Literature / Library / pneumocyte

pneumocyte

Real pictures of the pneumocyte delivered by gather.site, each with its paper.

13 pictures and 9 papers.

Gallery

(D) Representative transmission electron microscopy (TEM) images of monocystic alveolosphere. Microvilli (MVs) observed in spheres at the apical lumen. Mitochondria (MT) displayed with blue arrow heads. A monocystic organoid from fibrotic origin displays accumulations of numerous lamellar bodies on ultrastructural level (LB, black). Black window shows intracellular LBs, while yellow and green window display extracellular LBs. High magnification images in TEM show single AT-II cell from a monocystic organoid. NC (white), MV (red arrow heads), MT (blue arrow heads) and LB (black). Scale bar = 5 µm. (E) Details of a single AT-II cell within a monocystic alveolosphere. Scale bar = 5 µm. Presence of NC, MTs, LBs and MVs. (human (primary AT-II alveolar type II cells from lung organoids); Fig. 5, panels D-E (TEM of primary human AT-II alveolosphere; rows 540-1115 of figure).)

Schröder, Rückoldt, Schubert et al 2026, Respiratory Research · CC BY 4.0

Representative immunofluorescence labeling of AT2 marker pro-SPC (green), Hu-Mitochondria (red/MAB1273), Hu-LAMP3, AGER, and Hu-PDPN in transplanted P2-4 hALOs (panels B, upper) and P12-14 hALOs (panels C, lower). Micrographs shown at 20x and 40x with negative controls. Scale bars, 100 um (20x panels), 50 um (40x panels). (human (iPSC-derived alveolar organoids in mouse lung); Figure 4, panels B and C (confocal IF micrographs; schematic panel A and dot-plot panel D excluded; rows 104-571 of full figure).)

Li, Liu, Liu et al 2025, International Journal of Biological Sciences · CC BY 4.0

Histopathological analysis of lung sections of K18-hACE2 mice inoculated with PBS (A) and infected with SARS-CoV-2 (B-F). (A) A: Alveoli; AS: Alveolar sac; B: Bronchiole. Comparatively, note the difference between the alveolar architecture of non-infected and infected mice, particularly concerning the thickening of the alveolar septa in the infected group. (B) IP: Interstitial pneumonia; DS: Dead spaces; HI: Hyperinflation. (C) IC: Inflammatory cuffing; IP: Interstitial pneumonia; V: Vasculitis. (D) BS: Blood stasis; (E) BS: Blood stasis; H: Hemorrhage; (F) E: Edema. Bar: (A-E): 100 um, (F): 50 um. (mouse (K18-hACE2, PBS control and SARS-CoV-2 infected lung sections); Figure 1.)

de Almeida, da Silva, Souza et al 2026, Microorganisms · CC BY 4.0

Distal airway epithelial cells can survive infection by Mal04 and be identified using scRNA-seq. A) Confocal microscopy of the 3dpi lung section infected with Mal04-mNeon (green) and stained with Hoescht 33342 (blue) and ZO-1 (white) to define cell boundaries. B) Confocal microscopy of 14 dpi lung section infected with Mal04-Cre (red) and stained with Hoescht 33342 (blue) and ZO-1 (white). C) Diagram of 10x sc-RNA seq experiment cell collection and processing (n = 8, 2 mice were pooled for each time point). D) Representative flow cytometry of survivor cells collected at the indicated time points following Mal04-Cre infection in Cre-inducible tdTomato reporter mice. E) UMAP dimensionality reduction plot showing all epithelial cells sequenced. Clusters were identified using specific cell type markers. F) Dot plot displaying the expression of specific cell type markers used to determine cell type clusters in FIG. 1E. G) Feature plots of genes displayed in FIG. 1F. Clusters are colored based on their cell type determined by the expression of specific cell type markers. All scale bars = 100 um. (Fig 1.)

Nakano, Hamele, Tata et al 2024, mBio · CC BY 4.0

Ultrastructural analysis of lung sections of K18-hACE2 mice inoculated with PBS (A) and infected with SARS-CoV-2 (B-F). (A) A: Alveoli; AS: Alveolar sac; PI: Type I pneumocyte; RBC: Red blood cell; S: Alveolar septa. (B) C: Collagen; CD: Cellular debris; CR: Cytoplasmic rarefaction; F: Fibroblast; HPII: Hypertrophic type II pneumocyte; MC: Mononuclear inflammatory cell; P: Platelet; PII: Type II pneumocyte. (C) AC: Alveolar compression; P: Platelet; VC: Vascular congestion. (D) CD: Cellular debris; ED: Epithelial cell desquamation; PII: Type II pneumocyte; VT: Vesicle trafficking. (E) M: Macrophage; CP: Cytoplasmic protrusion; P: Platelet. (F) BM: Basal membrane thickening; C: Collagen; CP: Cytoplasmic protrusion; CR: Cytoplasmic rarefaction; LD: Lamellar bodies degeneration of type II pneumocyte; VT: Vesicle trafficking. Bar: (A-E) 5 um, (F) 2 um. (mouse (K18-hACE2 transgenic mice expressing human ACE2 under K18 promoter); Figure 4.)

de Almeida, da Silva, Souza et al 2026, Microorganisms · CC BY 4.0

Isolation, culture, and characterization of yak primary AT2 cells. ( A ) Morphological characterization of primary yak AT2 cells following 72 h of in vitro cultivation. ( B ) The cultured AT2 cells exhibited a cobblestone-like morphology on the 6th day. ( C , D ) Identification of AT2 cells was performed using transmission electron microscopy. The thick red arrows indicate the microvilli on the surface of AT2 cells, while the thin red arrows indicate osmiophilic multilamellar bodies. ( E ) AT2 cells were identified through immunofluorescence detection, visualizing the presence of the AT2-marker protein SPC while simultaneously confirming the absence of the AT1-marker protein Aqp5. The nucleus was stained blue with DAPI. ( F ) The presence of EGF and EGFR in AT2 cells was ascertained through immunofluorescence staining. The nucleus was stained blue with DAPI. (Figure 1.)

Wang, Zhang, Cui et al 2026, Cells · CC BY 4.0

Morphological, ultrastructural, and barrier function characterization of the multi-lineage lung model (LM). (a) Schematic workflow of differentiation from lung progenitors to the multi-lineage model and characterization. (b) Bright-field images and H&E-stained longitudinal sections of day-27 models. Red arrow: duct-like lumina; yellow arrow: alveolus-like cavities; B: basal layer; U: upper layer. Bright-field scale bar: 200 um; H&E scale bars: left 50 um, right 10 um. (c) Scanning electron microscopy (SEM) images showing surface topography and cellular diversity. (i-iv) Overall surface morphology of the model; (v) branched ridges and undulating textures; (vi) surface spherical cell clusters and microvilli-like protrusions; (vii) pore-like cavities; (viii) cells with ciliary structures; (ix) spindle-shaped cells and interwoven fibrous network; (x) cells with surface undulating membrane ruffling characteristics. Arrows: microvilli-like protrusions (vi), pore-like cavities (vii), cilia (viii), fibroblasts (ix), membrane ruffling (x); C: spherical cell clusters. Scale bars: 200, 100, 50, 20, 50, 30, 30, 10, 10, and 10 um, respectively. (d) Transmission electron microscopy (TEM) images. Arrows: microvilli (i), tight junctions, cilia (iii); scale bars: 2, 1, and 1 um, respectively. (e) ZO-1 immunofluorescence staining. Scale bar: 50 um. (FIGURE 2.)

Hua, Qu, Yang et al 2026, Frontiers in Cell and Developmental Biology · CC BY 4.0

Impaired branching morphogenesis and surfactant production in Sri-/- mice lungs. (A) E13.5 lung tissue: Embryonic Sri-/- mice show significantly decreased expression of branching morphogenesis genes (Fgf10, Sox9), compared to WT mice. Surfactant genes (Sp-b, Sp-c) exhibit no significant difference between the two groups at this stage. (B) 3-week-old lung tissue: significantly reduced expression of surfactant genes (Sp-b, Sp-c), and of the phospholipid transporter Abca3 is observed in Sri-/- mice compared to WT controls. Data are presented as mean +/- SEM. *p < 0.05; **p < 0.01; ***p < 0.001 (determined by Student's t-test). (C) Oil Red O staining of lung sections from 3-week-old WT and Sri-/- mice: Sri-/- mice exhibit decreased lipid droplet accumulation, indicative of impaired total lipid surfactant content, compared to WT. Scale bars, 20 and 50 um. (D) Quantification of lipid droplets from Oil Red O stained sections. Data are presented as mean +/- SEM. ***p < 0.001 (Student's t-test). (E) Periodic acid-Schiff (PAS) staining of lung sections from 3-week-old WT and Sri-/- mice. Sri-/- mice show increased glycogen staining, indicative of pneumocyte immaturity, compared to WT. Scale bars, 50 um. (Fig. 2.)

Tito, De Angelis, Iaiza et al 2025, Cellular and Molecular Life Sciences · CC BY 4.0

Z-AAT polymers accumulation in alveolar type-2 epithelial cells is associated with mitochondria dysfunction in Z-AAT Serpina1 Null mice and AATD lung. ( A ) Representative TEM images of in situ murine AT2 of Z-AAT Serpina1 Null , Serpina1 Null and WT mice; scale bar: 2 um. Note higher numbers of fused mitochondria (white arrows head), but unchanged number of surfactant-containing lamellar bodies (black star) in greater than 12-month-old Z-AAT Serpina1 Null versus normal mitochondria (white arrow) Serpina1 Null and WT mice. ( B ) Number of mitochondria per AT2 cell quantified by manual counting of 5 different TEM images per mouse. ( C and D ) Quantification of Mitofusin 2 (red) and pro-SPC (green) and representative immunofluorescence in lungs of 7-month-old Z-AAT Serpina1 Null , Serpina1 Null and WT mice. Colocalization Mitofusin 2 and pro-SPC (yellow) and quantified by ImageJ analysis of 5 different fields /slide from 3 different mice / genotype. Scale bar: 100 um. ( E ) Representative immunofluorescence images of healthy, never smoker and AATD lungs stained for Mitofusin 2 (red, mitochondrial marker), HTII-280 (green), and DAPI (nuclei); scale bar: 100 um. (mouse (Z-AAT Serpina1 Null, Serpina1 Null, and WT murine AT2 cells); human (healthy, never smoker, and AATD lung tissue); Figure 5.)

Magallon Serrano, Khodayari, Bowers et al 2026, JCI Insight · CC BY 4.0

Areg activates EGFR and accelerates AT2 proliferation and differentiation. (A) Immunofluorescence staining of 2D-cultured AT2 cells treated with recombinant AREG and collected at days 3, 5, and 7. GFP marks lineage-labeled AT2-derived cells. Left panels show staining for the AT1 marker PDPN and the AT2 marker pro-SPC. Right panels show staining for the transitional AT2 (PATS) marker Krt8 and phosphorylated EGFR (p-EGFR), indicating EGFR pathway activation. Scale bars, 50 um. (B-E) Quantification of marker expression corresponding to (A): (B) pro-SPC (AT2 marker), (C) PDPN (AT1 marker), (D) Krt8 (transitional AT2/PATS marker), (E) p-EGFR (EGFR pathway activation). All values are presented as mean +/-SD; *p < 0.05, **p < 0.01, ***p < 0.001; nonsignificant (NS) (unpaired, two-tailed Student's t-test). (F) Immunofluorescence staining of lung sections on day 14 after bleomycin injury. EdU (red) labels proliferating cells, p-EGFR (white) marks EGFR activation, and Traced (green) indicates lineage-labeled AT2 cells. (G-I) Immunofluorescence staining and quantification of p-EGFR (red), p-mTOR (red), and p-AKT (red) activation in transitional AT2 cells (Krt8+, green) following bleomycin injury. Traced (white) marks lineage-labeled cells. Scale bars, 50 um. Data are presented as mean +/-SD from n = 4 mice per group; analyzed by Two-tailed unpaired Student's t test, *P < 0.05. (mouse (lineage-traced Alkbh5 conditional knockout and control AT2 cells; 2D culture and bleomycin lung injury model); Figure 5.)

Lv J et al. 2026, International journal of biological scie · CC BY 4.0

Papers

Hua C, Qu C, Yang L, Zhao W, Zhao J, Jia Y, et al. An hiPSC-derived multi-lineage lung model exhibiting proximal-distal epithelial features for modeling pulmonary fibrosis. Front Cell Dev Biol. 2026;14:1914941. PMID: 42712523.
Magallón Serrano M, Khodayari N, Bowers W, Manning EP, Liu X, Lee J, et al. Polymerized Z-α-1 antitrypsin leads to lung injury in a murine model of emphysema. JCI Insight. 2026;11:e199029. PMID: 42579796.
Lv J, Chen K, Wang X, Liu Y, Li L, Chen S, et al. Loss of Alkbh5 enhances AT2 cell differentiation and alveolar repair across diverse injury models via m6A-dependent Areg signaling. Int J Biol Sci. 2026;22:6465-6482. PMID: 42524630.
Wang B, Zhang X, Cui Y, He J, Yu S, Zhang Q, et al. EGF and EGFR Facilitate Alveolar Development by Promoting the Proliferation of Alveolar Type II Cells in the Yak (Bos grunniens). Cells. 2026;15:1167. PMID: 42439644.
de Almeida ALT, da Silva AMV, Souza MME, Rodrigues MPMD, Coelho FS, da Rosa LC, et al. SARS-CoV-2 Effects on Respiratory and Neurological Systems: Morphological Findings and Gene Expression in K18-hACE2 Mice Model. Microorganisms. 2026;14:852. PMID: 42075250.
Schröder LJ, Rückoldt J, Schubert S, Knudsen L, Janciauskiene SM, Werlein C, et al. Optimized culture of primary human alveolar type II cell-derived 3D organoids from fibrotic lung tissue with phenotypic and metabolic profiling. Respir Res. 2026;27:164. PMID: 41792753.
Li L, Liu Y, Liu L, Zhao S, Feng J, Zhou J, et al. Human Pluripotent Stem Cell-Derived Alveolar Organoids for Gene-editing and Lung Adenocarcinomas Modeling. Int J Biol Sci. 2025;21:6285-6304. PMID: 41208901.
Tito C, De Angelis L, Iaiza A, Abbinantefina AP, Benedetti A, Mazzanti G, et al. Sorcin regulates alveolarization and airway tissue remodeling during lung morphogenesis. Cell Mol Life Sci. 2025;82:367. PMID: 41148307.
Nakano S, Hamele CE, Tata A, Tata PR, Heaton NS. Influenza B virus infection alters the regenerative potential of murine alveolar type 2 pneumocytes. mBio. 2025;16:e0274324. PMID: 39745393.