scholarly journals Non-Squamous Epithelial Cell Count

2020 ◽  
Author(s):  
Keyword(s):  
Epithelial Cell ◽  
Cell Count ◽  
Squamous Epithelial Cell

scholarly journals Impact of sex, androgens, and prostate size on C57BL/6J mouse urinary physiology: urethral histology

2020 ◽  
Vol 318 (3) ◽  
pp. F617-F627
Author(s):  
Hannah Ruetten ◽  
Kyle A. Wegner ◽  
Conner L. Kennedy ◽  
Anne Turco ◽  
Helen L. Zhang ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Count ◽  
National Institutes Of Health ◽  
Male Mice ◽  
Male And Female ◽  
Future Studies ◽  
Biological Variable ◽  
Prostate Size ◽  
Hematoxylin And Eosin ◽  
The Impact

The National Institutes of Health leveled new focus on sex as a biological variable with the goal of understanding sex-specific differences in health and physiology. We previously published a functional assessment of the impact of sex, androgens, and prostate size on C57BL/6J mouse urinary physiology (Ruetten H, Wegner KA, Zhang HL, Wang P, Sandhu J, Sandhu S, Mueller B, Wang Z, Macoska J, Peterson RE, Bjorling DE, Ricke WA, Marker PC, Vezina CM. Am J Physiol Renal Physiol 317: F996–F1009, 2019). Here, we measured and compared five characteristics of urethral histology (urethral lumen diameter and area, epithelial cell count, epithelial and rhabdosphincter thickness, epithelial cell area, and total urethral area) in male and female 9-wk-old C57BL/6J mice using hematoxylin and eosin staining. We also compared male mice with castrated male mice, male and female mice treated with the steroid 5α-reductase inhibitor finasteride or testosterone, or male mice harboring alleles ( Pbsn4cre/+; R26RDta/+) that reduce prostate lobe mass. The three methods used to reduce prostate mass (castration, finasteride, and Pbsn4cre/+; R26RDta/+) changed urethral histology, but none feminized male urethral histology (increased urethral epithelial area). Exogenous testosterone caused increased epithelial cell count in intact females but did not masculinize female urethral histology (decrease epithelial area). Our results lay a critical foundation for future studies as we begin to parse out the influence of hormones and cellular morphology on male and female urinary function.

scholarly journals Nasal Colonisation by Staphylococcus aureus Depends upon Clumping Factor B Binding to the Squamous Epithelial Cell Envelope Protein Loricrin

2012 ◽  
Vol 8 (12) ◽  
pp. e1003092 ◽  
Author(s):  
Michelle E. Mulcahy ◽  
Joan A. Geoghegan ◽  
Ian R. Monk ◽  
Kate M. O'Keeffe ◽  
Evelyn J. Walsh ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Epithelial Cell ◽  
Envelope Protein ◽  
Cell Envelope ◽  
Factor B ◽  
Squamous Epithelial Cell ◽  
Clumping Factor B

scholarly journals P027 Epithelial cells of patients with ulcerative colitis do not show an increased sensitivity after microbiota stimulation compared to non-IBD controls

2021 ◽  
Vol 15 (Supplement_1) ◽  
pp. S142-S143
Author(s):  
K Arnauts ◽  
C Lapierre ◽  
B Verstockt ◽  
S Verstockt ◽  
P Sudhakar ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Count ◽  
Rna Sequencing ◽  
Principal Component ◽  
Cell Permeability ◽  
Patient Specific ◽  
P Value ◽  
Sequencing Data ◽  
Different Response

Abstract Background Alterations in the intestinal microbiota play a pivotal role in the pathogenesis of Inflammatory Bowel Diseases (IBD). Although there is a lot of interest in restoring dysbiosis, the effects of microbial alterations are not fully understood. In addition, it is known that epithelial cells from IBD patients maintain intrinsic defects1. For that reason, our aim was to unravel if epithelial cells of UC patients are more sensitive towards microbiota stimulation, compared to non-IBD controls. Methods Intestinal organoids of UC patients (n=8) and non-IBD controls (n=8) were grown as monolayers on Transwell inserts. Upon confluency (evaluated by transepithelial electrical resistance (TEER)), monolayers were stimulated for 24 hours with TNF-α (100 ng/ml), IL-1β (20 ng/ml) and Flagellin (1 µg/ml) to mimic inflammation. Fresh fecal samples of a selected donor (n=1, high microbial cell count and presence of selected phyla2) and UC patients (n=3, endoscopic sub-mayo ≥2) were filtered and stored in 0.9% NaCl. Monolayers were stimulated for 6 hours with 3.108 microbial cells (cell count by Flow Cytometry). RNA sequencing was performed by Truseq for Illumina. Differentially expressed genes (DEG) were studied by DESeq2 (FDR <0.05). Results Although TEER measurements indicated a higher epithelial cell permeability upon UC microbiota stimulation in UC patients compared to non-IBD controls (p=0.038; Mann-Whitney; Figure 1), we could not confirm this distinct response based on RNA sequencing data at principal component analysis (PCA). Several epithelial barrier genes were significantly upregulated between UC and non-IBD epithelium at nominal p-value, while only CLDN1 and 18 were significant for FDR <0.05 (Figure 2). Clustering on PCA was driven by microbial treatment and not by epithelial origin (Figure 3). Inflamed monolayers of UC patients showed different baseline characteristics (129 DEG; e.g. HLA-G, MUC2, CLDN1, IL23A, PARP8; Figure 4A), but did not propagate in a different response upon microbiota exposure compared to non-IBD controls. Treatment with microbiota of UC patients (23 DEG; e.g. PARP9, TGFBI, ANXA13) or the selected donor (58 DEG; e.g. CCL5, CLDN18, TGFBI) only induced minor differences between epithelial cell types (Figure 4B). Conclusion We observed no different response in epithelial cells of UC patients towards microbiota stimulation compared to non-IBD epithelial cells on transcriptomic level. Further validation on barrier integrity is needed. We observed no indications that microbial treatment would be less beneficial to UC patients, based on the epithelial cell response. Addition of (patient specific) immune cells will contribute to unraveling host-microbiota interactions in IBD patients. References

The Microvascular Organization of the Gas exchange Organs of the Australian Lungfish, Neoceratodus forsteri (Krefft)

1983 ◽  
Vol 31 (5) ◽  
pp. 651 ◽  
Author(s):  
BJ Gannon ◽  
DJ Randall ◽  
J Browing ◽  
RJG Lester ◽  
LJ Rogers
Keyword(s):  
Epithelial Cell ◽  
Corpus Cavernosum ◽  
Leading Edge ◽  
Ciliary Epithelium ◽  
Microvascular Network ◽  
Squamous Epithelial Cell ◽  
Pillar Cell ◽  
Secondary Lamellae ◽  
General Organization ◽  
Australian Lungfish

The general organization of the gill microvasculature of Neoceratodus is similar to that reported for elasmobranchs. A corpus cavernosum is situated between the afferent filamental artery and afferent lamellar arterioles. The microvascular network of the lamellar blood sheet consists of a series of major channels, curving in concentric arcs from afferent to efferent lamellar arterioles, with minor radial cross-connections between these major channels; the basal lamellar channels are not buried in the filament. The afferent filamental arteries also supply blood to the interbranchial septum, which extends almost to the filament tip. The water-blood barrier of 3-4 �m consists of up to three cells: the surface epithelial cell, the pillar cell flange. plus a frequently interposed interstitial cell; there is a prominent basal lamina immediately external to the pillar cell flange. Adjacent gill secondary lamellae are commonly fused at their free margins near the leading edge into groups of from two to five. The micro-organization of the pseudobranch is in general similar to that of the posterior holobranchs. The lung is divided into a series of air sacs by stout septae which contain large amounts of smooth muscle. The respiratory epithelium is of two types: a squamous epithelium underlain by a dense capillary sheet, and isolated patches of a columnar muco-ciliary epithelium associated with only few capillaries. The air-blood barrier (approximately 3 �m thick) consists of a squamous epithelial cell process and attenuated vesiculated endothelial cell cytoplasm, with two basal laminae and intervening interstitial space situated between these.

scholarly journals Force-Induced Strengthening of the Interaction between Staphylococcus aureus Clumping Factor B and Loricrin

mBio ◽  
2017 ◽  
Vol 8 (6) ◽  
Author(s):  
Pauline Vitry ◽  
Claire Valotteau ◽  
Cécile Feuillie ◽  
Simon Bernard ◽  
David Alsteens ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Epithelial Cell ◽  
Envelope Protein ◽  
Cell Envelope ◽  
Surface Protein ◽  
Binding Mechanism ◽  
Factor B ◽  
Squamous Epithelial Cell ◽  
High Affinity ◽  
Clumping Factor B

ABSTRACT Bacterial pathogens that colonize host surfaces are subjected to physical stresses such as fluid flow and cell surface contacts. How bacteria respond to such mechanical cues is an important yet poorly understood issue. Staphylococcus aureus uses a repertoire of surface proteins to resist shear stress during the colonization of host tissues, but whether their adhesive functions can be modulated by physical forces is not known. Here, we show that the interaction of S. aureus clumping factor B (ClfB) with the squamous epithelial cell envelope protein loricrin is enhanced by mechanical force. We find that ClfB mediates S. aureus adhesion to loricrin through weak and strong molecular interactions both in a laboratory strain and in a clinical isolate. Strong forces (~1,500 pN), among the strongest measured for a receptor-ligand bond, are consistent with a high-affinity “dock, lock, and latch” binding mechanism involving dynamic conformational changes in the adhesin. Notably, we demonstrate that the strength of the ClfB-loricrin bond increases as mechanical force is applied. These findings favor a two-state model whereby bacterial adhesion to loricrin is enhanced through force-induced conformational changes in the ClfB molecule, from a weakly binding folded state to a strongly binding extended state. This force-sensitive mechanism may provide S. aureus with a means to finely tune its adhesive properties during the colonization of host surfaces, helping cells to attach firmly under high shear stress and to detach and spread under low shear stress. IMPORTANCE Staphylococcus aureus colonizes the human skin and the nose and can cause various disorders, including superficial skin lesions and invasive infections. During nasal colonization, the S. aureus surface protein clumping factor B (ClfB) binds to the squamous epithelial cell envelope protein loricrin, but the molecular interactions involved are poorly understood. Here, we unravel the molecular mechanism guiding the ClfB-loricrin interaction. We show that the ClfB-loricrin bond is remarkably strong, consistent with a high-affinity “dock, lock, and latch” binding mechanism. We discover that the ClfB-loricrin interaction is enhanced under tensile loading, thus providing evidence that the function of an S. aureus surface protein can be activated by physical stress. IMPORTANCE Staphylococcus aureus colonizes the human skin and the nose and can cause various disorders, including superficial skin lesions and invasive infections. During nasal colonization, the S. aureus surface protein clumping factor B (ClfB) binds to the squamous epithelial cell envelope protein loricrin, but the molecular interactions involved are poorly understood. Here, we unravel the molecular mechanism guiding the ClfB-loricrin interaction. We show that the ClfB-loricrin bond is remarkably strong, consistent with a high-affinity “dock, lock, and latch” binding mechanism. We discover that the ClfB-loricrin interaction is enhanced under tensile loading, thus providing evidence that the function of an S. aureus surface protein can be activated by physical stress.

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