Distribution of leucocyte populations, and milk composition, in milk fractions of healthy quarters in dairy cows

2005 ◽  
Vol 72 (4) ◽  
pp. 486-492 ◽  
Author(s):  
Hande Sarikaya ◽  
Claudia Werner-Misof ◽  
Melanie Atzkern ◽  
Rupert M Bruckmaier
Keyword(s):  
Dairy Cows ◽  
Cell Types ◽  
Milk Composition ◽  
Polymorphonuclear Neutrophils ◽  
Cell Type ◽  
Maximum Value ◽  
Predominant Cell Type ◽  
Teat Canal ◽  
Main Entrance

The goal of the study was to evaluate the composition of leucocyte populations in different milk fractions as a basis on which to judge their possible role in the immune response in different compartments of the udder. The milk of one healthy quarter of nine dairy cows (SCC/quarter [les ]125000/ml; bacteriologically negative) was removed separately and during the course of milking divided into: cisternal milk (C), alveolar milk 0–25%, 25–50%, 50–75%, 75–100% (A25; A50; A75; A100, respectively) and residual milk (R). Each fraction was analysed for the main constituents, SCC and distribution of leucocyte populations and their viability. The content of fat increased steadily during milking and reached highest values in R. Protein and lactose increased from C to A25, decreased from A25 to A100 and reached their minimum in R. Na and Cl ion levels diminished from C to A25 and thereafter increased from A50 to R. Electrical Conductivity (EC) also decreased from C to A25 but remained similar within the alveolar samples and reached a minimum in R. SCC decreased from C to a minimum in A25 and increased subsequently to a significant maximum in R. Somatic cell viability increased throughout consecutive fractions with a maximum value in R. The ratio of cell populations in the various milk fractions showed a reverse trend of macrophages (M) and polymorphonuclear neutrophils (PMN). M values were highest in C while PMN levels increased to their maximum in the R fraction. The lymphocyte (L) fraction remained similar in C, A25, A50, A75 and R but was higher in A100. Proportions of L, PMN and M were, respectively, 9·3%, 38·2%, 52·3% in C, 10·9%, 64%, 25·1% in A25–A100 and 10·2%, 64·9%, 24·8% in R. Numbers of L, PMN and M in milk showed a similar pattern for all three cell types: high levels in C decreased to a minimum at A25 and increased steadily thereafter to their maxima in R. It is concluded that, for healthy quarters, M, the predominant cell type in C, are located near the teat canal, the main entrance of pathogens. Obviously they are the first immunological barriers for invading pathogens. In contrast, PMN are the most important population in the alveolar compartment. However, each leucocyte fraction had a higher concentration in C than in early alveolar fractions, thus indicating the crucial role of immune defence in the cisternal compartment.

scholarly journals Role for a Glycan Phosphoinositol Anchor in Fcγ Receptor Synergy

1997 ◽  
Vol 139 (5) ◽  
pp. 1209-1217 ◽  
Author(s):  
Jennifer M. Green ◽  
Alan D. Schreiber ◽  
Eric J. Brown
Keyword(s):  
T Cells ◽  
Cell Types ◽  
Polymorphonuclear Neutrophils ◽  
Fcγ Receptor ◽  
Fcγ Receptors ◽  
Jurkat T Cells ◽  
Gpi Anchor ◽  
Transmembrane Anchor ◽  
Activation Motif

While many cell types express receptors for the Fc domain of IgG (FcγR), only primate polymorphonuclear neutrophils (PMN) express an FcγR linked to the membrane via a glycan phosphoinositol (GPI) anchor. Previous studies have demonstrated that this GPI-linked FcγR (FcγRIIIB) cooperates with the transmembrane FcγR (FcγRIIA) to mediate many of the functional effects of immune complex binding. To determine the role of the GPI anchor in Fcγ receptor synergy, we have developed a model system in Jurkat T cells, which lack endogenously expressed Fcγ receptors. Jurkat T cells were stably transfected with cDNA encoding FcγRIIA and/or FcγRIIIB. Cocrosslinking the two receptors produced a synergistic rise in intracytoplasmic calcium ([Ca2+]i) to levels not reached by stimulation of either FcγRIIA or FcγRIIIB alone. Synergy was achieved by prolonged entry of extracellular Ca2+. Cocrosslinking FcγRIIA with CD59 or CD48, two other GPI-linked proteins on Jurkat T cells also led to a synergistic [Ca2+]i rise, as did crosslinking CD59 with FcγRIIA on PMN, suggesting that interactions between the extracellular domains of the two Fcγ receptors are not required for synergy. Replacement of the GPI anchor of FcγRIIIB with a transmembrane anchor abolished synergy. In addition, tyrosine to phenylalanine substitutions in the immunoreceptor tyrosine-based activation motif (ITAM) of the FcγRIIA cytoplasmic tail abolished synergy. While the ITAM of FcγRIIA was required for the increase in [Ca2+]i, tyrosine phosphorylation of crosslinked FcγRIIA was diminished when cocrosslinked with FcγRIIIB. These data demonstrate that FcγRIIA association with GPI-linked proteins facilitates FcγR signal transduction and suggest that this may be a physiologically significant role for the unusual GPI-anchored FcγR of human PMN.

scholarly journals Revisiting the role of IRF3 in inflammation and immunity by conditional and specifically targeted gene ablation in mice

2018 ◽  
Vol 115 (20) ◽  
pp. 5253-5258 ◽  
Author(s):  
Hideyuki Yanai ◽  
Shiho Chiba ◽  
Sho Hangai ◽  
Kohei Kometani ◽  
Asuka Inoue ◽  
...  
Keyword(s):  
Immune Cell ◽  
Cell Types ◽  
Type I ◽  
Type I Ifn ◽  
Cell Type ◽  
Gene Ablation ◽  
Cell Type Specific

IFN regulatory factor 3 (IRF3) is a transcription regulator of cellular responses in many cell types that is known to be essential for innate immunity. To confirm IRF3’s broad role in immunity and to more fully discern its role in various cellular subsets, we engineered Irf3-floxed mice to allow for the cell type-specific ablation of Irf3. Analysis of these mice confirmed the general requirement of IRF3 for the evocation of type I IFN responses in vitro and in vivo. Furthermore, immune cell ontogeny and frequencies of immune cell types were unaffected when Irf3 was selectively inactivated in either T cells or B cells in the mice. Interestingly, in a model of lipopolysaccharide-induced septic shock, selective Irf3 deficiency in myeloid cells led to reduced levels of type I IFN in the sera and increased survival of these mice, indicating the myeloid-specific, pathogenic role of the Toll-like receptor 4–IRF3 type I IFN axis in this model of sepsis. Thus, Irf3-floxed mice can serve as useful tool for further exploring the cell type-specific functions of this transcription factor.

Immunocytochemical localization of oestrogen receptors in the endometrium of the ewe

1991 ◽  
Vol 3 (3) ◽  
pp. 321 ◽  
Author(s):  
RA Cherny ◽  
LA Salamonsen ◽  
JK Findlay
Keyword(s):  
Stromal Cells ◽  
Cellular Response ◽  
Individual Cell ◽  
Cell Types ◽  
Staining Intensity ◽  
Steroid Treatment ◽  
Positive Staining ◽  
Cell Type ◽  
Peak Intensity

Immunocytochemistry with monoclonal antibodies to the oestrogen receptor (ER) was used to localize ERs in sections of endometrium obtained from cycling and pregnant Corriedale ewes. Representative tissue from Days 4, 10, 14, 15, 16 and 17 of the cycle (Day 0 = onset of oestrus) and Day 15 of pregnancy was used. ER localization was also examined in tissue obtained from ovariectomized (ovex) ewes with and without subcutaneous implants containing oestrogen, progesterone, or oestrogen and progesterone. ER distribution was examined in caruncular endometrium and intercaruncular endometrium. Staining intensity varied according to cell type, stage of the cycle, steroid treatment and pregnancy. No staining was observed in endothelial cells. In all cases, ER was localized within the nuclei of positive cells. Generally, ER levels were high on Day 4 and declined to negligible values by Day 10 (corresponding to peak progesterone values) except in the deep stroma of caruncular endometrium. Positive staining reappeared in stromal cells of caruncles on Day 13 and in the luminal epithelium of intercaruncular tissue on Day 14. Peak intensity was reached on Day 15 for caruncular tissue and Day 16 for intercaruncular tissue. Ovariectomy did not cause an overall reduction in ER levels, whereas treatment with oestrogen and progesterone had variable effects depending on cell type. Progesterone did not suppress overall ER. In Day 15 pregnant tissue, ER was undetectable in all compartments except deep stroma of caruncles, indicating that factors other than progesterone, perhaps embryonic in origin, were responsible. The observation that individual cell types display differential sensitivities to oestrogen and progesterone as regards their expression of ER is consistent with the role of cell-cell interactions as modulators of cellular response to steroids through the oestrous cycle and in pregnancy.

scholarly journals Differential Expression of Genes Associated with Oncogene-Induced Senescence and Senescence Associated Secretory Phenotype in the Absence of Differential Expression of High Molecular Risk Genes and Genes Associated with JAK-STAT Pathway in Sorted Cells of Patients with Polycythemia Vera and Primary Myelofibrosis

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 4283-4283
Author(s):  
Chieh Lee Wong ◽  
Andrew Innes ◽  
Baoshan Ma ◽  
Gareth Gerrard ◽  
Zainul Abidin Norziha ◽  
...  
Keyword(s):  
Gene Expression ◽  
Differential Expression ◽  
Primary Myelofibrosis ◽  
Cell Types ◽  
Differentially Expressed ◽  
Cell Type ◽  
Expression Of Genes ◽  
A Cell ◽  
Stat Pathway

Abstract Introduction Despite significant progress in the understanding of the molecular pathogenesis of myeloproliferative neoplasms (MPN) and the identification of high molecular risk (HMR) genes (i.e. ASXL1, EZH2, IDH1 and IDH2 genes), the mechanisms by which different cell types predominate in the different disease subtypes and their implications for prognosis remain uncertain. Given the recently described association of senescence and fibrosis in a number of pathologies by Menoz-Espin et al, we hypothesized that genes implicated in oncogene-induced senescence (OIS) and senescence associated secretory phenotype (SASP) may contribute to the pathogenesis of these neoplastic bone marrow disorders that frequently show evidence of fibrosis. Specifically, we were interested in the gene expression levels in different disease subtypes, at a cell-type level, and whether these patterns of differential expression were distinct from the transforming JAK-STAT pathway and the HMR genes. Aim To elucidate the role of OIS and SASP genes in the pathogenesis of MPN subtypes by determining the differential expression of the genes in specific cell types in patients with MPN. Methods We performed gene expression profiling on normal controls (NC) and patients with MPN who were diagnosed with essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF) according to the 2008 WHO diagnostic criteria. Two cohorts of patients, the patient and validation cohorts, from 3 tertiary-level hospitals were recruited prospectively over 3 years. Peripheral blood samples were taken and sorted into polymorphonuclear cells (PMN), mononuclear cells (MNC) and T cells. RNA was extracted from each cell population. Gene expression profiling of the human transcriptome was performed using microarray and RNA sequencing on the patient and validation cohorts respectively. Gene expression analyses (GEA) were performed on 4 sets of genes derived from publicly available or custom derived gene set enrichment analysis: 92 OIS genes, 88 SASP genes (Gil et al), 4 HMR genes, and 126 genes associated with JAK-STAT pathway. Gene expression levels for each cell type in each disease were compared with NC to obtain the differential expression of the genes. RNA-seq analysis of samples from the validation cohort was used to validate the microarray results from the patient cohort. Results Twenty-eight patients (10 ET, 11 PV and 7 PMF) and 11 NC were recruited into the patient cohort. Twelve patients (4 ET, 4 PV and 4 PMF) and 4 NC were recruited into the validation cohort. After combination of the microarray and RNA-seq datasets, GEA of the OIS genes revealed the differential expressions of MCTP1 and SULT1B1 genes by PMN in PV but of none in PMF. In contrast, the BEX1 gene was identified as differentially expressed by MNC in PMF but none in PV. GEA of the SASP genes revealed differential expression of THBS1 gene by MNC in PMF but of none in PV. None of the SASP genes were differentially expressed by PMN in either PV or PMF. No differentially expressed genes were identified by PMN or MNC in ET, or by T cells in any of the diseases. Notably, GEA of the HMR genes and genes associated with the JAK-STAT pathways did not show any differential expression in any disease subtype by any cell type. Conclusions We have found strikingly distinct patterns of differential expression of senescence associated genes by PMN (in PV) and MNC (in PMF). These results provide a novel insight into the mechanisms underlying the different phenotype of the MPN subtypes and also to the cells responsible for mediating the differences. The lack of differential expression of OIS and SASP genes in ET may reflect the milder clinical phenotype of the disease. Although mutations in the HMR genes are associated with poor prognosis in PMF, the lack of differential expression in these genes and genes associated with the JAK-STAT pathway is in keeping with their mutated status and suggests that they give rise to the disease phenotypes via altering downstream expression of genes associated in other pathways such as the senescence pathways studied here. Further studies are warranted to investigate the role of these genes and the pathways involved in senescence at a cell-type specific level in order to gain further insight into how they can potentially give rise to the various disease phenotypes in MPN and unmask potential therapeutic targets. Disclosures Aitman: Illumina: Honoraria.

scholarly journals Defective Autophagy in Atherosclerosis: To Die or to Senesce?

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Mandy O. J. Grootaert ◽  
Lynn Roth ◽  
Dorien M. Schrijvers ◽  
Guido R. Y. De Meyer ◽  
Wim Martinet
Keyword(s):  
Cell Types ◽  
Special Focus ◽  
Oxygen Species ◽  
Cell Type ◽  
Mitochondrial Quality Control ◽  
Targeted Treatments ◽  
Wide Range ◽  
Autophagic Process ◽  
Progression Of Atherosclerosis

Autophagy is a subcellular process that plays an important role in the degradation of proteins and damaged organelles such as mitochondria (a process termed “mitophagy”) via lysosomes. It is crucial for regulating protein and mitochondrial quality control and maintaining cellular homeostasis, whereas dysregulation of autophagy has been implicated in a wide range of diseases including atherosclerosis. Recent evidence has shown that the autophagic process becomes dysfunctional during the progression of atherosclerosis, regardless of whether there are many autophagy-stimulating factors (e.g., reactive oxygen species, oxidized lipids, and cytokines) present within the atherosclerotic plaque. This review highlights the recent insights into the causes and consequences of defective autophagy in atherosclerosis, with a special focus on the role of autophagy and mitophagy in plaque macrophages, vascular smooth muscle cells (VSMCs), and endothelial cells (ECs). It has been shown that defective autophagy can promote apoptosis in macrophages but that it accelerates premature senescence in VSMCs. In the ECs, defective autophagy promotes both apoptosis and senescence. We will discuss the discrepancy between these three cell types in their response to autophagy deficiency and underline the cell type-dependent role of autophagy, which may have important implications for the efficacy of autophagy-targeted treatments for atherosclerosis.

scholarly journals Synovial Macrophages in Osteoarthritis: The Key to Understanding Pathogenesis?

2021 ◽  
Vol 12 ◽  
Author(s):  
Amanda Thomson ◽  
Catharien M. U. Hilkens
Keyword(s):  
Immune Cell ◽  
Cell Types ◽  
Disease Development ◽  
Cell Type ◽  
Major Research ◽  
Genetic Characteristics ◽  
Clinical Challenge ◽  
Great Heterogeneity ◽  
Different Tissues

Effective treatment of osteoarthritis (OA) remains a huge clinical challenge despite major research efforts. Different tissues and cell-types within the joint contribute to disease pathogenesis, and there is great heterogeneity between patients in terms of clinical features, genetic characteristics and responses to treatment. Inflammation and the most abundant immune cell type within the joint, macrophages, have now been recognised as possible players in disease development and progression. Here we discuss recent findings on the involvement of synovial inflammation and particularly the role of synovial macrophages in OA pathogenesis. Understanding macrophage involvement may hold the key for improved OA treatments.

The Response of Leukocytes in the Peripheral Blood During and Following Exchange Transfusion in the Newborn

PEDIATRICS ◽  
1973 ◽  
Vol 51 (3) ◽  
pp. 570-574
Author(s):  
M. Xanthou ◽  
D. Nicolopoulos ◽  
A. Gizas ◽  
N. Matsaniotis
Keyword(s):  
Peripheral Blood ◽  
Marked Reduction ◽  
Exchange Transfusion ◽  
Cell Types ◽  
Polymorphonuclear Neutrophils ◽  
Cell Type ◽  
Significant Difference ◽  
Before And After ◽  
Leukocyte Counts ◽  
Monocytes And Lymphocytes

Serial leukocyte counts were done on 12 full-term and eight premature jaundiced babies during exchange transfusions and daily thereafter until the ninth day, in order to study changes in each cell type. The main changes were found to be (1) a marked reduction in all cell types during the procedure with a statistically significant difference in absolute values before and after; (2) significantly lower values of the polymorphonuclear neutrophils and eosinophils in the baby's blood at the end of the transfusion compared with those of the donor's blood, with the monocytes and lymphocytes showing no statistically significant change; and (3) a remarkable rise in each cell type starting soon after the procedure and reaching a peak within the week following the transfusions. Comparison of absolute values during the post-transfusion days with those found in normal babies of corresponding postnatal age showed that the polymorphonuclear neutrophils and eosinophils were significantly increased, the lymphocytes unchanged, and the absolute values of monocytes decreased compared to those of normal babies.

Endothelial cells in human cytomegalovirus infection: One host cell out of many or a crucial target for virus spread?

2009 ◽  
Vol 102 (12) ◽  
pp. 1057-1063 ◽  
Author(s):  
Christian Sinzger ◽  
Barbara Adler
Keyword(s):  
Endothelial Cells ◽  
Human Cytomegalovirus ◽  
Cell Types ◽  
The Body ◽  
Cell Type ◽  
Cell Culture Systems ◽  
Human Cytomegalovirus Infection ◽  
Productive Replication

SummaryEndothelial cells (EC) are assumed to play a central role in the spread of human cytomegalovirus (HCMV) throughout the body. Results from in-situ analyses of infected tissues and data from cell culture systems together strongly suggest that vascular EC can support productive replication of HCMV and thus contribute to its haematogeneous dissemination. By inducing an angiogenic response, HCMV may even promote growth of its own habitat. The particular role of EC is further supported by the fact that entry of HCMV into EC is dependent on a complex of the envelope glycoproteins gH and gL with a set of proteins (UL128–131A) which is dispensable for HCMV entry into most other cell types. These molecular requirements may also be reflected by cell type-dependent differences in entry routes, i.e. endocytosis versus fusion at the plasma membrane. An animal model with trackable murine CMV is now available to clarify the pathogenetic role of EC during haematogeneous dissemination of this virus.

Lung redox homeostasis: emerging concepts

2000 ◽  
Vol 279 (3) ◽  
pp. L413-L417 ◽  
Author(s):  
Marilyn P. Merker ◽  
Bruce R. Pitt ◽  
Augustine M. Choi ◽  
Paul M. Hassoun ◽  
Christopher A. Dawson ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Electron Transport ◽  
Nadph Oxidase ◽  
Redox Homeostasis ◽  
Cell Types ◽  
Xanthine Dehydrogenase ◽  
Zinc Binding ◽  
Cell Type ◽  
Predominant Cell Type ◽  
Lung Endothelium

This symposium was organized to present some aspects of current research pertaining to lung redox function. Focuses of the symposium were on roles of pulmonary endothelial NADPH oxidase, xanthine oxidase (XO)/xanthine dehydrogenase (XDH), heme oxygenase (HO), transplasma membrane electron transport (TPMET), and the zinc binding protein metallothionein (MT) in the propagation and/or protection of the lung or other organs from oxidative injury. The presentations were chosen to reflect the roles of both intracellular (metallothionein, XO/XDH, and HO) and plasma membrane (NADPH oxidase, XO/XDH, and unidentified TPMET) redox proteins in these processes. Although the lung endothelium was the predominant cell type under consideration, at least some of the proposed mechanisms operate in or affect other cell types and organs as well.

scholarly journals Cell Type-Specific Imaging of Calcium Signaling in Arabidopsis thaliana Seedling Roots Using GCaMP3

2020 ◽  
Vol 21 (17) ◽  
pp. 6385
Author(s):  
William Krogman ◽  
J. Alan Sparks ◽  
Elison B. Blancaflor
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Types ◽  
Root Cell ◽  
Cauliflower Mosaic Virus ◽  
Cell Type ◽  
Root Cells ◽  
Cell Tissue ◽  
Seedling Roots ◽  
Cell Type Specific

Cytoplasmic calcium ([Ca2+]cyt) is a well-characterized second messenger in eukaryotic cells. An elevation in [Ca2+]cyt levels is one of the earliest responses in plant cells after exposure to a range of environmental stimuli. Advances in understanding the role of [Ca2+]cyt in plant development has been facilitated by the use of genetically-encoded reporters such as GCaMP. Most of these studies have relied on promoters such as Cauliflower Mosaic Virus (35S) and Ubiquitin10 (UBQ10) to drive expression of GCaMP in all cell/tissue types. Plant organs such as roots consist of various cell types that likely exhibit unique [Ca2+]cyt responses to exogenous and endogenous signals. However, few studies have addressed this question. Here, we introduce a set of Arabidopsis thaliana lines expressing GCaMP3 in five root cell types including the columella, endodermis, cortex, epidermis, and trichoblasts. We found similarities and differences in the [Ca2+]cyt signature among these root cell types when exposed to adenosine tri-phosphate (ATP), glutamate, aluminum, and salt, which are known to trigger [Ca2+]cyt increases in root cells. These cell type-targeted GCaMP3 lines provide a new resource that should enable more in depth studies that address how a particular environmental stimulus is linked to specific root developmental pathways via [Ca2+]cyt.

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