microbial effectors that modulate this key host system may have diverse effects on infected cells and mediate many aspects of eukaryotic-prokaryotic interactions.

Animals↗
PubMed2026

First Report and Integrated Characterization of Aeromonas veronii Associated with the Protected Fish Diptychus maculatus in Xinjiang, China.

Aeromonas veronii is a widely distributed opportunistic aquatic pathogen associated with diseases in freshwater fish. Despite the ecological and conservation significance of Diptychus maculatus, a protected cold-water fish inhabiting high-altitude ecosystems, information regarding its associated bacterial communities remains limited. This study aimed to isolate and characterize A. veronii recovered from D. maculatus and provide baseline information on its occurrence and phenotypic characteristics. Eight bacterial isolates were recovered from various tissues, including skin, gills, eye, intestine, dorsal fin, body kidney, gonad, and spleen of randomly sampled fish individuals from Xinjiang, China. Phenotypic and biochemical characterization, together with 16S rRNA sequencing, supported their identification as A. veronii, while gyrB analysis of a representative isolate provided additional species-level confirmation. Antimicrobial susceptibility testing revealed a consistent multidrug-resistance phenotype among all isolates. The isolates were susceptible to enrofloxacin, cefotaxime, ceftriaxone, and florfenicol. Intermediate responses were observed for ciprofloxacin, ofloxacin, doxycycline, oxytetracycline, and trimethoprim-sulfamethoxazole, whereas resistance was detected against norfloxacin, neomycin, penicillin, amoxicillin, tetracycline, and erythromycin. In vitro biofilm assays demonstrated weak to moderate biofilm-forming capacity among isolates. These findings provide baseline data for wildlife microbial surveillance and conservation-oriented monitoring of protected fish populations, supporting future investigations into environmental monitoring, genomic characterization, and host-microbe interactions.

Aeromonas veronii↗
PubMed1991

Bacteriologic monitoring of periodontal diseases: cultural, enzymatic, immunologic, and nucleic acid studies.

Evidence supporting the bacteriologic etiology of periodontal diseases has led investigators to monitor the microbiologic species associated with each disease. The type of study performed has evolved at different levels over the years and is predominantly influenced by available technologies. As the technology has advanced, so too have attempts at monitoring specific microorganisms. The ultimate goal in most research efforts on clinical bacteriologic monitoring of the periodontal diseases has been to obtain a method of measuring microorganisms in a specific, rapid, low-cost fashion. The method would be used on a daily basis at chairside in the dental operatory to direct treatment at a target microbial population, evaluate treatment, or predict future areas of attachment loss. It is suggested that future efforts try to incorporate microbiologic-host interactions that are likely to be important in the etiology and pathogenesis of the periodontal diseases.

Aggregatibacter actinomycetemcomitans↗
PubMed1990

Bacterial overgrowth.

Small bowel bacterial overgrowth is a syndrome manifested by malabsorption, weight loss, and diarrhea. Human intestinal flora is part of a complex ecosystem regulated by host mechanisms, environmental factors, and bacterial interactions. Numerous conditions can tilt this balance to favor bacterial contamination of the gut. Knowledge of intestinal microbial control enables the clinician to better understand the pathophysiology and the clinical features of this disorder. Current strategies in diagnosis and therapy are discussed.

Bacteria↗
PubMed2006

Symbiotic bacteria direct expression of an intestinal bactericidal lectin.

The mammalian intestine harbors complex societies of beneficial bacteria that are maintained in the lumen with minimal penetration of mucosal surfaces. Microbial colonization of germ-free mice triggers epithelial expression of RegIIIgamma, a secreted C-type lectin. RegIIIgamma binds intestinal bacteria but lacks the complement recruitment domains present in other microbe-binding mammalian C-type lectins. We show that RegIIIgamma and its human counterpart, HIP/PAP, are directly antimicrobial proteins that bind their bacterial targets via interactions with peptidoglycan carbohydrate. We propose that these proteins represent an evolutionarily primitive form of lectin-mediated innate immunity, and that they reveal intestinal strategies for maintaining symbiotic host-microbial relationships.

Animals↗
PubMed2006

Variola virus IL-18 binding protein interacts with three human IL-18 residues that are part of a binding site for human IL-18 receptor alpha subunit.

Interleukin-18 (IL-18) plays an important role in host defense against microbial pathogens. Many poxviruses encode homologous IL-18 binding proteins (IL-18BP) that neutralize IL-18 activity. Here, we examined whether IL-18BP neutralizes IL-18 activity by binding to the same region of IL-18 where IL-18 receptor (IL-18R) binds. We introduced alanine substitutions to known receptor binding sites of human IL-18 and found that only the substitution of Leu5 reduced the binding affinity of IL-18 with IL-18BP of variola virus (varvIL-18BP) by more than 4-fold. The substitutions of Lys53 and Ser55, which were not previously known to be part of the receptor binding site but that are spatially adjacent to Leu5, reduced the binding affinity to varvIL-18BP by approximately 100- and 7-fold, respectively. These two substitutions also reduced the binding affinity with human IL-18R alpha subunit (hIL-18Ralpha) by 4- and 2-fold, respectively. Altogether, our data show that varvIL-18BP prevents IL-18 from binding to IL-18R by interacting with three residues that are part of the binding site for hIL-18Ralpha.

Amino Acid Sequence↗
PubMed2026

Involvement of cross-genus phages in bacterial resistance to chlorine disinfection.

Chlorine disinfection resistance in pathogenic microorganisms poses severe environmental concerns and public health risks. While phages play critical roles in host adaptation to environmental stress, how poly-host phages contribute to bacterial resistance to chlorine disinfectants remains poorly understood. Here, we investigated shifts in the population dynamics, transcriptional profiles, and function potentials of cross-genus phage-bacterial communities under exposure to chlorine disinfectants in a continuously operated anaerobic-anoxic-oxic system over a 92-day period, using integrated metagenomic and metatranscriptomic approaches. In the presence and absence of chlorine disinfectants, the genomic abundance and diversity of phage and bacterial communities showed similar variation trends, and the community structures of both exhibited clear differences. A strong significant positive correlation was observed between phage and bacterial diversity under chlorine exposure (R&#x202f;=&#x202f;0.975, p&#x202f;=&#x202f;0.00,057), whereas no significant correlation was detected in the absence of chlorine disinfection (R&#x202f;=&#x202f;-0.314, p&#x202f;=&#x202f;0.613), suggesting that chlorine disinfectants may enhance phage-bacteria interactions. Host-associated phages exhibited high consistency with their corresponding putative hosts in terms of genomic abundance (M2&#x202f;=&#x202f;0.0945, p&#x202f;=&#x202f;0.001) and transcript abundance (M2&#x202f;=&#x202f;0.3668, p&#x202f;=&#x202f;0.001), and they were also significantly correlated with cross-genus phages in both genomic abundance (R&#x202f;=&#x202f;0.97, p&#x202f;<&#x202f;2.2e-16) and transcript abundance (R&#x202f;=&#x202f;0.83, p&#x202f;<&#x202f;2.2e-16), which collectively suggests the critical role of cross-genus phages in the resistance of microbial communities to chlorine disinfectants. Bipartite association network analysis shows that cross-genus phages carry highly homologous genes to their putative hosts and may be involved in the horizontal transfer of these genes among bacteria. These homologous genes are involved in DNA repair, redox balance regulation, environmental stress adaptation and efflux pump functions, suggesting a synergistic role between cross-genus phages and their putative hosts in chlorine resistance. Our findings reveal that cross-genus phages can contribute to the resistance of bacterial communities to chlorine disinfectants, providing the theoretical foundation for evaluating the role of poly-host phages in microbial communities.

Chlorine resistance↗
PubMed1999

Fluorescence image analysis of the association between Porphyromonas gingivalis and gingival epithelial cells.

We have developed a fluorescence imaging technique using a DNA-binding dye to visualize, over time, the physical interactions between Porphyromonas gingivalis and human gingival epithelial cells in vitro. The results extend previous observations of P. gingivalis invasion of gingival epithelial cells based on indirect measurements. An intracellular location for P. gingivalis was established by optical sectioning of images in the z-plane. Kinetic analysis showed that P. gingivalis invasion of epithelial cells is a rapid and efficient process, reaching completion after 12 min. Imaging of infected monolayers revealed that over 90% of a population of gingival epithelial cells contained bacteria. Furthermore, only vital bacteria were capable of invasion, and intracellular bacteria congregated in the perinuclear region of the epithelial cells. P. gingivalis remained inside the epithelial cells over a 24 h period and induced rearrangement of the actin cytoskeleton along with alteration of the size and shape of the epithelial cells. These findings provide direct evidence that entry rates of P. gingivalis into gingival epithelial cells are high and rapid, and that internalized bacteria initially localize in a specific region of the epithelial cells.

Cell Nucleus↗