Fate of the fish pathogen Aeromonas salmonicida in the peritoneal cavity of rainbow trout

1993 ◽  
Vol 39 (11) ◽  
pp. 1051-1058 ◽  
Author(s):  
Rafael A. Garduño ◽  
Julian C. Thornton ◽  
William W. Kay
Keyword(s):  
Rainbow Trout ◽  
Peritoneal Cavity ◽  
Peritoneal Fluid ◽  
Aeromonas Salmonicida ◽  
Lytic Activity ◽  
Fish Pathogen ◽  
Phagocytic Cells ◽  
Fish Pathogens

A model was developed to study the fate of the fish pathogen Aeromonas salmonicida in vivo, inside a specialized intraperitoneal chamber implanted in rainbow trout, Oncorhynchus mykiss. Although normally recalcitrant to lytic agents in vitro, owing to the presence of its regular surface array (S layer), A. salmonicida was rapidly killed in the peritoneal cavity by a host-derived, soluble lytic activity present in peritoneal fluid. Peritoneal fluid was also found to kill other bacteria and lyse various types of erythrocytes, but was particularly lytic to A. salmonicida. Intraperitoneal survival of injected (free) A. salmonicida cells was several orders of magnitude higher than survival of implanted (restrained) cells. Injected free cells could evade the lytic activity of peritoneal fluid because they readily spread, initiating lethal infections. One evasion strategy was envisioned to be the penetration of peritoneal and (or) tissue macrophages. In spite of the killing mechanisms of these phagocytic cells, A. salmonicida was still able to survive and even replicate inside head kidney macrophages, thereby supporting the notion of A. salmonicida as a facultatively intracellular pathogen. Intraperitoneal chambers in rainbow trout may constitute a valuable experimental tool for studying the in vivo fate of A. salmonicida, and perhaps of other fish pathogens as well.Key words: Aeromonas salmonicida, intraperitoneal chambers, rainbow trout, complement-mediated cell lysis.

scholarly journals In Vitro and In Vivo Phagocytic Ability of Mouse B-1 Cells

2010 ◽  
Vol 2 ◽  
pp. III.S6156 ◽  
Author(s):  
RR Novaes E Brito ◽  
BA Cortez ◽  
GM Machado-Santelli ◽  
P Xander ◽  
BH De Lorenzo ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
B Cells ◽  
Peritoneal Cavity ◽  
Mononuclear Phagocyte ◽  
Phagocytic Cells ◽  
Phagocytic Ability ◽  
Escherichia Coli Bacteria ◽  
Pathogen Clearance

B-1 cells are a peculiar subpopulation of B cells found in the peritoneal and pleural cavities in mice. These cells are typically IgM+ and CD11b+. B-1 cells are able to migrate from the peritoneal cavity to non-specific inflammatory sites in mice. In addition, they can differentiate into mononuclear phagocyte-like cells in vitro; however, it is still unknown whether B-1 cells are capable of performing phagocytosis in vivo. Here we further characterized B-1 cells as phagocytes in vitro, and we investigated their ability to phagocytose apoptotic cells and bacteria in vivo. Our results demonstrate that B-1 phagocytes are able to uptake apoptotic thymocytes and Escherichia coli bacteria, both in vitro and in vivo. These findings indicate that along with macrophages, B-1 phagocytic cells might play a role in fundamental processes such as tissue remodeling, resolution of inflammation and pathogen clearance.

scholarly journals BIOLOGICAL ACTIVITY OF COMPLEMENT IN VIVO

1971 ◽  
Vol 134 (5) ◽  
pp. 1131-1143 ◽  
Author(s):  
Ralph Snyderman ◽  
Jean K. Phillips ◽  
Stephan E. Mergenhagen
Keyword(s):  
Peritoneal Cavity ◽  
Peritoneal Fluid ◽  
Chemotactic Activity ◽  
Rapid Accumulation ◽  
Inflammatory Stimuli ◽  
Early Phases ◽  
Deficient Mice ◽  
Local Accumulation

The importance of C5 in the generation of complement (C)-dependent chemotactic activity in vitro is well recognized. However, the actual role C5 may play in the accumulation of polymorphonuclear leukocytes (PMN) at inflammatory sites in vivo has not been established. Injection of glycogen or endotoxin into the peritoneal cavities of guinea pigs resulted, shortly thereafter, in the local accumulation of PMN. Preceding the influx of leukocytes, the peritoneal fluid became chemotactic for rabbit PMN in vitro. The majority of this activity could be attributed to a cleavage product of C5 (C5a). Similarly, injection of endotoxin into the peritoneal cavity of C5-normal mice resulted in the generation of a chemotactic factor for mouse PMN which was followed by the accumulation of PMN in the peritoneal fluid. In contrast, injection of endotoxin into the peritoneal cavity of C5-deficient mice resulted in the generation of virtually no detectable chemotactic activity and a markedly depressed accumulation of PMN during the first 24 hr after injection. The data suggest that C5 plays an important role in the early phases of PMN accumulation in response to inflammatory stimuli. The rapid accumulation of PMN in response to an inflammatory stimulus such as bacterial endotoxin would be expected to be a major factor in host defense against proliferation and dissemination of infectious agents.

scholarly journals Comparative studies on Salmonella typhi grown in vivo and in vitro III. The immunizing potencies of acetone-killed vaccines prepared from in vivo and in vitro grown bacteria and the immunizing potency of substances isolated from infected organs

1963 ◽  
Vol 61 (3) ◽  
pp. 353-363 ◽  
Author(s):  
A. L. Olitzki ◽  
Dina Godinger
Keyword(s):  
Comparative Studies ◽  
Guinea Pigs ◽  
Peritoneal Fluid ◽  
Parent Strain ◽  
Salmonella Typhi ◽  
Challenge Strain

1. Salmonella typhi, strain Ty2, grown in vivo and employed as acetone-dried vaccine possessed a higher immunizing potency than the descendants of the same parent strain grown in vitro and employed as vaccine.2. When 2 × 108in vitro-grown bacteria were employed as challenge, the immunizing effects of both types of vaccine were more marked than after administration of 2 × 108in vivo-grown bacteria as challenge.3. The higher potency of the in vivo-grown vaccine was apparent in all experiments, whether the challenge strain was grown in vivo or in vitro.4. Immunogenic substances were isolated from infected organs of mice and guinea-pigs, and an immunogenic substance from the peritoneal fluid of the infected guinea-pigs was concentrated by precipitation with ethanol.

The in vitro effect of kynurenic acid on the rainbow trout (Oncorhynchus mykiss) leukocyte and splenocyte activity

2014 ◽  
Vol 17 (3) ◽  
pp. 453-458 ◽  
Author(s):  
J. Małaczewska ◽  
A. K. Siwicki ◽  
R. Wójcik ◽  
W. a. Turski ◽  
E. Kaczorek
Keyword(s):  
Rainbow Trout ◽  
Immune Cells ◽  
Kynurenic Acid ◽  
Kynurenine Pathway ◽  
Phagocytic Cells ◽  
Mitogenic Response ◽  
Tryptophan Degradation ◽  
Selective Ligand ◽  
Vitro Effect

Abstract Kynurenic acid (KYNA), an endogenous neuroprotectant formed along the kynurenine pathway of tryptophan degradation, is a selective ligand of the GPR35 receptor, which can be found on the surface of various populations of human immune cells. In infections and inflammations, KYNA produces an anti-inflammatory effect through this receptor, by depressing the synthesis of reactive oxygen species and pro-inflammatory cytokines. However, it is still unrecognized whether receptors for kynurenic acid are also localized on immune cells of poikilothermic animals, or whether KYNA is able to affect these cells. The objective of this study has been to determine the effect of different concentrations of kynurenic acid (12.5 μM to 10 mM) on the viability and mitogenic response of lymphocytes and on the activity of phagocytic cells isolated from blood and the spleen of rainbow trout. The results imply low toxicity of kynurenic acid towards fish immune cells, and the proliferative effect observed at the two lowest concentrations of KYNA (12.5 μM and 25 μM) seems indicative of endogenous kynurenic acid being capable of activating fish lymphocytes. Non-toxic, micromole concentrations of KYNA, however, had no influence on the mitogenic response of lymphocytes nor on the activity of phagocytes in rainbow trout under in vitro conditions. There is some likelihood that such an effect could be observed at lower, nanomole concentrations of KYNA.

In Vivo and In Vitro Debromination of Decabromodiphenyl Ether (BDE 209) by Juvenile Rainbow Trout and Common Carp

2006 ◽  
Vol 40 (15) ◽  
pp. 4653-4658 ◽  
Author(s):  
Heather M. Stapleton ◽  
Brian Brazil ◽  
R. David Holbrook ◽  
Carys L. Mitchelmore ◽  
Rae Benedict ◽  
...  
Keyword(s):  
Rainbow Trout ◽  
Common Carp ◽  
Decabromodiphenyl Ether ◽  
Juvenile Rainbow Trout ◽  
Bde 209

scholarly journals Estrogen-Like Activity of Perfluoroalkyl Acids In Vivo and Interaction with Human and Rainbow Trout Estrogen Receptors In Vitro

2010 ◽  
Vol 120 (1) ◽  
pp. 42-58 ◽  
Author(s):  
Abby D. Benninghoff ◽  
William H. Bisson ◽  
Daniel C. Koch ◽  
David J. Ehresman ◽  
Siva K. Kolluri ◽  
...  
Keyword(s):  
Rainbow Trout ◽  
Estrogen Receptors ◽  
Perfluoroalkyl Acids

Cigarette smoking, emphysema, and damage to alpha 1-proteinase inhibitor

1994 ◽  
Vol 266 (6) ◽  
pp. L593-L611 ◽  
Author(s):  
M. D. Evans ◽  
W. A. Pryor
Keyword(s):  
Cigarette Smoke ◽  
Proteinase Inhibitor ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Lung Lavage ◽  
Tissue Destruction ◽  
Phagocytic Cells ◽  
Lung Fluid

The proteinase-antiproteinase theory for the pathogenesis of emphysema proposes that the connective tissue destruction associated with emphysema arises from excessive proteinase activity in the lower respiratory tract. For this reason, the relative activities of neutrophil elastase and alpha 1-proteinase inhibitor (alpha 1-PI) are considered important. Most emphysema is observed in smokers; therefore, alpha 1-PI has been studied as a target for smoke-induced damage. Damage to alpha 1-PI in lung fluid could occur by several mechanisms involving species delivered to the lung by cigarette smoke and/or stimulated inflammatory cells. Oxidative damage to alpha 1-PI has received particular attention, since both cigarette smoke and inflammatory cells are rich sources of oxidants. In this article we review almost two decades of research on mechanistic studies of damage to alpha 1-PI by cigarette smoke and phagocytic cells in vitro, studies emphasizing the importance of elastinolytic activity in the pathogenesis of emphysema in vivo and studies of human lung lavage fluid to detect defects in alpha 1-PI at the molecular and functional levels.

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