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NORMAL GIT, Innate lymphoid cells (ILCs) - Coggle Diagram

- - - - broken down by amylase in saliva to lactose, maltose and sucrose
        
        disaccharidases (lactase, maltase, sucrase) in brush border of SI break them all down into glucose (as well as lactose to galactose, sucrose to fructose)
        
        glucose, galactose absorbed via SGLT using energy of Na+ gradient
        
        Facilitated diffusion through GLUT2 out of epithelial cell
        
        fructose diffuses via GLUT5 through apical membrane
    - - there are dietary and endogenous proteins (digestive enzymes, mucosal turnover, leaking plasma proteins)
        
        broken down by pepsin in stomach to amino acids
        
        amino acids transported into epithelial cell by cotransporter (small peptides by H+ cotransporters)
        
        small peptides broken down into amino acids by intracellular peptidases in lysosomes
        
        amino acids enter circulation by facilitated diffusion
    - - triglycerides emulsified by bile salts into fat droplets
        
        pancreatic lipase breaks down into monoglycerides and FFAs
        
        bile salts form micelles (water-soluble)
        
        passively diffuse into epithelial cells
        
        resynthesised into triglycerides coated in layer of lipoprotein to form chylomicrons
        
        chylomicrons diffuse into lymph
        
        1 more item...
        
        bile salts reabsorbed in terminal ileum by special active transport
    - - heme iron
        
        enters via heme transporter
        
        converted by oxygenase to ferrous iron
      - ferrous iron
        
        enters via DMT1
        
        ferrous iron leaves via ferroportin 1
    - - water-soluble
        
        passive diffusion with water or via carriers
        
        vitamin B12 must be with IF to be absorbed via receptor-mediated endocytosis
      - fat-soluble
        
        included in micelles
    - - passive diffusion
      - transport via TRPV6 channels
        
        leaves via PMCA1b or exocytosis
  - - - submucosal plexus
        
        mainly influences secretory epithelium and vasculature
      - myenteric plexus
        
        mainly influences smooth muscle (located between inner circular and outer longitudinal layers)
      - distension activates enterochromaffin cells
        
        secrete 5-HT
        
        acts via 5-HT4 receptor to activate interneurons
        
        secrete excitatory neurotransmitters e.g. ACh/substance P rostrally and inhibitory hormones e.g. NO, VIP caudally
        
        contraction proximally and relaxation distally
        
        peristaltic reflex
      - parasympathetic input from vagus nerve (oesophagus to ascending colon) and pelvic splanchnics (distal colon/rectum)
        
        main neurotransmitter: ACh
      - sympathetic input from thoracolumbar spinal cord
        
        main neurotransmitter: NA
- - - - secrete mucin
    - - sense parasites
        
        secrete IL-25
        
        stimulates ILC2 and Th2 response
        
        ILC2 drives helminth expulsion
        
        IL-13
        
        tuft and goblet cell expansion
        
        1 more item...
        
        IL-5
        
        activates eosinophils to degrade outer integument of helminth
        
        AREG
        
        drives epithelial differentiation/proliferation
    - - secrete antimicrobial peptides (AMPs)
        
        α-defensins, lysozyme C, REGIII
    - - sample luminal antigens and transport across epithelium (do not process)
        
        deliver to DCs
        
        Dendritic cells take up antigens from M cells or directly from lumen
        
        sample/process antigens to present to T cells in Peyer's patches, lymphoid follicles and lymph nodes
        
        induce protective T cell and Treg responses
        
        T cells
        
        3 more items...
    - - recognise PAMPs
        
        cytokines
        
        immune cell migration/differentiation
        
        T-independent IgA class switching/IgA release
        
        IgA-producing B cells in lamina propria
        
        produce dimeric IgA (bound to poly-Ig receptor)
        
        transported into lumen by transcytosis
        
        1 more item...
  - - - Peyer's patches not encapsulated like nodes, antigens deliver directly via M cells without lymphatics
      - Peyer's patches B:T cell ratio 5x greater than lymph nodes
  - - - tolerogenic DCs
        
        IL-10
        
        TLR2
      - CD4+CD25+ Treg cells
        
        dampened immune response
- - - - increases solubility to maximise function by preventing passive reabsorption in SI
      - rate limiting step: catalysis by cholesterol-7α-hydroxylase and CYP7A1 and CYP8B1
      - +reuptake of bile acids from enterohepatic recirculation via OATP2 and NTCP transporters
        
        secreted by hepatocytes into bile canaliculi (contains large amounts of cholesterol and other organic constituents)
        
        empties into terminal bile ducts, then hepatic duct and common bile duct to empty into duodenum
        
        lined by cholangiocytes
        
        secrete bicarbonate via Cl-/HCO3- exchanger and water
        
        stimulated by secretin or inhibited by somatostatin
        
        reabsorb bile acids, glucose and amino acids
        
        travels through cystic duct to be stored in gallbladder
        
        water and electrolytes (except Ca2+) absorbed
        
        remaining bile constituents concentrated 5-20x
        
        1 more item...
        
        bile salts in GIT
        
        emulsification of dietary fat
        
        increases SA for lipase activity
        
        activate pancreatic cholesterol esterase
        
        catalyses hydrolysis of cholesterol esters
        
        secretion stimulated by secretin, VIP
        
        secretion inhibited by somatostatin, gastrin, dopamine
- - - - converted to biliverdin, then free bilirubin, which is then bound to albumin
        
        absorbed by hepatocytes
        
        ligandin added
        
        glucuronidation
        
        conjugated bilirubin
        
        excreted in bile
        
        1 more item...
        
        bilirubin buildup in ECF causes jaundice
  - - - glycolysis
        
        TCA or ketone bodies
        
        ATP
      - glycogenesis
      - conversion of glucose to fat
        
        acetyl CoA to malonyl CoA
        
        note that fatty acids cannot be converted back to glucose since pyruvate --> acetyl CoA is only irreversible step
      - gluconeogenesis
    - - storage
      - ß-oxidation of fatty acids
        
        acetyl CoA
      - compound synthesis
        
        cholesterol
        
        bile salt formation
        
        lipoproteins (LDL, HDL, VLDL)
        
        important for fat transport
        
        phospholipids
        
        cell membranes and myelin
      - fat synthesis
    - - deamination or transamination of amino acids
        
        generates intermediates of TCA
        
        ammonium generated from deamination
      - synthesis of compounds from amino acids
        
        urea
        
        excreted via kidneys (75%) or intestines
        
        carbohydrates and fats (via deamination)
        
        proteins (via transamination transfer of amino group to alpha-keto acid)
        
        plasma proteins (albumin, clotting factors, transporters)
  - - - synthesis of coagulation factors II, VII, IX, X in liver
      - bone formation
    - - important for DNA and myelin synthesis, and RBC maturation
      - fatty acid and amino acid metabolism
  - - - hepatocytes store iron bound to ferritin
        
        iron release regulated by hepcidin
  - - - CTR1 transports copper into hepatocytes
        
        metallothionein binds copper for storage
        
        ATP7A binds copper to enter trans-Golgi network for incorporation into ceruloplasmin, or excretion via bile
        
        COX17 binds copper to transport to mitochondria to make cytochrome C oxidase
  - - - Phase 1: cytochrome P450 enzymes (makes drug mildly soluble)
        
        Phase 2: conjugation by transferases (makes drug highly soluble)
        
        Phase 3: elimination via urine, plasma, bile
      - 1st pass metabolism
        
        high clearance (dependent on blood flow)
        
        intermediate/low clearance (dependent on intrinsic clearance and protein binding)
- - - - protects barrier