Effects of Inhaled Hexachlorobenzene Aerosols on Rat Pulmonary Host Defenses

1989 ◽  
Vol 5 (3) ◽  
pp. 451-461 ◽  
Author(s):  
Robert L. Sherwood ◽  
Peter T. Thomas ◽  
William J. O'shea ◽  
Jeannie N. Bradof ◽  
Helen V. Ratajczak ◽  
...  
Keyword(s):  
Lymph Nodes ◽  
B Cell ◽  
Bactericidal Activity ◽  
Peritoneal Macrophages ◽  
Sprague Dawley ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph ◽  
Sprague Dawley Rats ◽  
Cell Mitogen

Pulmonary bactericidal activity, macrophage phagocytic activity, alveolar macrophage (AM) enzyme activity, and T- and B-cell mitogenesis of lymphocytes from lung associated lymph nodes (LALN) or mesenteric lymph nodes (MESLN) were assessed in Sprague-Dawley rats exposed 4 hr/d, 4 days/wk for 1, 4, or 16 days to hexachlorobenzene (HCB) aerosols. Pulmonary bactericidal activity was depressed after 1 or 4 but not 16 exposures to 35 mg/m3 of HCB. AM phagocytosis of 51Cr-RBC in vitro was increased after 4 but not 1 or 16 exposures to HCB, and no effect was observed in peritoneal macrophages. HCB significantly enhanced mitogenesis in MESLN to the B-cell mitogen Salmonella typhimurium lipopolysaccharide (STM) after 4 exposures; LALN STM mitogenesis and LALN and MESLN mitogenesis to phytohemagglutinin (PHA) were not affected. After 16 exposures, however, the PHA responses in LALN and MESLN were significantly increased and decreased, respectively.

STUDY OF LYMPHOCTYE INTERACTION IN HUMAN MESENTERIC LYMPH NODES IN VITRO

1984 ◽  
Vol 62 (5) ◽  
pp. 531-537
Author(s):  
AW Cripps ◽  
RL Clancy ◽  
H Chipchase ◽  
EJ Hennessy
Keyword(s):  
Lymph Nodes ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph

Inability of human clinical strains of Helicobacter pylori to colonize the alimentary tract of germfree rodents

1990 ◽  
Vol 36 (4) ◽  
pp. 237-241 ◽  
Author(s):  
Margherita T. Cantorna ◽  
Edward Balish
Keyword(s):  
Helicobacter Pylori ◽  
Lymph Nodes ◽  
Alimentary Tract ◽  
Sprague Dawley ◽  
Mesenteric Lymph Nodes ◽  
Immunodeficient Mice ◽  
Mesenteric Lymph ◽  
H Pylori ◽  
Rats And Mice ◽  
Culture Negative

Several attempts were made to colonize the alimentary tract and infect germfree BALB/c mice and germfree Sprague-Dawley rats with two human isolates of Helicobacter pylori. The alimentary tracts of mice, sacrificed at intervals between 1 day and 20 weeks after oral challenge, were culture negative for H. pylori. The alimentary tract, kidney, liver, and mesenteric lymph nodes were culture negative for H. pylori 5 h after intravenous challenge. Growth of H. pylori was inhibited by homogenates of murine stomach, small intestine, liver, and mesenteric lymph nodes. Germfree rats and mice do not appear to be readily colonized or infected by human strains of H. pylori. Key words: Helicobacter pylori, germfree mice, congenitally immunodeficient mice.

scholarly journals Analysis of IL-2 Production in Hookworm Infected Hamsters Using Generated Polyclonal Antibodies

2012 ◽  
Vol 56 (1) ◽  
pp. 37-42
Author(s):  
Ewa Długosz ◽  
Jarosław Cendrowski ◽  
Piotr Bąska ◽  
Anna Siwińska ◽  
Halina Wędrychowicz ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Lymph Nodes ◽  
Cell Cultures ◽  
Polyclonal Antibodies ◽  
Mesenteric Lymph Nodes ◽  
Ancylostoma Ceylanicum ◽  
Specific Antibodies ◽  
Mesenteric Lymph ◽  
Race Pcr

Abstract The aim of the study was cloning and analysis of the entire coding sequence of hamster IL-2 by the method of RACE-PCR, its expression in Escherichia coli cells, and production of IL-2 specific antibodies. These antibodies were used to determine in vitro IL-2 production by cells derived from the spleen and mesenteric lymph nodes of Ancylostoma ceylanicum infected hamsters. The highest concentration of IL-2 was noted in supernatants from cell cultures coming from the oldest, most resistant hamsters.

B-Cell Leukemia in a Sheep

2003 ◽  
Vol 40 (1) ◽  
pp. 117-119 ◽  
Author(s):  
B. A. Valentine ◽  
S. P. Mcdonough
Keyword(s):  
Lymph Nodes ◽  
Respiratory Distress ◽  
B Cell ◽  
Mononuclear Cells ◽  
Final Diagnosis ◽  
Cell Leukemia ◽  
Mesenteric Lymph Nodes ◽  
Tissue Sections ◽  
Mesenteric Lymph ◽  
B Cell Leukemia

Necropsy examination was performed on an 8.5-year-old Finnish ewe euthanatized because of progressive respiratory distress, cachexia, and weakness. Significant postmortem findings included a diffusely enlarged, dark-red friable liver, mild splenomegaly, and mild mesenteric lymphadenopathy. Examination of multiple tissue sections revealed intravascular atypical mononuclear cells in all tissues examined, with a leukemic pattern of infiltration of mesenteric lymph nodes, liver, lung, and spleen. Neoplastic cells were positive for CD79a and negative for CD-3, BLA.36, and CD68 leukocytic markers. The final diagnosis was B-cell leukemia.

scholarly journals Endothelium-dependent hyperpolarization-mediated relaxation pathway in bovine mesenteric lymph nodes

2019 ◽  
Vol 484 (5) ◽  
pp. 645-648
Author(s):  
G. I. Lobov ◽  
D. P. Dvoretskii
Keyword(s):  
Lymph Nodes ◽  
Physiological Saline ◽  
Relaxation Mechanism ◽  
Mesenteric Lymph Nodes ◽  
Tetraethylammonium Chloride ◽  
K Channels ◽  
Mesenteric Lymph ◽  
Lymph Node Capsule ◽  
Endothelium Dependent Relaxation

In vitro, endothelium-dependent relaxation mechanisms of smooth muscle cells of the bovine mesenteric lymph node capsule have been studied. The addition of L-NAME and indomethacin to physiological saline inhibited the production of endothelium NO and prostacyclin. In this solution, tetraethylammonium chloride and TRAM-34 increased the tone of the precontracted lymph nodes. Thus, in bovine mesenteric lymph nodes there is an relaxation mechanism mediated by endothelial hyperpolarization, realized by activating Ca2+-dependent K+-channels of large- and intermediate conductance.

scholarly journals Arachidonic acid in postshock mesenteric lymph induces pulmonary synthesis of leukotriene B4

2008 ◽  
Vol 104 (4) ◽  
pp. 1161-1166 ◽  
Author(s):  
Janeen R. Jordan ◽  
Ernest E. Moore ◽  
Eric L. Sarin ◽  
Sagar S. Damle ◽  
Sara B. Kashuk ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Lung Injury ◽  
Ischemia Reperfusion ◽  
Leukotriene B4 ◽  
Polymorphonuclear Neutrophil ◽  
Sprague Dawley ◽  
Bioactive Lipids ◽  
Mesenteric Lymph ◽  
Sprague Dawley Rats

Mesenteric lymph is the mechanistic link between splanchnic hypoperfusion and acute lung injury (ALI), but the culprit mediator(s) remains elusive. Previous work has shown that administration of a phospholipase A2(PLA2) inhibitor attenuated postshock ALI and also identified a non-ionic lipid within the postshock mesenteric lymph (PSML) responsible for polymorphonuclear neutrophil (PMN) priming. Consequently, we hypothesized that gut-derived leukotriene B4(LTB4) is a key mediator in the pathogenesis of ALI. Trauma/hemorrhagic shock (T/HS) was induced in male Sprague-Dawley rats and the mesenteric duct cannulated for lymph collection/diversion. PSML, arachidonic acid (AA), and a LTB4receptor antagonist were added to PMNs in vitro. LC/MS/MS was employed to identify bioactive lipids in PSML and the lungs. T/HS increased AA in PSML and increased LTB4and PMNs in the lung. Lymph diversion decreased lung LTB4by 75% and PMNs by 40%. PSML stimulated PMN priming (11.56 ± 1.25 vs. 3.95 ± 0.29 nmol O2−/min; 3.75 × 105cells/ml; P < 0.01) that was attenuated by LTB4receptor blockade (2.64 ± 0.58; P < 0.01). AA stimulated PMNs to produce LTB4, and AA-induced PMN priming was attenuated by LTB4receptor antagonism. Collectively, these data indicate that splanchnic ischemia/reperfusion activates gut PLA2-mediated release of AA into the lymph where it is delivered to the lungs, provoking LTB4production and subsequent PMN-mediated lung injury.

B-cell activation in the mesenteric lymph nodes of resistant BALB/c mice infected with the murine nematode parasite Trichuris muris

1999 ◽  
Vol 85 (3) ◽  
pp. 194-199 ◽  
Author(s):  
Koichi Koyama ◽  
Hidekazu Tamauchi ◽  
Masahiro Tomita ◽  
Takashi Kitajima ◽  
Yoichi Ito
Keyword(s):  
Lymph Nodes ◽  
B Cell ◽  
Cell Activation ◽  
Nematode Parasite ◽  
B Cell Activation ◽  
Mesenteric Lymph Nodes ◽  
Trichuris Muris ◽  
Mesenteric Lymph

scholarly journals AvrA effector protein of Salmonella enterica serovar Enteritidis is expressed and translocated in mesenteric lymph nodes at late stages of infection in mice

Microbiology ◽  
2014 ◽  
Vol 160 (6) ◽  
pp. 1191-1199 ◽  
Author(s):  
Mónica N. Giacomodonato ◽  
Mariángeles Noto Llana ◽  
María del Rosario Aya Castañeda ◽  
Fernanda R. Buzzola ◽  
Sebastián H. Sarnacki ◽  
...  
Keyword(s):  
Lymph Nodes ◽  
Culture Conditions ◽  
Effector Protein ◽  
Post Inoculation ◽  
Mesenteric Lymph Nodes ◽  
Salmonella Enterica Serovar Enteritidis ◽  
Major Health Problem ◽  
Mesenteric Lymph

Salmonellosis is a major health problem worldwide. Salmonella enterica serovar Enteritidis (S. Enteritidis) has been a primary cause of Salmonella outbreaks in many countries. AvrA is an SPI-1 effector protein involved in the enteritis pathway, with critical roles in inhibiting inflammation and apoptosis. In this work, we constructed an AvrA-FLAG-tagged strain of S. Enteritidis to analyse the expression profile of AvrA in vitro, in cell culture and in vivo. AvrA expression and secretion were observed in vitro under culture conditions that mimicked intestinal and intracellular environments. In agreement, bacteria isolated from infected cell monolayers expressed and translocated AvrA for at least 24 h post-inoculation. For in vivo experiments, BALB/c mice were inoculated by the natural route of infection with the AvrA-FLAG strain. Infecting bacteria and infected cells were recovered from mesenteric lymph nodes (MLN). Our results showed that AvrA continues to be synthesized in vivo up to day 8 post-inoculation. Moreover, AvrA translocation was detected in the cytosol of cells isolated from MLN 8 days after infection. Interestingly, we observed that AvrA is secreted by both type three secretion system (T3SS)-1 and T3SS-2. In summary, these findings indicate that AvrA expression is not constrained to the initial host–bacteria encounter in the intestinal environment as defined previously. The AvrA effector may participate also in systemic S. Enteritidis infection.

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