Murine Respiratory Mycoplasmosis in LEW and F344 Rats: Strain Differences in Lesion Severity

1982 ◽  
Vol 19 (3) ◽  
pp. 280-293 ◽  
Author(s):  
J. K. Davis ◽  
G. H. Cassell
Keyword(s):  
Strain Differences ◽  
Inflammatory Cells ◽  
Lymphoid Cells ◽  
Model Systems ◽  
Mycoplasma Pulmonis ◽  
Weanling Rats ◽  
Colony Forming Units ◽  
Gross Lesions ◽  
F344 Rats

Pathogen-free weanling rats of the LEW and F344 strains were caged together for two months to eliminate microbial and environmental differences, and then infected intranasally with 10-fold dilutions of viable Mycoplasma pulmonis. At necropsy 28 days postinoculation, F344 rats had no gross lung lesions, even those given the maximum dose of 1.4 X 109 colony-forming units of M. pulmonis. LEW rats often had extensive gross lesions with a gross-pneumonia-dose50 of 1.1 X 107 colony-forming units/rat. Histological examination of the respiratory tract (nasal passages, larynges, tracheae, and lungs) and tympanic cavities showed both qualitative and quantitative differences in lesions between the two strains, particularly in the lungs. Hyperplasia of bronchus-associated lymphoid tissue occurred in both strains, but was more extensive in LEW rats. Atelectasis, alveolar consolidation (due primarily to mononuclear inflammatory cells), and suppurative bronchitis and bronchiolitis were seen only in LEW rats. Infiltrates of lymphoid cells into the lungs distal to bronchi and around blood vessels also were seen primarily in LEW rats. These differences between the two rat strains provide excellent model systems with which to dissect the role of cell responses in the pathogenesis of a naturally occurring chronic lung disease.

Exacerbation of Murine Respiratory Mycoplasmosis by Sialodacryoadenitis Virus Infection in Gnotobiotic F344 Rats

1987 ◽  
Vol 24 (5) ◽  
pp. 392-399 ◽  
Author(s):  
T. R. Schoeb ◽  
J. R. Lindsey
Keyword(s):  
Virus Infection ◽  
Culture Medium ◽  
Lung Lesion ◽  
Mycoplasma Pulmonis ◽  
Experimental Conditions ◽  
Sterile Culture ◽  
Naturally Occurring ◽  
Colony Forming Units ◽  
Nasal Passages ◽  
F344 Rats

To test the hypothesis that sialodacryoadenitis virus infection could exacerbate respiratory mycoplasmosis in rats, four groups of 40 7- to 9-week-old gnotobiotic F344/N rats were given two intranasal inoculations 7 days apart: Mycoplasma pulmonis, then sialodacryoadenitis virus; M. pulmonis followed by sterile culture medium; medium initially, then virus; or two doses of medium. Immediately and 3, 5, 10, and 20 days after the second inoculation, the nasal passages, middle ears, larynges, tracheas, lungs, and salivary and lacrimal glands of four rats from each group were prepared for histologic examination, and the respiratory organs from four other rats were collected for quantitative culture of M. pulmonis and sialodacryoadenitis virus. To test statistically the effect of virus infection on mycoplasmosis lesions, we determined indices of the severity of respiratory tract lesions by subjective scoring. In rats given both organisms, indices of nasal and tracheal lesions were significantly ( P < 0.05) greater at 3 days and after than in rats given M. pulmonis alone, and middle ear, laryngeal, and lung lesion indices were significantly greater at 5 days and after. Rats given both mycoplasma and virus had significantly more mycoplasmal colony-forming units in the nasal passages at 3 days and after, and in the larynges, tracheas, and lungs at 10 and 20 days, than rats given only mycoplasma. These results show that sialodacryoadenitis virus infection can exacerbate respiratory mycoplasmosis in rats under experimental conditions; therefore, the virus probably also contributes to expression of naturally occurring mycoplasmosis.

A pro-inflammatory role of type 2 innate lymphoid cells in murine immune-mediated hepatitis

2015 ◽  
Vol 53 (12) ◽  
Author(s):  
K Karimi ◽  
K Neumann ◽  
J Meiners ◽  
R Voetlause ◽  
W Dammermann ◽  
...  
Keyword(s):  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Immune Mediated

Regulation of microRNAs in Inflammation-Associated Colorectal Cancer: A Mechanistic Approach

2020 ◽  
Vol 20 ◽  
Author(s):  
Sridhar Muthusami ◽  
Ilangovan Ramachandran ◽  
Sneha Krishnamoorthy ◽  
Yuvaraj Sambandam ◽  
Satish Ramalingam ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Molecular Mechanisms ◽  
Colorectal Carcinogenesis ◽  
Model Systems ◽  
Necrosis Factor Alpha ◽  
Multi Stage ◽  
Mechanistic Approach ◽  
Tnf Α ◽  
Factor Alpha

: The development of colorectal cancer (CRC) is a multi-stage process. The inflammation of the colon as in inflammatory bowel disease (IBD) such as ulcerative colitis (UC) or Crohn’s disease (CD) is often regarded as the initial trigger for the development of CRC. Many cytokines such as tumor necrosis factor alpha (TNF-α) and several interleukins (ILs) are known to exert proinflammatory actions, and inflammation initiates or promotes tumorigenesis of various cancers, including CRC through differential regulation of microRNAs (miRNAs/miRs). miRNAs can be oncogenic miRNAs (oncomiRs) or anti-oncomiRs/tumor suppressor miRNAs, and they play key roles during colorectal carcinogenesis. However, the functions and molecular mechanisms of regulation of miRNAs involved in inflammation-associated CRC are still anecdotal and largely unknown. Consolidating the published results and offering perspective solutions to circumvent CRC, the current review is focused on the role of miRNAs and their regulation in the development of CRC. We have also discussed the model systems adapted by researchers to delineate the role of miRNAs in inflammation-associated CRC.

Role of inflammation in the development of colorectal cancer

2020 ◽  
Vol 20 ◽  
Author(s):  
Sridhar Muthusami ◽  
R. Ileng Kumaran ◽  
Kokelavani Nampalli Babu ◽  
Sneha Krishnamoorthy ◽  
Akash Guruswamy ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Chronic Inflammation ◽  
Interleukin 1 ◽  
Cell Types ◽  
Model Systems ◽  
Cytokine Gene Expression ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Proinflammatory Molecules

: Chronic inflammation can lead to the development of many diseases including cancer. Inflammatory bowel disease (IBD) that includes both ulcerative colitis (UC) and Crohn's disease (CD) are risk factors for the development of colorectal cancer (CRC). Many cytokines produced primarily by the gut immune cells either during or in response to localized inflammation in the colon and rectum are known to stimulate the complex interactions between the different cell types in the gut environment resulting in acute inflammation. Subsequently, chronic inflammation together with genetic and epigenetic changes has been shown to lead to the development and progression of CRC. Various cell types present in the colon such as enterocytes, Paneth cells, goblet cells and macrophages express receptors for inflammatory cytokines and respond to tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), IL-6 and other cytokines. Among the several cytokines produced, TNF-α and IL-1β are the key proinflammatory molecules that play critical roles in the development of CRC. The current review is intended to consolidate the published findings to focus on the role of proinflammatory cytokines, namely TNF-α and IL-1β, on inflammation (and the altered immune response) in the gut, to better understand the development of CRC in IBD, using various experimental model systems, preclinical and clinical studies. Moreover, this review also highlights the current therapeutic strategies available (monotherapy and combination therapy), to alleviate the symptoms or treat inflammationassociated CRC by using monoclonal antibodies or aptamers to block proinflammatory molecules, inhibitors of tyrosine kinases in inflammatory signaling cascade, competitive inhibitors of proinflammatory molecules, and the nucleic acid drugs like small activating RNAs (saRNAs) or microRNA (miRNA) mimics to activate tumor suppressor or repress oncogene/proinflammatory cytokine gene expression.

On the Structure of Lead(II) Complexes in Aqueous Solutions. I. Trinuclear Clusters

1995 ◽  
Vol 60 (4) ◽  
pp. 527-536 ◽  
Author(s):  
Martin Breza ◽  
Alena Manová
Keyword(s):  
Quantum Chemistry ◽  
Aqueous Solutions ◽  
Electronic Structures ◽  
Mndo Method ◽  
Model Systems ◽  
Trinuclear Clusters ◽  
The Stability ◽  
Semiempirical Mndo

Using semiempirical MNDO method of quantum chemistry the optimal geometries and corresponding electronic structures of [Pb3(OH)n]6-n model systems as well as of their hydrated [Pb3(OH)n(H2O)8-n]6-n analogues (n = 4, 5) are investigated. The most stable trinuclear lead(II) complexes present in aqueous solutions correspond to cyclo-(μ3-OH)(μ2-OH)3Pb32+, Pb(μ-OH)2Pb(μ-OH)2Pb2+, cyclo-(μ3-OH)2(μ2-OH)3Pb3+, Pb(OH)(μ-OH)2Pb(μ-OH)Pb(OH)+ and Pb(OH)(μ-OH)2Pb(μ-OH)2Pb+ systems. The key role of OH bridges (by vanishing direct Pb-Pb bonds) on the stability of individual isomers is discussed.

The localized electron: magnetic properties

2018 ◽  
Author(s):  
Jean-Pierre Launay ◽  
Michel Verdaguer
Keyword(s):  
Single Molecule ◽  
Model Systems ◽  
Ferromagnetic Coupling ◽  
Single Chain ◽  
Single Molecule Magnets ◽  
Magnetic Systems ◽  
Orbital Interactions ◽  
Prussian Blue Analogues ◽  
Mononuclear Complexes

After preliminaries about electron properties, and definitions in magnetism, one treats the magnetism of mononuclear complexes, in particular spin cross-over, showing the role of cooperativity and the sensitivity to external perturbations. Orbital interactions and exchange interaction are explained in binuclear model systems, using orbital overlap and orthogonality concepts to explain antiferromagnetic or ferromagnetic coupling. The phenomenologically useful Spin Hamiltonian is defined. The concepts are then applied to extended molecular magnetic systems, leading to molecular magnetic materials of various dimensionalities exhibiting bulk ferro- or ferrimagnetism. An illustration is provided by Prussian Blue analogues. Magnetic anisotropy is introduced. It is shown that in some cases, a slow relaxation of magnetization arises and gives rise to appealing single-ion magnets, single-molecule magnets or single-chain magnets, a route to store information at the molecular level.

scholarly journals Cyclo-oxygenase 2, a putative mediator of vessel remodeling, is expressed in the brain AVM vessels and associates with inflammation

2021 ◽  
Author(s):  
Sara Keränen ◽  
Santeri Suutarinen ◽  
Rahul Mallick ◽  
Johanna P. Laakkonen ◽  
Diana Guo ◽  
...  
Keyword(s):  
Quantitative Polymerase Chain Reaction ◽  
Rank Correlation ◽  
Inflammatory Cells ◽  
Vessel Remodeling ◽  
Brain Avm ◽  
Inflammatory Drugs ◽  
Polymerase Chain ◽  
The Brain ◽  
Cox2 Expression

Abstract Background Brain arteriovenous malformations (bAVM) may rupture causing disability or death. BAVM vessels are characterized by abnormally high flow that in general triggers expansive vessel remodeling mediated by cyclo-oxygenase-2 (COX2), the target of non-steroidal anti-inflammatory drugs. We investigated whether COX2 is expressed in bAVMs and whether it associates with inflammation and haemorrhage in these lesions. Methods Tissue was obtained from surgery of 139 bAVMs and 21 normal Circle of Willis samples. The samples were studied with immunohistochemistry and real-time quantitative polymerase chain reaction (RT-PCR). Clinical data was collected from patient records. Results COX2 expression was found in 78% (109/139) of the bAVMs and localized to the vessels’ lumen or medial layer in 70% (95/135) of the bAVMs. Receptors for prostaglandin E2, a COX2-derived mediator of vascular remodeling, were found in the endothelial and smooth muscle cells and perivascular inflammatory cells of bAVMs. COX2 was expressed by infiltrating inflammatory cells and correlated with the extent of inflammation (r = .231, p = .007, Spearman rank correlation). COX2 expression did not associate with haemorrhage. Conclusion COX2 is induced in bAVMs, and possibly participates in the regulation of vessel wall remodelling and ongoing inflammation. Role of COX2 signalling in the pathobiology and clinical course of bAVMs merits further studies.

scholarly journals Loss of IL-33 enhances elastase-induced and cigarette smoke extract-induced emphysema in mice

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Daisuke Morichika ◽  
Akihiko Taniguchi ◽  
Naohiro Oda ◽  
Utako Fujii ◽  
Satoru Senoo ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Intratracheal Instillation ◽  
Inflammatory Cells ◽  
Cigarette Smoke Extract ◽  
Lymphoid Cells ◽  
Chronic Obstructive ◽  
Porcine Pancreas ◽  
Obstructive Pulmonary Disease ◽  
Quantitative Morphometry ◽  
Cytokines And Chemokines

Abstract Background IL-33, which is known to induce type 2 immune responses via group 2 innate lymphoid cells, has been reported to contribute to neutrophilic airway inflammation in chronic obstructive pulmonary disease. However, its role in the pathogenesis of emphysema remains unclear. Methods We determined the role of interleukin (IL)-33 in the development of emphysema using porcine pancreas elastase (PPE) and cigarette smoke extract (CSE) in mice. First, IL-33−/− mice and wild-type (WT) mice were given PPE intratracheally. The numbers of inflammatory cells, and the levels of cytokines and chemokines in the bronchoalveolar lavage (BAL) fluid and lung homogenates, were analyzed; quantitative morphometry of lung sections was also performed. Second, mice received CSE by intratracheal instillation. Quantitative morphometry of lung sections was then performed again. Results Intratracheal instillation of PPE induced emphysematous changes and increased IL-33 levels in the lungs. Compared to WT mice, IL-33−/− mice showed significantly greater PPE-induced emphysematous changes. No differences were observed between IL-33−/− and WT mice in the numbers of macrophages or neutrophils in BAL fluid. The levels of hepatocyte growth factor were lower in the BAL fluid of PPE-treated IL-33−/− mice than WT mice. IL-33−/− mice also showed significantly greater emphysematous changes in the lungs, compared to WT mice, following intratracheal instillation of CSE. Conclusion These observations suggest that loss of IL-33 promotes the development of emphysema and may be potentially harmful to patients with COPD.

scholarly journals Anatomy and Neural Pathways Modulating Distinct Locomotor Behaviors in Drosophila Larva

Biology ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 90
Author(s):  
Swetha B. M. Gowda ◽  
Safa Salim ◽  
Farhan Mohammad
Keyword(s):  
Motor Neurons ◽  
Model Systems ◽  
Neural Pathways ◽  
Animal Movements ◽  
Drosophila Larvae ◽  
The Central Nervous System ◽  
Drosophila Larva ◽  
Locomotor Behaviors ◽  
Basic Level

The control of movements is a fundamental feature shared by all animals. At the most basic level, simple movements are generated by coordinated neural activity and muscle contraction patterns that are controlled by the central nervous system. How behavioral responses to various sensory inputs are processed and integrated by the downstream neural network to produce flexible and adaptive behaviors remains an intense area of investigation in many laboratories. Due to recent advances in experimental techniques, many fundamental neural pathways underlying animal movements have now been elucidated. For example, while the role of motor neurons in locomotion has been studied in great detail, the roles of interneurons in animal movements in both basic and noxious environments have only recently been realized. However, the genetic and transmitter identities of many of these interneurons remains unclear. In this review, we provide an overview of the underlying circuitry and neural pathways required by Drosophila larvae to produce successful movements. By improving our understanding of locomotor circuitry in model systems such as Drosophila, we will have a better understanding of how neural circuits in organisms with different bodies and brains lead to distinct locomotion types at the organism level. The understanding of genetic and physiological components of these movements types also provides directions to understand movements in higher organisms.

scholarly journals Impaired eIF5A function causes a Mendelian disorder that is partially rescued in model systems by spermidine

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Víctor Faundes ◽  
Martin D. Jennings ◽  
Siobhan Crilly ◽  
Sarah Legraie ◽  
Sarah E. Withers ◽  
...  
Keyword(s):  
De Novo ◽  
Model Systems ◽  
Yeast Growth ◽  
Related Disorder ◽  
Optimal Position ◽  
Human Phenotype ◽  
Mendelian Disorder ◽  
Growth Defects ◽  
Polysome Profiling

AbstractThe structure of proline prevents it from adopting an optimal position for rapid protein synthesis. Poly-proline-tract (PPT) associated ribosomal stalling is resolved by highly conserved eIF5A, the only protein to contain the amino acid hypusine. We show that de novo heterozygous EIF5A variants cause a disorder characterized by variable combinations of developmental delay, microcephaly, micrognathia and dysmorphism. Yeast growth assays, polysome profiling, total/hypusinated eIF5A levels and PPT-reporters studies reveal that the variants impair eIF5A function, reduce eIF5A-ribosome interactions and impair the synthesis of PPT-containing proteins. Supplementation with 1 mM spermidine partially corrects the yeast growth defects, improves the polysome profiles and restores expression of PPT reporters. In zebrafish, knockdown eif5a partly recapitulates the human phenotype that can be rescued with 1 µM spermidine supplementation. In summary, we uncover the role of eIF5A in human development and disease, demonstrate the mechanistic complexity of EIF5A-related disorder and raise possibilities for its treatment.

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