scholarly journals Transcriptomic Analysis of Long-Term Protective Immunity Induced by Vaccination With Mycoplasma gallisepticum Strain ts-304

2021 ◽  
Vol 11 ◽  
Author(s):  
Sathya N. Kulappu Arachchige ◽  
Neil D. Young ◽  
Anna Kanci Condello ◽  
Oluwadamilola S. Omotainse ◽  
Amir H. Noormohammadi ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Cells ◽  
Mycoplasma Gallisepticum ◽  
Tracheal Mucosa ◽  
Chemokine Production ◽  
Live Attenuated Vaccine ◽  
Motor Movement ◽  
Transcriptional Changes ◽  
Protein Classes ◽  
Cellular Cytoskeleton

Live attenuated vaccines are commonly used to control Mycoplasma gallisepticum infections in chickens. M. gallisepticum ts-304 is a novel live attenuated vaccine strain that has been shown to be safe and effective. In this study, the transcriptional profiles of genes in the tracheal mucosa in chickens challenged with the M. gallisepticum wild-type strain Ap3AS at 57 weeks after vaccination with ts-304 were explored and compared with the profiles of unvaccinated chickens that had been challenged with strain Ap3AS, unvaccinated and unchallenged chickens, and vaccinated but unchallenged chickens. At two weeks after challenge, pair-wise comparisons of transcription in vaccinated-only, vaccinated-and-challenged and unvaccinated and unchallenged birds detected no differences. However, the challenged-only birds had significant up-regulation in the transcription of genes and enrichment of gene ontologies, pathways and protein classes involved in infiltration and proliferation of inflammatory cells and immune responses mediated through enhanced cytokine and chemokine production and signaling, while those predicted to be involved in formation and motor movement of cilia and formation of the cellular cytoskeleton were significantly down-regulated. The transcriptional changes associated with the inflammatory response were less severe in these mature birds than in the relatively young birds examined in a previous study. The findings of this study demonstrated that vaccination with the attenuated M. gallisepticum strain ts-304 protects against the transcriptional changes associated with the inflammatory response and pathological changes in the tracheal mucosa caused by infection with M. gallisepticum in chickens for at least 57 weeks after vaccination.

scholarly journals Differential Response of the Chicken Trachea to Chronic Infection with Virulent Mycoplasma gallisepticum Strain Ap3AS and Vaxsafe MG (Strain ts-304): a Transcriptional Profile

2020 ◽  
Vol 88 (5) ◽  
Author(s):  
Sathya N. Kulappu Arachchige ◽  
Neil D. Young ◽  
Pollob K. Shil ◽  
Alistair R. Legione ◽  
Anna Kanci Condello ◽  
...  
Keyword(s):  
Cytokine Production ◽  
Mycoplasma Gallisepticum ◽  
Chronic Respiratory Disease ◽  
Tracheal Mucosa ◽  
Content Type ◽  
Motor Movement ◽  
Cilia Formation ◽  
Junctional Complexes ◽  
Protein Classes ◽  
Gene Ontologies

ABSTRACT Mycoplasma gallisepticum is the primary etiological agent of chronic respiratory disease in chickens. Live attenuated vaccines are most commonly used in the field to control the disease, but current vaccines have some limitations. Vaxsafe MG (strain ts-304) is a new vaccine candidate that is efficacious at a lower dose than the current commercial vaccine strain ts-11, from which it is derived. In this study, the transcriptional profiles of the trachea of unvaccinated chickens and chickens vaccinated with strain ts-304 were compared 2 weeks after challenge with M. gallisepticum strain Ap3AS during the chronic stage of infection. After challenge, genes, gene ontologies, pathways, and protein classes involved in inflammation, cytokine production and signaling, and cell proliferation were upregulated, while those involved in formation and motor movement of cilia, formation of intercellular junctional complexes, and formation of the cytoskeleton were downregulated in the unvaccinated birds compared to the vaccinated birds, reflecting immune dysregulation and the pathological changes induced in the trachea by infection with M. gallisepticum. Vaccination appears to protect the structural and functional integrity of the tracheal mucosa 2 weeks after infection with M. gallisepticum.

scholarly journals Transcriptional Profiling of the Chicken Tracheal Response to Virulent Mycoplasma gallisepticum Strain Rlow

2017 ◽  
Vol 85 (10) ◽  
Author(s):  
J. Beaudet ◽  
E. R. Tulman ◽  
K. Pflaum ◽  
X. Liao ◽  
G. F. Kutish ◽  
...  
Keyword(s):  
Gene Expression ◽  
Ex Vivo ◽  
Virulent Strain ◽  
Current Model ◽  
Inflammatory Cells ◽  
Mycoplasma Gallisepticum ◽  
Immune Dysregulation ◽  
Mitogen Activated Protein Kinase ◽  
Tracheal Mucosa ◽  
Content Type

ABSTRACT Mycoplasma gallisepticum, the primary etiologic agent of chronic respiratory disease (CRD) in poultry, leads to prolonged recruitment and activation of inflammatory cells in the respiratory mucosa. This is consistent with the current model of immune dysregulation that ostensibly allows the organism to evade clearance mechanisms and establish chronic infection. To date, studies using quantitative reverse transcription-PCR (qRT-PCR) and microarrays have shown a significant transient upregulation of cytokines and chemokines from tracheal epithelial cells (TECs) in vitro and tracheal tissue ex vivo in response to virulent strain Rlow that contributes to the infiltration of inflammatory cells into the tracheal mucosa. To expand upon these experiments, RNA was isolated from tracheas of 20 chickens infected with M. gallisepticum Rlow and 20 mock-infected animals at days 1, 3, 5, and 7 postinoculation, and samples were analyzed for differential gene expression using Illumina RNA sequencing. A rapid host response was observed 24 h postinfection, with over 2,500 significantly differentially expressed genes on day 3, the peak of infection. Many of these genes have immune-related functions involved in signaling pathways, including Toll-like receptor (TLR), mitogen-activated protein kinase, Jak-STAT, and the nucleotide oligomerization domain-like receptor pathways. Of interest was the increased expression of numerous cell surface receptors, including TLR4 and TLR15, which may contribute to the production of cytokines. Metabolic pathways were also activated on days 1 and 3 postinfection, ostensibly due to epithelial cell distress that occurs upon infection. Early perturbations in tissue-wide gene expression, as observed here, may underpin a profound immune dysregulation, setting the stage for disease manifestations characteristic of M. gallisepticum infection.

scholarly journals Urokinase Attenuates Pulmonary Thromboembolism in an Animal Model by Inhibition of Inflammatory Response

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Ying Shi ◽  
Zhirong Zhang ◽  
Danli Cai ◽  
Jing Kuang ◽  
Shuifang Jin ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Animal Model ◽  
Inflammatory Response ◽  
Inflammatory Cell ◽  
Pulmonary Thromboembolism ◽  
Thrombus Formation ◽  
Inflammatory Cells ◽  
Hemodynamic Instability ◽  
Synergistic Action ◽  
Determining Factor

Inflammatory response is an important determining factor for the mortality of patients with pulmonary thromboembolism. Inflammatory mediators can promote thrombus formation and increase hemodynamic instability. Urokinase is a commonly used drug for the treatment of PTE. The effect of urokinase on inflammatory reaction in PTE is still unclear. Our study was aimed at evaluating the effects of the intervention of urokinase and urokinase combined with aspirin in PTE rats. Results revealed that a large amount of infiltrated inflammatory cells surrounding the bronchus, vessels, and pulmonary mesenchyme, and even pulmonary abscess were observed in the PTE rats. CX3CL1/CX3CR1 coexpression, CX3CL1/NF-κB coexpression, and TXA2 were significantly higher. After treatment with urokinase, pulmonary embolism was partially dissolved and inflammatory cell infiltration was significantly reduced. The expression of TNNI3, BNP, D2D, PASP, PADP, PAMP, and TXA2, as well as CX3CL1/CX3CR1 coexpression and CX3CL1/NF-κB coexpression were significantly lowered. Aspirin showed no synergistic action. Therefore, these findings suggested the occurrence of inflammation during the process of PTE in rats. Urokinase treatment reduced the inflammatory response.

Use of Vicryl (Polyglactin 910) Mesh to Limit Epidural Scar Formation after Laminectomy

Neurosurgery ◽  
1990 ◽  
Vol 26 (4) ◽  
pp. 649-654 ◽  
Author(s):  
Charles E. Nussbaum ◽  
Joseph V. McDonald ◽  
Raymond B. Baggs
Keyword(s):  
Inflammatory Response ◽  
Subcutaneous Fat ◽  
Inflammatory Cells ◽  
Scar Formation ◽  
Good Survival ◽  
Polyglactin 910 ◽  
Chronic Inflammatory Response ◽  
Fat Grafts ◽  
Free Grafts ◽  
Vicryl Mesh

Abstract A variety of substances have been used at laminectomy sites to prevent postoperative epidural scarring. Free grafts of autologous subcutaneous fat are commonly used both clinically and experimentally. The free fat grafts usually survive, but decrease in size by about 50%. Postoperatively, subcutaneous seroma has been observed with the use of fat grafts, as well as recurrent symptoms of neural compression by the graft that required additional operations. When compared to the use of free fat grafts after laminectomy in dogs, Vicryl mesh produced slightly more scarring, but consistently less than that observed in control animals. The Vicryl mesh was resorbed by a minimal chronic inflammatory response over about 45 days. Seven of 11 fat-grafted zones showed signs of necrosis, at times with a greater collection of inflammatory cells than that associated with the Vicryl mesh. Of the 4 fat-grafted zones that showed good survival. 2 had gross evidence of neural compression. No surgical zone treated with Vicryl mesh exhibited evidence of neural compression. In view of these results, the use of Vicryl mesh at laminectomy sites may be a safer method of limiting postoperative epidural scar formation.

Proteases from Inflammatory Cells: Regulation of Inflammatory Response

2011 ◽  
pp. 73-100 ◽  
Author(s):  
Magali Pederzoli-Ribeil ◽  
Julie Gabillet ◽  
Véronique Witko-Sarsat
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Cells

scholarly journals Il6/Sil6R Regulates Tnfα-Inflammatory Response In Synovial Fibroblasts Through Modulation of Transcriptional and Post-Transcriptional Mechanisms

2020 ◽  
Author(s):  
Alvaro Valin ◽  
Manuel J. Del Rey ◽  
Cristina Municio ◽  
Alicia Usategui ◽  
Marina Romero ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Mononuclear Cells ◽  
De Novo ◽  
Inflammatory Cells ◽  
Synovial Fibroblasts ◽  
Matrix Metalloproteases ◽  
P Value ◽  
Polymorphonuclear Cells ◽  
Expression Of Genes

Abstract Introduction: The clinical efficacy of specific interleukin-6 inhibitors has confirmed the central role of IL6 in rheumatoid arthritis (RA). However the local role of IL6, in particular in synovial fibroblasts (SF) as a direct cellular target to IL6/sIL6R signal is not well characterized. The purpose of the study was to characterize the crosstalk between TNFα and IL6/sIL6R signaling to the effector pro-inflammatory response of SF. Methods SF lines were stimulated with either TNFα or IL6 and sIL6R for the time and dose indicated for each experiment, and where indicated, cells were treated with inhibitors actinomycin D, adalimumab, ruxolitinib and cicloheximide. mRNA expression of cytokines, chemokines and matrix metalloproteases (MMPs) were analyzed by quantitative RT-PCR. Level of IL8 and CCL8 in culture supernatants was measured by ELISA. Mononuclear and polymorphonuclear cells migration assays were assesed by transwell using conditioned medium from SF cultures. Statistical analyses were performed as indicated in the corresponding figure legends and a p-value < 0.05 was considered statistically significant. Results IL6/sIL6R stimulation of TNFα treated SF cooperatively promotes the expression of mono- and lymphocytic chemokines such as IL6, CCL8 and CCL2, as well as matrix degrading enzymes such as MMP1, while inhibiting the induction of central neutrophil chemokines such as IL8. These changes in the pattern of chemokines expression resulted in reduced polymorphonuclear (PMN) and increased mononuclear cells (MNC) chemoattraction by SF. Mechanistic analyses of the temporal expression of genes demonstrated that the cooperative regulation mediated by these two factors is mostly induced through de novo transcriptional mechanisms activated by IL6/sIL6R. Furthermore, we also demonstrate that TNFα and IL6/sIL6R cooperation is partially mediated by the expression of secondary factors signaling through JAK/STAT pathways. Conclusions These results point out to a highly orchestrated response to IL6 in TNFα-induced SF and provide additional insights into the role of IL6/sIL6R in the context of RA, highlighting the contribution of IL6/sIL6R to the interplay of SF with other inflammatory cells.

Cyclopentenone Prostaglandins Inhibit Cytokine-Induced NF-κB Activation and Chemokine Production by Human Mesangial Cells

2001 ◽  
Vol 12 (8) ◽  
pp. 1659-1667
Author(s):  
BRAD H. ROVIN ◽  
LING LU ◽  
ANNA COSIO
Keyword(s):  
Inflammatory Response ◽  
Mesangial Cells ◽  
Gene Activation ◽  
Chemokine Production ◽  
Human Mesangial Cells ◽  
Renal Inflammation ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Cyclopentenone Prostaglandins

Abstract. In the kidney an uncontrolled inflammatory response to an acute insult may lead to chronic inflammation, permanent tissue damage, and progressive renal insufficiency. Resolution of acute inflammation likely is dependent on endogenous regulatory mechanisms activated in parallel with mediators of renal inflammation. These mechanisms are postulated to attenuate the renal expression of proinflammatory cytokines, including the chemokines responsible for recruiting leukocytes to the kidney, thus facilitating the transition from inflammation to healing. To understand the regulation of the inflammatory response within the kidney, the effects of anti-inflammatory J series cyclopentenone prostaglandins on chemokine production by human mesangial cells were examined. Treatment of mesangial cells with prostaglandin J2and 15-deoxy-Δ12,14-prostaglandin J2blocked interleukin-1β—induced monocyte chemoattractant protein-1 mRNA expression and protein production. This correlated with failure of the transcription factor nuclear factor-κB (NF-κB) to translocate to the nucleus and bind to its recognition motif, a step required for cytokine-induced monocyte chemoattractant protein-1 gene activation. NF-κB failed to translocate because the cyclopentenone prostaglandins attenuated degradation of the NF-κB inhibitor IκB-α. These data suggest that certain prostaglandins can limit the extent of renal chemokine expression and thus may have an important role in resolving renal inflammation.

Molecular and Cellular Mediators of the Inflammatory Response

2015 ◽  
Author(s):  
Amy T. Makley ◽  
Michael D. Goodman ◽  
Timothy A. Pritts
Keyword(s):  
Inflammatory Response ◽  
Activated Protein C ◽  
Inflammatory Cells ◽  
Cellular Responses ◽  
Sepsis Syndrome ◽  
Reactive Oxygen Metabolites ◽  
Therapeutic Implications ◽  
Susceptibility To Infection ◽  
Cellular Mediators ◽  
Definition Of

Inflammation is a highly complex process involving vascular, neurogenic, humoral, and cellular responses. Although the descriptive features of acute inflammation have long been known (i.e., heat, redness, pain, swelling), a single satisfactory definition of this phenomenon is still lacking. Successful therapy for inflammation rests not only on investigating the type of injury, but also on the timing of the intervention. This review focuses on humoral and cellular responses to injury, defining essential and interrelated inflammatory pathways. Systemic inflammatory response system (SIRS), in relation to sepsis syndrome, is defined by the global proinflammatory physiologic response to a stimulus. In contrast, compensatory antiinflammatory response (CARS) results from a predominant antiinflammatory response to an insult, also causing immunosuppression and increased susceptibility to infection. Also discussed are the roles of cytokines, adhesion molecules, inflammatory cells such as neutrophils, mast cells, and lymphocytes, extracellular vesicles, sphingolipids, reactive oxygen metabolites, nitric oxide, the complement cascade, and eicosanoids. Therapeutic implications and trials are examined in relation to cytokines in SIRS and CARS, activated protein C, and inflammatory bowel disease. This review contains 11 figures, 4 tables, and 79 references.

scholarly journals Different experimental multiple trauma models induce comparable inflammation and organ injury

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Borna Relja ◽  
Bing Yang ◽  
Katrin Bundkirchen ◽  
Baolin Xu ◽  
Kernt Köhler ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Multiple Trauma ◽  
Inflammatory Cells ◽  
Organ Damage ◽  
Organ Injury ◽  
Local Inflammatory Response ◽  
Healthy Control ◽  
Post Traumatic ◽  
Tissue Trauma ◽  
Trauma Group

AbstractMultiple injuries appear to be a decisive factor for experimental polytrauma. Therefore, our aim was to compare the inflammatory response and organ damage of five different monotrauma with three multiple trauma models. For this, mice were randomly assigned to 10 groups: Healthy control (Ctrl), Sham, hemorrhagic shock (HS), thoracic trauma (TxT), osteotomy with external fixation (Fx), bilateral soft tissue trauma (bsTT) or laparotomy (Lap); polytrauma I (PT I, TxT + HS + Fx), PT II (TxT + HS + Fx + Lap) and one multi-trauma group (MT, TxT + HS + bsTT + Lap). The inflammatory response and organ damage were quantified at 6 h by analyses of IL-6, IL-1β, IL-10, CXCL1, SAA1, HMGB1 and organ injury. Systemic IL-6 increased in all mono and multiple trauma groups, while CXCL1 increased only in HS, PT I, PT II and MT vs. control. Local inflammatory response was most prominent in HS, PT I, PT II and MT in the liver. Infiltration of inflammatory cells into lung and liver was significant in all multiple trauma groups vs. controls. Hepatic and pulmonary injury was prominent in HS, PT I, PT II and MT groups. These experimental multiple trauma models closely mimic the early post-traumatic inflammatory response in human. Though, the choice of read-out parameters is very important for therapeutic immune modulatory approaches.

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