Infection and Immunity, August 2008, p. 3360-3373, Vol. 76, No. 8

Schematic diagrams of small intestine mucosa in normal and infected intestines. (A) Normal intestinal mucosa, including the epithelial layer with the associated brush border, tight junctions, mucosa, and the microbiota. There are small cells at the intestinal crypts (Paneth cells) that secrete large amounts of antimicrobial peptides (defensins). A large M cell with a closely associated phagocyte is also shown. Even during the resting state some of these entrocytes express the cytoplasmic microbial pattern recognition receptors (PRR) (i.e., NOD2). (B) Infected intestinal mucosa. A typical diseased intestinal epithelium during bacterial insult is shown. On the left side (cells labeled A to C) an M cell (cell A) takes up S. enterica serovar Typhimurium after the bacterium injects its effectors through the type III secretion system (TTSS), leading to the formation of a Salmonella-containing vacuole (SCV) and eventual host cell death. Cell death liberates the bacteria, which can invade the incoming phagocytes. For a neighboring cell (cell C) the key events of the host cell response are shown, which includes LPS activation of a surface pattern recognition receptor (TLR4), leading to MyD88-dependent activation of NF-B and basolateral release of IL-8 (CXCL8). At the same time the intracellular pattern recognition receptor, NOD2, recognizes a bacterial peptidoglycan (PG) derivative and triggers a pathway that culminates in NF-B activation. The epithelial cells also secrete the PMN chemoattractant hepoxilin A3 (HXA3) at the apical surface, resulting in an influx of neutrophils into the mucosa and lumen from the underlying vascular bed. On the right side (cells D and E) EPEC and V. cholerae infection is shown. Cell D loosens the brush border and tight junction due to the bacterial effectors secreted by the type III secretion system. In the case of cell E the result is almost same, but the outcome is due to a toxin secreted by V. cholerae. FA, fatty acid.

GIF animation showing the synthesis of peptidoglycan.
GIF animation illustrating how penicillins inhibit peptidoglycan synthesis.
GIF animation illustrating how vancomycin inhibit peptidoglycan synthesis.
Flash animation of a normal bacterial enzyme reaction.
Flash animation illustrating how antimicrobial agents may inactivate a bacterial enzyme.
Flash animation illustrating the early stages of translation during bacterial protein synthesis.
Flash animation illustrating aminoglycosides preventing the translocation of tRNA from the A-site to the P-site of bacterial ribosomes.
Flash animation illustrating aminoglycosides causing a misreading of codons.
Flash animation illustrating how tetracyclines bind to the 30S ribosomal subunit and block translation.
Flash animation illustrating how macrolides bind to the 50S ribosomal subunit and block translation by blocking peptidyltransferase.
Flash animation illustrating how macrolides bind to the 50S ribosomal subunit and block translation by preventing the transfer of the peptidyl tRNA from the A-site to the P-site.
Flash animation illustrating how oxazolidinones block the binding of the 50S ribosomal subunit to the initiation complex.

Flash animation showing a motile bacterium contacting a host cell by swimming through the mucus.
Flash animation showing spirochetes using motility to enter and exit blood vessels.
GIF animation showing induction of stomach ulcers by Helicobacter pylori.
Flash animation showing a bacterium using both pili and adhesins to adhere to a host cell.
GIF animation showing bacteria lacking pili being flushed out of the urethra.
GIF animation showing how bacteria with pili may resist being flushed out of the urethra.
Flash animation showing bacteria using invasions to enter a hoist cell
Gif animation of Shigella invading an intestinal mucosal epithelial cell.
Flash animation illustrating the function of endocytic pattern-recognition receptors on phagocytes.
Flash animation summarizing phagocytosis through unenhanced attachment.
Flash animation illustrating the function of enhanced attachment by way of IgG.
Flash animation summarizing phagocytosis through enhanced attachment.
Flash animation illustrating how capsules can block unenhanced attachment of pathogen-associated molecular patterns to endocytic pattern-recognition receptors on phagocytes.
Flash animation showing phagocytosis of an encapsulated bacterium through opsonization.
Flash animation showing an encapsulated bacterium resisting phagocytosis by blocking C3b.
GIF animation showing bacteria depolymerizing actin in order to resist phagocytosis.
GIF animation showing a bacterium resisting phagocytosis by escaping from a phagosome.
GIF animation showing a bacterium resisting phagocytosis by blocking the fusion of a lysosome and a phagosome.
Flash animation of a capillary prior to vasodilation.
Flash animation of vasodilation.
Flash animation showing toll-like receptors responding to lipoteichoic acid(LTA) from the gram-positive cell wall and signaling the synthesis inflammatory cytokines.
Flash animation showing toll-like receptors responding to lipopolysaccharide (LPS) from the gram-negative cell wall and signaling the synthesis inflammatory cytokines.
Flash animation showing binding of lipopolysaccharide (LPS) and chemokines to neutrophils triggering extracellular killing.
Flash animation showing binding of teichoic acids (TA) and chemokines to neutrophils triggering extracellular killing.
GIF animation of an A-B toxin binding to and penetrating a susceptible host cell.
Flash animation showing neutralization of an exotoxin by antibodies.