Absence Of Bacterial Colonization Research Articles

Differences in Decreasing Bacteria Colonization Wound Irrigation using 0.9% Nacl Compared with Wound Irrigation using Active Ingredients Polyhexanide 0.1% and 0.1% Betaine in Open Fractures of Long Bone

BACKGROUND: An open fracture is an emergency case that must be treated quickly to prevent infection. The use of an irrigation solution containing 0.1% of the antimicrobial polyhexanide and 0.1% of the surfactant betaine has been associated with more satisfactory wound healing. AIM: This study was comparing irrigation with polyhexanide 0.1% and betaine 0.1% (P + B) in reducing bacterial colonization of open fractures compared to using 0.9% natrium chloride (NaCl) solution. METHODS: This study uses a pre- and post-control group design. Sampling was carried out in the operation room of the emergency care installation, inpatient installation, and outpatient installation of prof. Hospital. Dr. I.G.N.G Ngoerah Denpasar, between September and November 2022. From a sample population suffering from open fractures of the lower extremities, samples of patients were taken who were irrigated with 0.9% NaCl solution with a mixture of polyhexanide 0.1% and betaine 0.1%. The presence or absence of bacterial colonization was examined using a surgical wound base swab with the Levine technique. RESULTS: In the 30 patients in this study, there was a significant decrease in bacterial levels (Log colony-forming unit [CFU]/g) after irrigation, both from irrigation with NaCl (p = 0.04) and NaCl + P + B (p < 0.001). The reduction in bacterial levels was more significant with NaCl + P + B compared with NaCl alone, at post-irrigation (p < 0.001), H+3 (p = 0.003), and H + 7 (p < 0.001). CONCLUSION: Wound irrigation using a combination of 0.9% NaCl, 0.1% polyhexanide, and 0.1% betaine reduced bacterial colonization more than using 0.9% NaCl-only solution in open fractures of long bones.

Breath Hydrogen Test in Lactose Malabsorption

Lactose is the most important source in mammalian milk. In normal children, Lactose is hydrolyzed by lactase, and directly absorbed into bloodstream by an active transport mechanism. The term of lactose malabsorption is reserved to patients in whom impaired intestinal lactose hydrolysis and uptake has been proven by an appropriate test. The severity of lactose malabsorption and the extent of symptoms vary widely and are the results of several factors such as the amount of ingested lactose, gastric emptying time, intestinal transit time, and colonic flora. The diagnosis of lactose malabsorption is based on clinical findings and the results of appropriate tests. The breath hydrogen test has obvious advantages for pediatric population because it is painless, non-invasive, sensitive and specific. In the absence of bacterial colonization in the small intestine, the elevation of the concentration of hydrogen in the expired air implies the arrival of lactose in the colon. The increasing respiratory excretion of hydrogen is indicative of a deficit of lactase in enterocyte brush border. This test can also be used to show the existence of bacterial growth. Dietary fiber, some drugs, preparation for colonoscopy, colonic pH, and diarrhea can influence the result of breath hydrogen test.

564 Genes Encoding E. coli Small Heat Shock Proteins IbpA/B Have a Protective Role in Experimental Colitis in E. coli Monoassociated Il10-Deficient Mice

Adult colonic mucosa is highly fucosylated relative to immature mucosa, and this fucosylation is dependent upon bacterial colonization. Toll-like receptor-4 (TLR4) was hypothesized to mediate this colonization-dependent fucosylation. Germ-free (GF) and bacteria-depleted (BD) mice were compared with conventional and mutant mice with regard to induction of epithelial fut2 mRNA levels and α1,2-fucosyltransferase (FUT2) activity. Induction of these activities by recolonization were compared with induction by LPS (TLR4 ligand) andmonocolonization by bacteriodes and E. coli strains. Cultured human erythroleukemia (Hel) cells were used to study fucosylated TLR4 In Vitro. Colonization-dependent induction of fucosylation occurs only in TLR2-/and wild-type mice but not in TLR4-/and MyD88-/mice, suggesting TLR4-MyD88 dependent signaling is important for fucosylation. TLR4 is fucosylated in the colonocytes of only GF and BD mice. LPS activate fut2 mRNA and FUT2 activity in the absence of bacterial colonization. Fucose-utilizing Bacteroides fragilis induce colonic fucosylation, but not a fucose-non-utilizing mutant. In Hel cells, which express fucosylated TLR4 activates fut2 mRNA and fucosylation. TLR4-specific siRNA inhibits this activation, and fucosidase treatment abolished TLR4-dependent activation of fut2 mRNA, confirming the central role of fucosylated-TLR4 in activating fut2 and cell surface fucosylation. Fucosylated-TLR4 expressed on uncolonized colonocytes mediates bacterially-induced activation of fut2 mRNA and FUT2 activity without activating inflammation, and is a necessary initial step in the communication between the colonizing bacteria and the host epithelium.

563 Colonization-Dependent Colonic Fucosylation is Mediated by Gram Negative Bacteria via Activation of a Novel Fucosylated TLR4

Adult colonic mucosa is highly fucosylated relative to immature mucosa, and this fucosylation is dependent upon bacterial colonization. Toll-like receptor-4 (TLR4) was hypothesized to mediate this colonization-dependent fucosylation. Germ-free (GF) and bacteria-depleted (BD) mice were compared with conventional and mutant mice with regard to induction of epithelial fut2 mRNA levels and α1,2-fucosyltransferase (FUT2) activity. Induction of these activities by recolonization were compared with induction by LPS (TLR4 ligand) andmonocolonization by bacteriodes and E. coli strains. Cultured human erythroleukemia (Hel) cells were used to study fucosylated TLR4 In Vitro. Colonization-dependent induction of fucosylation occurs only in TLR2-/and wild-type mice but not in TLR4-/and MyD88-/mice, suggesting TLR4-MyD88 dependent signaling is important for fucosylation. TLR4 is fucosylated in the colonocytes of only GF and BD mice. LPS activate fut2 mRNA and FUT2 activity in the absence of bacterial colonization. Fucose-utilizing Bacteroides fragilis induce colonic fucosylation, but not a fucose-non-utilizing mutant. In Hel cells, which express fucosylated TLR4 activates fut2 mRNA and fucosylation. TLR4-specific siRNA inhibits this activation, and fucosidase treatment abolished TLR4-dependent activation of fut2 mRNA, confirming the central role of fucosylated-TLR4 in activating fut2 and cell surface fucosylation. Fucosylated-TLR4 expressed on uncolonized colonocytes mediates bacterially-induced activation of fut2 mRNA and FUT2 activity without activating inflammation, and is a necessary initial step in the communication between the colonizing bacteria and the host epithelium.

Poly(D,L‐lactide) coating is capable of enhancing osseous integration of Schanz screws in the absence of infection

Pin loosening is a major complication in external fixation. Biological and mechanical conditions play an important role in the maintenance and enhancement of the implant-bone interface in fracture fixation. It is thought that biodegradable coatings may be capable of preventing pin track infection and pin loosening. The goal of this study was therefore to analyze the influence of a biodegradeable coating on the osseous integration of Schanz' screws during fracture treatment. Standardized osteotomies (3-mm fracture gap) of the right tibiae were performed on 16 sheep and stabilized by an AO mono-lateral external fixator. Additional, mechanically less loaded Schanz' screws were also mounted. All screws were randomly coated with biodegradable poly(D,L-lactide). The sheep were sacrificed after 9 weeks. All screws were removed and rolled on blood agar plates for microbiological analysis. Histological sections of the pin tracks were histochemically and morphometrically analyzed. Clinically, no signs of severe infection were visible. Microbiological analysis revealed 14.8% colonization by Staphylococcus aureus in the coated and 29% in the uncoated screws. Histomorphometry of the bone surrounding the Schanz' screws revealed that significantly more osseous integration had occurred on poly(D,L-lactide)-coated screws in the absence of bacterial colonization. Significantly more bone remodeling and a higher osteoclastic activity was seen near the screw-bone interface in the uncoated screw group. Up to a threefold increase in new bone formation and more severe remodeling was observed around the screw entry compared to the pin exit in all groups. Loaded screws showed significantly more callus formation around the exit sites than their less loaded counterparts. In the present study, poly(D,L-lactide) coating of Schanz' screws was found to enhance osseous integration in the absence of bacterial colonization in sheep by causing less cortical remodeling and less osteoclastic activity in the cortices compared to uncoated screws. Additionally, the coating appeared to reduce the instances of pin track infections. Mechanical loading showed an adverse effect on bone formation and remodeling. It has been shown that both biological and mechanical factors play an important role in the maintenance of osseous integrity of the pin-bone interface. Poly(D,L-lactide) coating of Schanz' screws does not prevent osseous destruction and severe bacterial colonization along the pin tracts, but can improve osseous integration of Schanz' screws in the absence of infection.

IL-2-deficient mice raised under germfree conditions develop delayed mild focal intestinal inflammation.

Interleukin-2 (IL-2) amplifies immune stimuli and influences B cell differentiation. IL-2-deficient mice spontaneously develop intestinal inflammation if raised under specific pathogen-free (SPF) conditions. We quantitatively determined the aggressiveness and kinetics of gastrointestinal and hepatic inflammation in the presence or absence of viable bacteria in IL-2-deficient mice. Breeding colonies were maintained under SPF and germfree (GF) conditions. Intestinal tissues, serum, and mesenteric lymph nodes were obtained from mice at different ages for blind histological scoring, immunoglobulin measurements, mucosal T cell infiltration, and cytokine secretion. GF IL-2 -/- mice developed mild, focal, and nonlethal intestinal inflammation with delayed onset, whereas the more aggressive inflammation in SPF IL-2 -/- mice led to their death between 28 and 32 wk. Periportal hepatic inflammation was equal in the presence or absence of bacterial colonization. Intestinal immunoglobulin secretion decreased significantly by 13 wk of age in IL-2 -/- mice in both GF and SPF environments. In contrast to other genetically engineered rodents, IL-2 -/- mice develop mild focal gastrointestinal and active portal tract inflammation in the absence of viable bacteria.

A Transient Exposure to Symbiosis-Competent Bacteria Induces Light Organ Morphogenesis in the Host Squid.

Recent studies of the symbiotic association between the Hawaiian sepiolid squid Euprymna scolopes and the luminous bacterium Vibrio fischeri have shown that colonization of juvenile squid with symbiosis-competent bacteria induces morphogenetic changes of the light organ. These changes occur over a 4-day period and include cell death and tissue regression of the external ciliated epithelium. In the absence of bacterial colonization, morphogenesis does not occur. To determine whether the bacteria must be present throughout the morphogenetic process, we used the antibiotic chloramphenicol to clear the light organ of bacteria at various times during the initial colonization. We provide evidence in this study that a transient, 12-hour exposure to symbiosis-competent bacteria is necessary and sufficient to induce tissue regression in the light organ over the next several days. Further, we show that successful entrance into the light organ is necessary to induce morphogenesis, suggesting that induction results from bacterial interaction with internal crypt cells and not with the external ciliated epithelium. Finally, no difference in development was observed when the light organ was colonized by a mutant strain of V. fischeri that did not produce autoinducer, a potential light organ morphogen.