scholarly journals Selectivity in the transport of spermatozoa to oviductal reservoirs in the menstruating fruit bat, Carollia perspicillata

Reproduction ◽  
2010 ◽  
Vol 140 (5) ◽  
pp. 743-757 ◽  
Author(s):  
John J Rasweiler ◽  
Nilima K Badwaik ◽  
Kiranmayi V Mechineni
Keyword(s):  
Epithelial Cells ◽  
Fine Particulate Matter ◽  
Uterine Cavity ◽  
Elastic Fibers ◽  
Carollia Perspicillata ◽  
Fruit Bat ◽  
Fine Particulate ◽  
Uterine Mucosa ◽  
Luminal Epithelial Cells ◽  
Gain Access

To better document the timing of ovulation and fertilization, female reproductive tracts were collected every 12 h from captive-bred fruit bats (Carollia perspicillata) on days 1–3 postcoitum and examined histologically. This also permitted observations on sperm transport, storage, and disposition. As the animals had previously been sexually segregated, most had been cycling and possessed menstrual uteri at the time of collection. Menstruation is periovulatory in this species. A widespread, headfirst orientation of spermatozoa to the uterine mucosa was observed in specimens apparently collected soon after insemination. Thereafter, however, this relationship was limited in most cases to the area around the entrance of each uterotubal junction (UTJ). A small number of spermatozoa also colonized the UTJs, which functioned as temporary sperm reservoirs on days 1–2. AlthoughC. perspicillatais monovular, no consistent differences were observed between the two oviducts in the pattern of sperm storage and release. Very few sperm were ever observed in the isthmus or ampulla (the site of fertilization). Menstrual debris (including fine particulate matter) and leukocytes present in the uterine cavity in most tracts did not gain access to the UTJ with the spermatozoa. Smooth muscle and abundant elastic fibers in the wall of the intramural UTJ, as well as receptors on its luminal epithelial cells, may play roles in the selective transport of spermatozoa to the fertilization site. While some spermatozoa are phagocytosed in the uterine lumen or by epithelial cells in the UTJ, the fate of most is probably expulsion into the vagina.

scholarly journals Development of a system for the detection of the inflammatory response induced by airborne fine particulate matter in rat tracheal epithelial cells

2020 ◽  
Vol 7 ◽  
pp. 859-866
Author(s):  
Nobuyuki Yamagishi ◽  
Tomoki Yamaguchi ◽  
Takahisa Kuga ◽  
Masanari Taniguchi ◽  
Mohammad Shahriar Khan ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Fine Particulate Matter ◽  
Tracheal Epithelial Cells ◽  
Fine Particulate ◽  
Tracheal Epithelial

scholarly journals Alteration of DNA methylation induced by PM2.5 in human bronchial epithelial cells

2020 ◽  
Vol 9 (4) ◽  
pp. 552-560
Author(s):  
Bingyu Wang ◽  
Runbing Li ◽  
Ying Cai ◽  
Boru Li ◽  
Shuangjian Qin ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Deoxyribonucleic Acid ◽  
Fine Particulate Matter ◽  
Bronchial Epithelial Cells ◽  
Differential Methylation ◽  
Functional Enrichment ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Cancer Pathways ◽  
Fine Particulate

Abstract This current study explored the effects of fine particulate matter (PM2.5) on deoxyribonucleic acid methylation in human bronchial epithelial cells. Human bronchial epithelial cells were exposed to PM2.5 for 24 h after which, deoxyribonucleic acid samples were extracted, and the differences between methylation sites were detected using methylation chips. Subsequent gene ontology functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed for the differential methylation sites. Functional epigenetic modules analysis of the overall differential methylation site interactions was also conducted. A total of 127 differential methylation sites in 89 genes were screened in the PM2.5 10 μg/ml group, of which 55 sites demonstrated increased methylation, with methylation levels decreasing in a further 72 sites. Following an exposure of 50 μg/ml PM2.5, a total of 238 differentially methylated sites were screened in 168 genes, of which methylation levels increased in 127 sites, and decreased in 111. KEGG analysis showed that the top 10 enrichment pathways predominantly involve hepatocellular carcinoma pathways and endometrial cancer pathways, whereas functional epigenetic modules analysis screened eight genes (A2M, IL23A, TPIP6, IL27, MYD88, ILE2B, NLRC4, TNF) with the most interactions. Our results indicate that exposure to PM2.5 for 24 h in human bronchial epithelial cells induces marked changes in deoxyribonucleic acid methylation of multiple genes involved in apoptosis and carcinogenesis pathways, these findings can provide a new direction for further study of PM2.5 carcinogenic biomarkers.

scholarly journals Effects of Fine Particulate Matter onPseudomonas aeruginosaAdhesion and Biofilm FormationIn Vitro

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Seon Hee Woo ◽  
Sang Moog Lee ◽  
Ki Cheol Park ◽  
Gyeong Nam Park ◽  
Byeolnimhee Cho ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Epithelial Cells ◽  
Biofilm Formation ◽  
Protein Concentration ◽  
Fine Particulate Matter ◽  
Surface Hydrophobicity ◽  
Laser Scanning Microscopy ◽  
Confocal Laser ◽  
Bacterial Surface ◽  
Fine Particulate

Respiratory infections ofPseudomonas aeruginosaare a major cause of mortality and morbidity for hospitalized patients. Fine particulate matter (FPM) is known to have interactions with some bacterial infection in the respiratory system. In this report, we investigate the effect of different concentration of FPM onP. aeruginosaattachment and biofilm formation usingin vitrocell culture systems.P. aeruginosawere cultured to form mature biofilms on hydroxyapatite-coated peg and the number of bacteria in the biofilms was enumerated. Morphology of biofilm was imaged with scanning electron microscopy and confocal laser scanning microscopy. Bacterial affinity change to the cell membrane was evaluated with attached colony counting and fluorescence microscopy images. Alteration of bacterial surface hydrophobicity and S100A4 protein concentration were explored as mechanisms ofP. aeruginosaadhesion to human cells. There were a concentration-dependent increase of thickness and surface roughness of biofilm mass.P. aeruginosaadherence to respiratory epithelial cells was increased after FPM treatment. Bacterial surface hydrophobicity and S1000A4 protein concentration were increased with proportionally the dose of FPM in media. FPM in the airway could enhance both the adhesion ofP. aeruginosato epithelial cells and biofilm formation. Bacterial surface hydrophobicity and human cell plasma membrane injury are associated with binding ofP. aeruginosaon airway epithelial cells and biofilm formation.

scholarly journals The Immune Barrier of Porcine Uterine Mucosa Differs Dramatically at Proliferative and Secretory Phases and Could Be Positively Modulated by Colonizing Microbiota

2021 ◽  
Vol 12 ◽  
Author(s):  
Deping Han ◽  
Peng Sun ◽  
Yanxin Hu ◽  
Jing Wang ◽  
Guoying Hua ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cross Talk ◽  
Mucosal Immunity ◽  
Immunoglobulin A ◽  
Uterine Cavity ◽  
Intraepithelial Lymphocytes ◽  
Mucosal Barrier ◽  
Lymphocyte Migration ◽  
Chemokine Signaling ◽  
Uterine Mucosa

Endometrial immune response is highly associated with the homeostatic balance of the uterus and embryo development; however, the underlying molecular regulatory mechanisms are not fully elucidated. Herein, the porcine endometrium showed significant variation in mucosal immunity in proliferative and secretory phases by single-cell RNA sequencing. The loose arrangement and high motility of the uterine epithelium in the proliferative phase gave opportunities for epithelial cells and dendritic cells to cross talk with colonizing microbial community, guiding lymphocyte migration into the mucosal and glandular epithelium. The migrating lymphocytes were primarily NK and CD8+ T cells, which were robustly modulated by the chemokine signaling. In the secretory phase, the significantly strengthened mechanical mucosal barrier and increased immunoglobulin A alleviated the migration of lymphocytes into the epithelium when the neuro-modulation, mineral uptake, and amino acid metabolism were strongly upregulated. The noticeably increased intraepithelial lymphocytes were positively modulated by the bacteria in the uterine cavity. Our findings illustrated that significant mucosal immunity variation in the endometrium in the proliferative and secretory phases was closely related to intraepithelial lymphocyte migration, which could be modulated by the colonizing bacteria after cross talk with epithelial cells with higher expressions of chemokine.

scholarly journals Inhalation of Salvianolic acid B Prevents Fine Particulate Matter-Induced Acute Airway Inflammation and Oxidative Stress by Downregulating the LTR4/MyD88/NLRP3 Pathway

2021 ◽  
Author(s):  
Liucheng Li ◽  
Liandi Kan ◽  
Qiangmin Xie
Keyword(s):  
Epithelial Cells ◽  
Airway Inflammation ◽  
Lung Tissue ◽  
Tumor Necrosis ◽  
Fine Particulate Matter ◽  
Protein Levels ◽  
Fine Particulate ◽  
Tnf Α ◽  
Tgf Β1 ◽  
Necrosis Factor

Abstract Background: Air pollution is a serious threat to human health. Inhaled fine particulate matter (PM2.5) can cause inflammation and oxidation in the airway; however, the mechanisms responsible for this effect have yet to be elucidated and there are no specific drugs that can prevent and treat this condition. In the present study, we investigated the effects and mechanisms underlying the inhalation of salvianolic acid B (SalB) on PM2.5-induced airway inflammation and oxidation.Methods: We used a PM2.5-induced mouse model of airway inflammation and oxidation, along with a human epithelial cell model, to study the action and mechanisms of SalB by histopathology, real-time quantitative polymerase chain reaction, enzyme-linked immunosorbent assays, flow cytometry, and western blotting. Results: SalB treatment markedly inhibited the PM2.5-induced increase in the number of neutrophils and macrophages in bronchoalveolar lavage fluid, improved the infiltration of inflammatory cells in lung tissue, and reduced injury in the alveolar septum. Furthermore, SalB reduced the mRNA and protein levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, keratinocyte (KC), and transforming growth factor (TGF)-β1 in lung tissues, and the protein levels of IL-1β, TNF-α, IL-8, IL-6 and TGF-β1 in human epithelial cells. SalB treatment also significantly reversed the reduction of levels of superoxide dismutase, catalase, glutathione and glutathione peroxidase in lung tissue and reduced the levels of reactive oxygen species in human epithelial cells induced by PM2.5. Furthermore, SalB and the myeloid differentiation primary response 88 (MyD88) inhibitor ST2825, inhibited the expression levels of toll-like receptor 4 (TLR4), MyD88, tumor necrosis factor receptor associated factor 6 (TRAF-6), and NOD-like receptor protein 3 (NLRP3), as well as the phosphorylation of downstream signals extracellular signal regulated kinase 1/2 (Erk1/2) and P38 MAP kinase (P38) in lung tissue and epithelial cells.Conclusion: SalB protects against PM2.5-induced airway inflammation and oxidation in a manner that is associated with the inhibition of the TLR4/MyD88/TRAF-6/NLRP3 pathway and downstream signals ERK1/2 and P38.

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