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. 2024 May 30;12:1379714. doi: 10.3389/fcell.2024.1379714

TABLE 2.

Summary of the ultrastructural lesions identified in human CD and UC.

Tissue Lesions in CD Lesions in UC
Luminal epithelium • Focal loss of the epithelium (Dvorak and Dickersin, 1979; Dvorak et al., 1979; Marin et al., 1983) • Focal loss of the epithelium (Delpre et al., 1989)
• Increased mucus secretion (Dvorak and Dickersin, 1979; Dvorak et al., 1979; Bertini et al., 1998) • Reduction in the number of crypts and crypt openings (Shields et al., 1985; Bertini et al., 1998)
• Glycocalyx reduction or loss (Bertini et al., 1998) • Crypt lesions (deformation, furrows, atrophy, and/or distorted and dilated openings) (Shields et al., 1985; Bertini et al., 1998; Fratila and Craciun, 2010)
• Crypt opening dilatation (Marin et al., 1983) • Increase in the number of undifferentiated, immature cells (Mughal and Filipe, 1992)
• Microulcerations (1–6 cells in diameter) (Marin et al., 1983) • Enterocytes
• Increase in the number of undifferentiated, immature cells (Mughal and Filipe, 1992) - Distortion and loss of hexagonal shape (Kavin et al., 1970; Shields et al., 1985)
• Enterocytes - Microvillus alterations (shortening, enlargement, and vacuolization) or loss (Myllarniemi and Nickels, 1980; Delpre et al., 1989; Mughal and Filipe, 1992; Bertini et al., 1998; Fratila and Craciun, 2010)
- Cell bridging or building (Marin et al., 1983; Nyhlin and Stenling, 1984; Nagel et al., 1995) - Hyperplasia and/or hypertrophy (Shields et al., 1985; Mughal and Filipe, 1992; Bertini et al., 1998)
- Loss of hexagonal shape (Myllarniemi and Nickels, 1980; Marin et al., 1983; Nyhlin and Stenling, 1984) - Large apical lysosomes (Bertini et al., 1998), cytoplasmic vacuolization (Delpre et al., 1989; Fratila and Craciun, 2010), and/or increase in the number of electron-dense vesicles (Mughal and Filipe, 1992)
- Tight junction fragmentation or loss (Marin et al., 1983) - ER swelling (Delpre et al., 1989)
- Microvillus alterations (shortening, thickening, enlargement, and fusion) or loss (Dvorak and Dickersin, 1979, 1980; Dvorak et al., 1979; Rickert and Carter, 1980; Marin et al., 1983; Nyhlin and Stenling, 1984; Nagel et al., 1995; Bertini et al., 1998) - Golgi zone swelling (Delpre et al., 1989)
- Abnormal small electron-dense, microvillus- and desmosome-associated bodies (Lewis et al., 1984) - Irregular, pycnotic nuclei (Mughal and Filipe, 1992; Fratila and Craciun, 2010) with a loosely arranged nuclear membrane (Mughal and Filipe, 1992)
- Increase in the number of electron-dense lysosomal granules (Ranlov et al., 1972; Dvorak and Dickersin, 1980; Thyberg et al., 1981; Marin et al., 1983) - Mitochondrial alterations (swelling with disarranged cristae) (Delpre et al., 1989; Fratila and Craciun, 2010)
- Mitochondrial lesions or pleomorphy (swelling with disarranged cristae) (Ranlov et al., 1972; Mughal and Filipe, 1992; Nazli et al., 2004) - Pseudopod-like extensions of the cell membrane (Delpre et al., 1989)
- ER swelling (Ranlov et al., 1972) - Dilation of the intercellular space (Delpre et al., 1989)
- Nuclei with a loosely arranged nuclear membrane (Mughal and Filipe, 1992) • Goblet cells
• Goblet cells - Hypoplasia (Kavin et al., 1970; Myllarniemi and Nickels, 1980; Bertini et al., 1998; Fratila and Craciun, 2010) or hyperplasia (Mughal and Filipe, 1992)
- Orifice dilation (Dvorak and Dickersin, 1979; Dvorak et al., 1979; Marin et al., 1983) - ER swelling (Fratila and Craciun, 2010)
- Hyperplasia and/or hypertrophy (Dvorak et al., 1979; Myllarniemi and Nickels, 1980; Marin et al., 1983; Nagel et al., 1995) - Heterogeneity (Mughal and Filipe, 1992) and decrease (Delpre et al., 1989) of mucin droplets
- Immature mucigenic granules (Dvorak and Dickersin, 1980)
- Abnormal small electron-dense, microvillus- and desmosome-associated bodies (Lewis et al., 1984)
• Paneth cells
- Irregular lysosomal inclusions/increased granule formation in Golgi areas (Dvorak and Dickersin, 1980)
- Hyperplasia (Dvorak and Dickersin, 1980)
Connective tissue and vasculature • Extracellular edema with marked infiltrates of inflammatory cells (Ranlov et al., 1972; Thyberg et al., 1981; Brewer et al., 1990) • Marked infiltrates of inflammatory cells (Delpre et al., 1989; Brewer et al., 1990)
• Activated fibroblasts and extracellular fibrin deposition (Ranlov et al., 1972) • Lymphatics
• Fragmented or irregularly arranged collagen (Dvorak et al., 1980b) - Intracellular edema in endothelial cells (Aluwihare, 1971)
• Lymphatics
- Distension (Dvorak et al., 1980a)
- Large inter-endothelial gaps (Dvorak et al., 1980a)
• Arterioles and arteries
- Intimal proliferation (Dvorak et al., 1980a)
- Fragmented elastic tissue (Dvorak et al., 1980a)
- Increased adventitial collagen (Dvorak et al., 1980a)
• Capillaries
- Endothelial swelling (Brewer et al., 1990)
• Venules
- Lumen filled with platelets and fibrin strands (Dvorak et al., 1980a)
- Focal endothelial necrosis (Dvorak et al., 1980a)
- Endothelial cells and pericytes with non-membrane-bound lipid bodies (Dvorak et al., 1980a)
- Basal lamina reduplications
• Macrophages
- Increase in the number of electron-dense lysosomal granules (Thyberg et al., 1981)
• Mast cells
- Granule alterations (size, number, and density/degranulation) (Dvorak et al., 1980a; Wang et al., 2007)
- Elongated surface villi (Dvorak et al., 1980a)
• Basophils
- Degranulation (Dvorak et al., 1980a)
• Eosinophils
- Granule alterations (size, number, and density) (Dvorak et al., 1980a)
• Lymphocytes
- Prominent nucleoli (Aluwihare, 1971)
• Lymphoid cells
- Poly-ribosomal structures (Ranlov et al., 1972)
- Golgi zone enlargement (Ranlov et al., 1972)
Musculature • Smooth muscle cells • Interstitial cells of Cajal
- Hyperplasia and/or hypertrophy (Dvorak et al., 1980b) - Lipid droplets (Rumessen, 1996; Rumessen et al., 2010)
- Necrosis (Dvorak et al., 1980b) - Disrupted glycogen vacuoles (Rumessen, 1996) and irregular vacuoles (Rumessen et al., 2010)
- Cytoplasmic vacuoles with collagen fibers or lipids (Dvorak et al., 1980b)
- Hypercontraction (Dvorak et al., 1980b)
- Myofibroblastic transformation (Dvorak et al., 1980b)
• Stellate cells
- Dilated Golgi area (Dvorak et al., 1980b)
- Increase in the rough ER (Dvorak et al., 1980b)
• Interstitial cells of Cajal
- Secondary lysosomes and vacuolization (Wang et al., 2007; Rumessen et al., 2011)
- Disrupted vacuoles associated with the rough ER and glycogen clumps (Rumessen et al., 2011)
- Mitochondrial swelling or loss (Wang et al., 2007)
- Lipid droplets (Wang et al., 2007)
- Cytoplasmic filament reduction or loss (Wang et al., 2007)
- Perinuclear damage (Wang et al., 2007)
Autonomic nervous system • Nerve trunk enlargement and distortion (Dvorak et al., 1980b) • Axons
• Axons - Damage (myelin figures, microtubule reduction, and terminal swelling) or necrosis (swollen and empty axons) (Brewer et al., 1990; Dvorak et al., 1993; Rumessen, 1996; Geboes and Collins, 1998; Rumessen et al., 2010)
- Damage (myelin figures, microtubule reduction, terminal swelling, and lipid droplets) or necrosis (swollen, empty axons) (Dvorak et al., 1980b; Dvorak and Silen, 1985; Steinhoff et al., 1988; Brewer et al., 1990; Dvorak et al., 1993; Geboes and Collins, 1998; Wang et al., 2007; Rumessen et al., 2011)
- Mitochondrial swelling (Dvorak et al., 1980b)
- Large membrane-bound vacuoles (Dvorak et al., 1980b)
- Dense core granules (Dvorak et al., 1980a)
- Neurofibril accumulation (Dvorak et al., 1980b)
• Synaptic membrane thickening (Dvorak et al., 1980b)
• Ganglion cell enlargement with an increase in the rough ER (Dvorak et al., 1980b)