Role Of Lec A / Gb-3 In Engulfment Of Bacteria

Introduction: The biological membranes are composed of phospholipid bilayers, each phospholipid with hydrophilic heads and hydrophobic tails, and proteins. This arrangement of the proteins and lipids produces a selectively permeable membrane. Many kinds of molecules surround or are contained within

Phospholipids make up most of the cell membrane, in a phospholipid bilayer. Phospholipid molecules form two layers, with the hydrophilic (water loving) head facing the extracellular fluid and the cytosol (intracellular) fluid, and the hydrophobic (not water loving) tails facing one another. The cell membrane is constructed in such a way that it is semipermeable, and allows oxygen, CO2 and lipid soluble molecules through easily, while other molecules like glucose, amino acids, water, and ions cannot pass through quite as easily. That is the meaning behind the chant “some things can pass, others cannot!”.

This phosphate will eventually end up dissolving in the water. Sterols are added to membranes to give is a stiffness and make it more durable. Cholesterol is one of the most rigid lipids in the membrane. The rigidity around the cholesterol makes the cell membrane tough and makes it harder for smaller molecules to pass through the membrane. Cholesterol also helps immobilize some of the lipid particles in the

Gram negative and gram positive bacteria differ from each other in many ways especially in the composition and size of their cell walls. Unlike Gram-positive bacteria, Gram-negative bacteria have a thin peptidoglycan layer surround by an outer membrane. This outer membrane contains many proteins one of them being lipopolysaccharides (LPS), which contributes to the bacteria’s negative charge. One part of this protein is a lipid, called Lipid A, which is considered an endotoxin because this lipid triggers an immune response stimulating fever

Carson, V. (2013). Microbiology Lab (1st ed.). Department of Cell Biology, Microbiology & Molecular Biology. University of South Florida.

When glucose carriers in the membrane were set to 500, the glucose transport rate for 2.00 mM of glucose was .0008 mM/min. Equilibrium was reached at 43 minutes. At 700 glucose carriers the rate was .0010 mM , and equilibrium was reached at 33 minutes. When the glucose carriers was set at 900 the rate was .012 mM/min, and equilibrium was reached at 27 minutes. After changing the glucose concentration to 8.0 mM, the glucose transport rate with 500 carrier proteins was .0023 mM/min, and equilibrium was reached at 58 minutes. With the simulation set at 700 carrier proteins the rate was .0031mM/min, and equilibrium was reached at 43 minutes. When the simulation was done with 900 carrier proteins the glucose transport rate was .0038, and equilibrium was reached at 35 minutes.

Our results show no growth whatsoever in those plates containing Ampicillin; this indicates that we encounter an error during our experiment. The agar plate's outcomes and bioluminescent response done by the bacterium that had the plasmid, it can be presumed due to scientific analysis that Escherichia coli is impervious to ampicillin and the plasmid combines itself with the DNA of Escherichia coli according to other experiments and based on science itself. We can predict that the impact of the bioluminescence in the cells of the microorganisms that is infested unmistakably gives affirmation that the plasmid infuses with Escherichia coli's DNA, guarding the cells that changed from dying, viably creating a gainful situation for the bacterial organisms. Since Escherichia coli is a negative prokaryotic call, it is within the phospholipid bilayer and on top of this is a peptide glycan

Biomedical research disclosed the toxically active part of LPS is its lipid A. It produces a wide variety of pathophysiological effects such as fever, septic shock, leucopenia, leucocytosis, Shwartzman rectivity and even death (Caroff and Karibian., 2003). LPS do not act directly against cells or organs but through the immune system, specifically speaking, the monocytes and macrophages, thereby enhancing immune responses. Bacterial LPS if released into the mammalian blood can bind with specific types of binding proteins called as LPS binding proteins (LBP) which are normally present in the circulating blood (McCuskey et al., 1996). LBP is a glycoprotein which is 60kDa in size, produced in the hepatocytes and continuously secreted into the circulating blood. LBP posses binding sites for lipid A and recognize molecules, fragments or intact bacteria containing LPS (Schumann., 1992). Lipid A receptor system plays the critical role in the binding of LPS with LBP. Lipid A, a glucosamine disaccharide with hydroxy and substituted nonhydroxyl fattyacids acts as potent immunostimulators by recognizing LBP. The number of fattyacids attached to the lipid A is a strong determinant in deciding the strength of immune reactions evoked by LPS. Until 1990 there were no enough evidence to explain how lipidA getting intercalated into the lipid bilayer of host immune cells. It was believed that a non specific binding is occurring between lipid A and mammalian cell surface lipid bilayer. The

Pathogenic L. monocytogenes go through an intracellular life cycle involving early escape from the phagocytic vacuole, rapid intracytoplasmic multiplication, bacterially induced actin-based motility, and direct spread to neighboring cells, in which they reinitiate the cycle. The bacterium is first phagocytosed by these cells and secretes a pore-forming toxin called listeriolysin, which allows the bacterium to escape from the phagosome. All virulent strains of L. monocytogenes synthesize and secrete listeriolysin. Phospholipase A and B are other virulence factors that facilitate escape of L. monocytogenes from the phagosome. Once out of the phagosome L. monocytogenes is capable of rapid division in the cytoplasm, evading the immune response and moving throughout the cytoplasm from cell to cell. L. monocytogenes is well known for its ability to propel itself like a rocket through the cell cytoplasm. This is the result of the bacterium’s ability to polymerize actin filaments at its tail end. Actin is arranged in subunits to form microfilaments that are capable of directing cell movement. L. monocytogenes accomplishes cell motility through a virulence factor called ActA that takes advantage of normal actin polymerization going on in the cell. The ActA protein shares sequence homology with a protein called WASP that is found in virtually all eukaryotic cells. WASP is responsible for recognizing and

After entry, the bacteria are trapped in a single membrane vacuole known as the phagosome. Lm must escape from the phagosome into the cytosol by the action of the secreted pore-forming toxin, Listeriolysin O (LLO) which is encoded by hly (Portnoy et al., 2002). Getting access to the cytosol is necessary for a successful infection and failure to escape from the phagosome results in the elimination of the bacteria from tissues (Le Monnier et al., 2007). LLO belongs to a family of cholesterol- dependent cytolysins (CDCs) which are secreted as a soluble monomers and characterized by their ability to bind to the cholesterol of host membranes, oligomerize, and form a large pores (Schnupf et al., 2007). Bacterial membranes lacking sterols are therefore not affected by the action of these toxins.

Summary of Lipid Dynamics Project. Lipid membranes are highly dynamic. Lipid membranes are highly dynamic. In 1972, Singer and Nicholson introduced the mosaic bilayer model, which suggests that membranes are two dimensional homogeneous liquid. Nowadays with a better understanding of the dynamics occurring at the molecular level of membranes, we are aware of their transverse and lateral heterogeneities. Studies suggest the existence of the so called lipid rafts. These are sub-domains with unique lipid and protein composition, in general with high concentrations of cholesterol and glycosphingolipids. They are believed to play an important role on cell

The Gram-positive cell wall is composed of peptidoglycans, a thick layer of protein-sugar complexes taking up 60-90% of their cell wall. Peptidoglycan is composed of two glucose derivatives, N-acetylmuramic acid and N-acetylglucosamine alternated and cross-linked by tetrapeptides that is composed of L-alanine, D-glutamine, L-lysine

Consequently, membrane permeability gets distorted, due to progressive release of lipopolysaccharide molecules and membrane proteins.

A large number of AMPs form amphipathic structures when they interact with the microbial plasma membrane. Amphipathicity is developed through the assembly of protein conformations. In case of AMPs, such amphipathicity is achieved via amphipathic helix. For example, the amphipathic α-helix has a periodicity of three monomers and is ideal for interactions with amphipathic membranes. The amphipathic helicity stimulates the peptide activity against anionic membranes, as well as zwitterionic membranes (neutral). A high degree of amphipathicity or helicity within the molecule forms hydrophobic domains with amino acids residues that is an important secondary structure of AMPs. This secondary structure increases the toxicity to cells made up of neutral phospholipids [Dathe] [Armand].

In all areas of biology, it is easy to see that structure is related to function. This statement holds true in microbiology as well, the study of microorganisms, including bacteria. One characterizing feature of bacteria is the cell wall, which can generally (although not in all situations) be categorized into one of two categories: either Gram positive or Gram negative. Gram positive bacteria’s cell walls are composed of a large peptidoglycan layer (up to 90% of their cell wall). Within this large peptidoglycan layer, one can find techoic acids, which contribute to the maintenance of cell wall structure, and lipotechoic acids, which attach to membrane lipids. Gram positive bacteria that act as pathogens can also potentially release exotoxins, which can have very dangerous effects on humans. Gram negative bacteria, on the other hand, have a very small layer of peptidoglycan in their cell wall, which is surrounded by an outer membrane. Within the outer membrane, one can find the lipopolysaccharide layer, which is one of the most distinguishing factors of Gram-negative bacteria. It is important to note that Gram negative bacteria fail to possess techoic