Substitution of the Radiation Requirement for Sporulation by Host Tissue in Dendrophoma obscurans

Mycologia ◽  
1975 ◽  
Vol 67 (5) ◽  
pp. 1025 ◽  
Author(s):  
F. L. Binder ◽  
V. G. Lilly
Keyword(s):  
Host Tissue ◽  
Dendrophoma Obscurans

Transfer of photosynthetically fixed carbon between the prokaryotic green alga Prochloron and its ascidian host

1983 ◽  
Vol 34 (3) ◽  
pp. 431 ◽  
Author(s):  
DJ Griffiths ◽  
L Thinh
Keyword(s):  
Light Intensity ◽  
Green Alga ◽  
Host Tissue ◽  
Total Carbon ◽  
Symbiotic Association ◽  
Fixed Carbon ◽  
Low Light ◽  
Ascidian Species ◽  
Dark Fixation ◽  
Efficient Transfer

In the symbiotic association between the prokaryotic green alga Prochloron and three didemnid host species (Diplosoma similis, Lissoclinum bistratum, Trididemnum cyclops), between 6 and 51 % of the total carbon fixed during exposure for 1 h to H14CO3- in the light (150 �E m-2 s-1) becomes associated with the host tissue. Dark fixation of 14CO2 in these ascidian species and in Lissoclinum punctatum never exceeds 6% of photosynthetic fixation at saturating light intensity. The corresponding values for dark fixation of 14CO2 in isolated Prochloron cells fall within the same range. There is very little excretion of photosynthate from whole colonies of the above ascidian species nor from Didemnum molle, Lissoclinum voeltzkowi and Trididemnum miniatum (usually less than 1 % of total photosynthate at saturation light intensity), suggesting an efficient transfer mechanism from Prochloron to host. Evidence from pulse-chase experiments suggests that transfer probably involves the early products of photosynthesis. The extent of transfer of photosynthate between Prochloron and T. cyclops varies with the rate of photosynthetic 14CO2 fixation into the whole colony but there is some transfer even at low light intensities, which strongly limit photosynthesis.

scholarly journals Genetic changes of Plasmodium vivax tempers host tissue-specific responses in Anopheles stephensi

2021 ◽  
Author(s):  
Seena Kumari ◽  
Charu Chauhan ◽  
Sanjay Tevatiya ◽  
Deepak Singla ◽  
Tanwee Das De ◽  
...  
Keyword(s):  
Plasmodium Vivax ◽  
Anopheles Stephensi ◽  
Host Tissue ◽  
Genetic Changes ◽  
Tissue Specific

THE ROLE OF MYELOPEROXIDASE AND NEUTROPHIL EXTRACELLULAR TRAPS IN THE PATHOGENESIS OF INFLAMMATORY BOWEL DISEASE

2021 ◽  
Vol 27 (Supplement_1) ◽  
pp. S4-S4
Author(s):  
Belal Chami ◽  
Gulfam Ahmad ◽  
Angie Schroder ◽  
Patrick San Gabriel ◽  
Paul Witting
Keyword(s):  
Disease Severity ◽  
Hypochlorous Acid ◽  
Tissue Injury ◽  
Activity Index ◽  
Critical Role ◽  
Neutrophil Migration ◽  
Sodium Sulphate ◽  
Host Tissue ◽  
Neutrophil Extracellular Trap

Abstract Neutrophils are short-lived immune cells that represent the major cell type recruited to the inflamed bowel releasing their azurophilic granules containing enzymes myeloperoxidase (MPO). Fecal and serum MPO levels has previously been shown to correlate to disease severity in IBD patients. MPO, in the presence of H2O2 and free Cl- undergoes a halogenation cycle, yielding the two-electron oxidant, hypochlorous acid (HOCl) - a potent bactericidal agent. However, chronic intestinal exposure to MPO/HOCl due to perpetual inflammation may cause secondary host-tissue injury and cell death. Neutrophil Extracellular Trap (NET)osis is a specialised form of neutrophil death where MPO is entrapped in a DNA scaffold and continues to elicit HOCl activity and may further contribute to host-tissue injury. We investigated the presence of NETs in surgically excised ileum samples from CD and healthy patients using advanced confocal microscopic techniques and found MPO, Neutrophil Elastase (NE) and Citrullinated Histone h3 (CitH3) - critical components of NET formation, individually positively correlate to the severity of histopathological intestinal injury. Furthermore, multiplex Opal™ IHC performed using LMS880 Airyscan-moduled microscopy with z-stacking revealed colocalization of NE, MPO, CitH3 and DAPI indicating the extensive presence of NETs in severely affected CD tissue. Using two pharmacological inhibitors of MPO in a dextran sodium sulphate (DSS) model of murine colitis, we demonstrated the pathological role of MPO in experimental colitis. MPO inhibitors, TEMPOL and AZD3241 delivered via daily i.p significantly rescued the course of colitis by abrogating clinical indices including body weight loss, disease activity index, inhibiting serum peroxidation, and preserving colon length, while significantly mitigating histoarchitectural damage associated with DSS-induced colitis. We also showed that MPO inhibition decreased neutrophil migration to the gut, suggesting MPO may play a role in perpetuating the inflammatory cell by further recruiting cells to the inflamed gut. Collectively, we have shown for the first time that MPO is not only an important clinical marker of disease severity but may also play a critical role in perpetuating host-tissue damage and inflammation.

Porcine Repeat Element DNA: In Situ Detection of Xenotransplanted Cells

1995 ◽  
Vol 4 (2) ◽  
pp. 253-256 ◽  
Author(s):  
Henry F. Oettinger ◽  
Amelie Rodrigue-Way ◽  
Joyce J. Bousquet ◽  
Albert S.B. Edge
Keyword(s):  
Southern Blotting ◽  
Host Tissue ◽  
Repeat Element ◽  
Tissue Analysis ◽  
Specific Staining ◽  
Tetrazolium Chloride ◽  
Tissue Sections ◽  
Blue Tetrazolium Chloride ◽  
In Situ Detection

Using a digoxygenin-labelled DNA probe derived from the porcine repeat element PRE-1, we have developed a protocol for the detection of transplanted porcine islets and hepatocytes against a background of murine host tissue. Analysis of this probe by Southern blotting indicated that PRE-1 hybridizes to pig genomic DNA but not to human or mouse DNA. On tissue sections, hybridizing probe was detected using alkaline phosphatase-conjugated anti-digoxygenin antibody visualized with 5-bromo-4-chloro-3-indolyl-phosphate/4-nitro-blue tetrazolium chloride (BCIP/ NBT) substrate. We have demonstrated sensitive and highly specific staining of porcine nuclei in fixed, paraffin embedded tissue sections, and have applied the technique to detect porcine pancreatic islets and hepatocytes transplanted into murine kidney and spleen. Applications of this technique include detection of transplanted cells or organs across a variety of xenogeneic barriers.

scholarly journals CXCR4 is a key regulator of neutrophil release from the bone marrow under basal and stress granulopoiesis conditions

Blood ◽  
2009 ◽  
Vol 113 (19) ◽  
pp. 4711-4719 ◽  
Author(s):  
Kyle J. Eash ◽  
Jacquelyn M. Means ◽  
Douglas W. White ◽  
Daniel C. Link
Keyword(s):  
Bone Marrow ◽  
Listeria Monocytogenes ◽  
Host Tissue ◽  
Microbial Pathogens ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Cxcr4 Signaling ◽  
Listeria Monocytogenes Infection ◽  
A Cell ◽  
Stimulating Factor

Abstract The number of neutrophils in the blood is tightly regulated to ensure adequate protection against microbial pathogens while minimizing damage to host tissue. Neutrophil homeostasis in the blood is achieved through a balance of neutrophil production, release from the bone marrow, and clearance from the circulation. Accumulating evidence suggests that signaling by CXCL12, through its major receptor CXCR4, plays a key role in maintaining neutrophil homeostasis. Herein, we generated mice with a myeloid lineage–restricted deletion of CXCR4 to define the mechanisms by which CXCR4 signals regulate this process. We show that CXCR4 negatively regulates neutrophil release from the bone marrow in a cell-autonomous fashion. However, CXCR4 is dispensable for neutrophil clearance from the circulation. Neutrophil mobilization responses to granulocyte colony-stimulating factor (G-CSF), CXCL2, or Listeria monocytogenes infection are absent or impaired, suggesting that disruption of CXCR4 signaling may be a common step mediating neutrophil release. Collectively, these data suggest that CXCR4 signaling maintains neutrophil homeostasis in the blood under both basal and stress granulopoiesis conditions primarily by regulating neutrophil release from the bone marrow.

Myogenic cell movement in the developing avian limb bud in presence and absence of the apical ectodermal ridge (AER)

Development ◽  
1984 ◽  
Vol 80 (1) ◽  
pp. 105-125
Author(s):  
Madeleine Gumpel-Pinot ◽  
D. A. Ede ◽  
O. P. Flint
Keyword(s):  
Cell Migration ◽  
Cell Movement ◽  
Host Tissue ◽  
Apical Ectodermal Ridge ◽  
Limb Bud ◽  
Myogenic Cell ◽  
Myogenic Cells ◽  
Apical Direction ◽  
Wing Bud ◽  
Presence And Absence

Fragments of quail wing bud containing myogenic cells of somitic origin and fragments of quail sphlanchopleural tissue were introduced into the interior of the wing bud of fowl embryo hosts. No movement of graft into host tissue occurred in the control, but myogenic cells from the quail wing bud fragments underwent long migrations in an apical direction to become incorporated in the developing musculature of the host. When the apical ectodermal ridge (AER), together with some subridge mesenchyme, was removed at the time of grafting, no such cell migration occurred. The capacity of grafted myogenic cells to migrate in the presence of AER persists to H.H. stage 25, when myogenesis has begun, but premyogenic cells in the somites, which normally migrate out into the early limb bud, do not migrate when somite fragments are grafted into the wing bud. Coelomic grafts of apical and proximal wing fragments showed that apical sections of quail wing buds become invaded by myogenic cells of the host, but grafts from proximal wing bud regions do not.

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