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Neisseria info
Gram-negative cocci, often diplococci, that use type IV pili for twitching motility and are naturally competent.
Neisseria disease
causes meningitis or gonorrhea
Neisseria human impact
major public health importance, resistant + reproductive complications
Neisseria function
depends on pili, Opa proteins, LOS, complement evasion, and extensive phase and antigenic variation. Invasive meningococci usually have a capsule, while gonococci rely heavily on surface variation and immune evasion
Neisseria host rxn
inflammation and mucosal immune activation, though immune evasion strategies can make reinfection and persistence easier
Neisseria paper
examined how commensal Neisseria release peptidoglycan fragments and how those fragments affect host immune sensing
Neisseria big question
how different Neisseria strains release peptidoglycan fragments and how those fragments influence NOD1/NOD2 activation
Neisseria solution
authors used metabolic labeling, chromatography, scintillation counting, and reporter assays to compare the inflammatory cell wall products released by different strains.
mycobacterium info
acid-fast, slow-growing intracellular bacteria with mycolic acid-rich cell walls.
mycobacterium disease
causes leprosy, a chronic infection w/ nerve and skin damage and tuberculosis, major global infectious killer
mycobacterium human impact
causes long term disease + requires special immune control
myco function
Mycobacterium tuberculosis survives in macrophages, blocks phagosome-lysosome fusion, uses lipids such as PDIM and PGL, and relies on factors like ESX-1 instead of classic toxins. Granuloma formation is a key feature of TB pathogenesis
myco host rxn
macrophage activation, T-cell responses, granuloma formation, and long-term latent infection
myco paper
whether bacteriophages can enter mammalian cells and kill intracellular mycobacteria
myco big question
whether phages can enter mammalian cells and reduce intracellular mycobacterial burden
myco solution
authors used fluorescence microscopy, reporter phages, electron microscopy, and intracellular burden assays to show that phages can access intracellular bacteria
bacteriophage info
viruses that infect bacteria. They can follow lytic or lysogenic life cycles
bacteriophage disease
bacteriophage function
Lytic phages kill bacteria directly, while lysogenic phages can persist in the host genome. Host range depends on receptor recognition, and bacteria counter phages using restriction systems, CRISPR-Cas, and other defenses
bacteriophage human impact
bacteriophage host rxn
bacteriophage paper
phage communication during lysogeny
bacteriophage big question
whether lysogens continue to communicate using arbitrium and use that signal to regulate exit from lysogeny
bacteriophage solution
authors used gene-expression assays, signaling perturbation, DNA-damage induction, and reporter systems to show that lysogens continue to signal and that the signal represses induction when lysogens are abundant
microbiome info
community of microorganisms, helps maintain a healthy state, supports colonization resistance & affects immunity, mucosal barriers + inflammation
microbiome disease
gastrointestinal disease, inflammation, bacterial vaginosis + increase for infection
possible obesity, diabetes, colorectal cancer, crohns disease + gastroenteritis
microbiome human impact
broad because it influences colonization resistance, barrier function, metabolism, and immune education
microbiome function
competing for nutrients and niches, producing metabolites such as short-chain fatty acids, supporting mucin and barrier function, and shaping host defenses like antimicrobial peptides and IgA
microbiome host rxn
tightly linked to microbiome state: a healthy microbiome supports homeostasis, while disturbed communities can contribute to inflammation and infection susceptibility
microbiome paper
asked whether a major gut commensal changes Shigella virulence
microbiome big question
whether Bacteroides thetaiotaomicron can directly change Shigella virulence
microbiome solution
authors used conditioned medium, invasion assays, plaque assays, protein detection, gene-expression assays, and fractionation to show that outer membrane vesicles from B. thetaiotaomicron repress Shigella virulence