Induction of Interleukin-8 and Interleukin-12 in Neonatal Ovine Lung Following Experimental Inoculation of Bovine Respiratory Syncytial Virus

Redondo, E.; Gázquez, Antonio; Vadillo, S.; García, Alfredo; Franco, A; Masot, A. J.

doi:10.1016/j.jcpa.2013.08.002

Cited by 3 publications

(2 citation statements)

References 37 publications

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“…Interleukin-8 is a chemotactic factor that correlates with neutrophil accumulation in distal airspaces of patients with ARDS and is a predictor of mortality (48)(49)(50). IL-8 is secreted by bronchial epithelial cells and can be induced by Mycoplasma pneumoniae antigen or live M. pneumoniae (51) as well as by severe acute respiratory syndrome coronavirus spike protein or respiratory syncytial virus infection (52,53). The rate of AFC is impaired by high levels of IL-8 and is significantly lower in patients who have a pulmonary edema fluid concentration of IL-8 above 4,000 pg/ml (54).…”

Section: Interleukin-8mentioning

confidence: 99%

Inflammatory Responses Regulating Alveolar Ion Transport during Pulmonary Infections

et al. 2017

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The respiratory epithelium is lined by a tightly balanced fluid layer that allows normal O2 and CO2 exchange and maintains surface tension and host defense. To maintain alveolar fluid homeostasis, both the integrity of the alveolar–capillary barrier and the expression of epithelial ion channels and pumps are necessary to establish a vectorial ion gradient. However, during pulmonary infection, auto- and/or paracrine-acting mediators induce pathophysiological changes of the alveolar–capillary barrier, altered expression of epithelial Na,K-ATPase and of epithelial ion channels including epithelial sodium channel and cystic fibrosis membrane conductance regulator, leading to the accumulation of edema and impaired alveolar fluid clearance. These mediators include classical pro-inflammatory cytokines such as TGF-β, TNF-α, interferons, or IL-1β that are released upon bacterial challenge with Streptococcus pneumoniae, Klebsiella pneumoniae, or Mycoplasma pneumoniae as well as in viral infection with influenza A virus, pathogenic coronaviruses, or respiratory syncytial virus. Moreover, the pro-apoptotic mediator TNF-related apoptosis-inducing ligand, extracellular nucleotides, or reactive oxygen species impair epithelial ion channel expression and function. Interestingly, during bacterial infection, alterations of ion transport function may serve as an additional feedback loop on the respiratory inflammatory profile, further aggravating disease progression. These changes lead to edema formation and impair edema clearance which results in suboptimal gas exchange causing hypoxemia and hypercapnia. Recent preclinical studies suggest that modulation of the alveolar–capillary fluid homeostasis could represent novel therapeutic approaches to improve outcomes in infection-induced lung injury.

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Section: Interleukin-8mentioning

confidence: 99%

Inflammatory Responses Regulating Alveolar Ion Transport during Pulmonary Infections

et al. 2017

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“…An increase in IL8 expression has been observed in challenges with BRSV and Mannheimia haemolytica as well as a significant association between increased expressions of IL8 with lung lesions. Therefore, it has been suggested that IL8 antagonist drugs be used to prevent inflammatory lung lesions ( Caswell et al, 1998 ; Malazdrewich et al, 2001 ; Singh et al, 2011 ; Redondo et al, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Integrated Network Analysis to Identify Key Modules and Potential Hub Genes Involved in Bovine Respiratory Disease: A Systems Biology Approach

et al. 2021

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Background: Bovine respiratory disease (BRD) is the most common disease in the beef and dairy cattle industry. BRD is a multifactorial disease resulting from the interaction between environmental stressors and infectious agents. However, the molecular mechanisms underlying BRD are not fully understood yet. Therefore, this study aimed to use a systems biology approach to systematically evaluate this disorder to better understand the molecular mechanisms responsible for BRD.Methods: Previously published RNA-seq data from whole blood of 18 healthy and 25 BRD samples were downloaded from the Gene Expression Omnibus (GEO) and then analyzed. Next, two distinct methods of weighted gene coexpression network analysis (WGCNA), i.e., module–trait relationships (MTRs) and module preservation (MP) analysis were used to identify significant highly correlated modules with clinical traits of BRD and non-preserved modules between healthy and BRD samples, respectively. After identifying respective modules by the two mentioned methods of WGCNA, functional enrichment analysis was performed to extract the modules that are biologically related to BRD. Gene coexpression networks based on the hub genes from the candidate modules were then integrated with protein–protein interaction (PPI) networks to identify hub–hub genes and potential transcription factors (TFs).Results: Four significant highly correlated modules with clinical traits of BRD as well as 29 non-preserved modules were identified by MTRs and MP methods, respectively. Among them, two significant highly correlated modules (identified by MTRs) and six nonpreserved modules (identified by MP) were biologically associated with immune response, pulmonary inflammation, and pathogenesis of BRD. After aggregation of gene coexpression networks based on the hub genes with PPI networks, a total of 307 hub–hub genes were identified in the eight candidate modules. Interestingly, most of these hub–hub genes were reported to play an important role in the immune response and BRD pathogenesis. Among the eight candidate modules, the turquoise (identified by MTRs) and purple (identified by MP) modules were highly biologically enriched in BRD. Moreover, STAT1, STAT2, STAT3, IRF7, and IRF9 TFs were suggested to play an important role in the immune system during BRD by regulating the coexpressed genes of these modules. Additionally, a gene set containing several hub–hub genes was identified in the eight candidate modules, such as TLR2, TLR4, IL10, SOCS3, GZMB, ANXA1, ANXA5, PTEN, SGK1, IFI6, ISG15, MX1, MX2, OAS2, IFIH1, DDX58, DHX58, RSAD2, IFI44, IFI44L, EIF2AK2, ISG20, IFIT5, IFITM3, OAS1Y, HERC5, and PRF1, which are potentially critical during infection with agents of bovine respiratory disease complex (BRDC).Conclusion: This study not only helps us to better understand the molecular mechanisms responsible for BRD but also suggested eight candidate modules along with several promising hub–hub genes as diagnosis biomarkers and therapeutic targets for BRD.

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How efficacious are vaccines against bovine respiratory syncytial virus in cattle?

Ellis

2017

Veterinary Microbiology

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Induction of Interleukin-8 and Interleukin-12 in Neonatal Ovine Lung Following Experimental Inoculation of Bovine Respiratory Syncytial Virus

Cited by 3 publications

References 37 publications

Inflammatory Responses Regulating Alveolar Ion Transport during Pulmonary Infections

Inflammatory Responses Regulating Alveolar Ion Transport during Pulmonary Infections

Integrated Network Analysis to Identify Key Modules and Potential Hub Genes Involved in Bovine Respiratory Disease: A Systems Biology Approach

How efficacious are vaccines against bovine respiratory syncytial virus in cattle?

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