Role of monocyte chemotactic protein-3 and -4 in children with virus exacerbation of asthma

Santiago, Julio; Hernández-Cruz, José Luis; Manjarrez-Zavala, M E; Montes-Vizuet, R.; Rosete-Olvera, Dora Patricia; Tapia-Díaz, A M; Zepeda-Peney, H; Terán, Luis M.

doi:10.1183/09031936.00085107

Cited by 25 publications

(23 citation statements)

References 20 publications

(24 reference statements)

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“…A role of CCL7 in macrophage recruitment is further highlighted by the observation of a correlation between nasal CCL7 production and the recruitment of macrophages in children with virus-induced asthma (31). A previous report showed IFN-a and IFN-b production by macrophages upon norovirus infection, which was abolished in IRF-3 and IRF-7 double knockout cells (32).…”

Section: Discussionmentioning

confidence: 98%

CCL7 and IRF-7 Mediate Hallmark Inflammatory and IFN Responses following Rhinovirus 1B Infection

Girkin

Hatchwell

Foster

et al. 2015

The Journal of Immunology

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Rhinovirus infections are common and have the potential to exacerbate asthma. We have determined the lung transcriptome in RV strain 1B (RV1B) infected naïve BALB/c mice (non-allergic) and identified CCL7 and IRF7 amongst the most upregulated mRNA transcripts in the lung. To investigate their roles we employed anti-CCL7 antibodies and an IRF7-targeting small interfering RNA in vivo. Neutralising CCL7 or inhibiting IRF7 limited neutrophil and macrophage influx and IFN responses in non-allergic mice. Neutralising CCL7 also reduced activation of NF-κB p65 and p50 subunits, as well as airways hyperreactivity (AHR) in non-allergic mice. However, neither NF-κB subunit activation nor AHR were abolished with infection of allergic mice after neutralising CCL7, despite a reduction in the number of neutrophils, macrophages and eosinophils. IRF7 siRNA primarily suppressed IFN-α and -β levels during infection of allergic mice. Our data highlight a pivotal role of CCL7 and IRF7 in RV-induced inflammation and IFN responses and link NF-κB signalling to the development of AHR.

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Section: Discussionmentioning

confidence: 98%

CCL7 and IRF-7 Mediate Hallmark Inflammatory and IFN Responses following Rhinovirus 1B Infection

Girkin

Hatchwell

Foster

et al. 2015

The Journal of Immunology

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“…CCL7 has been observed in nasal aspirates of influenza virus-infected children (40), but its role in influenza pathogenesis has not been determined. Our qPCR validation experiments revealed a Ͼ380-fold increase in CCL7 expression in Calu-3 cells; in mice, CCL7 exhibited profound early upregulation, supporting a role for airway epithelium in CCL7 production.…”

Section: Discussionmentioning

confidence: 99%

“…on May 10, 2018 by guest http://jvi.asm.org/ Downloaded from regulated inflammatory mediators (e.g., RAGE, CCL5, CCL7, and IL-17F) were not identified as differentially expressed in the previously published mouse study (8) but have been implicated in influenza virus pathogenesis (11,13,40,47). Thus, we also assessed the expression dynamics of two of these factors (CCL7 and IL-17F) by qPCR in Calu-3 cells and mice infected with VN1203 (Fig.…”

Section: Vol 85 2011 Hpai H5n1 Host Cell Response Network 10959mentioning

confidence: 96%

Host Regulatory Network Response to Infection with Highly Pathogenic H5N1 Avian Influenza Virus

Liu

Bankhead

Eisfeld

et al. 2011

J Virol

107

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During the last decade, more than half of humans infected with highly pathogenic avian influenza (HPAI) H5N1 viruses have died, yet virus-induced host signaling has yet to be clearly elucidated. Airway epithelia are known to produce inflammatory mediators that contribute to HPAI H5N1-mediated pathogenicity, but a comprehensive analysis of the host response in this cell type is lacking. Here, we leveraged a system approach to identify and statistically validate signaling subnetworks that define the dynamic transcriptional response of human bronchial epithelial cells after infection with influenza A/Vietnam/1203/2004 (H5N1, VN1203). Importantly, we validated a subset of transcripts from one subnetwork in both Calu-3 cells and mice. A more detailed examination of two subnetworks involved in the immune response and keratinization processes revealed potential novel mediators of HPAI H5N1 pathogenesis and host response signaling. Finally, we show how these results compare to those for a less virulent strain of influenza virus. Using emergent network properties, we provide fresh insight into the host response to HPAI H5N1 virus infection and identify novel avenues for perturbation studies and potential therapeutic interventions for fatal HPAI H5N1 disease.

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“…Eosinophils are involved in allergic inflammation in asthma via several processes, including adhesion to endothelial cells, transendothelial migration, and chemotaxis through monocyte chemoattractant proteins (MCPs) 3,4. The three MCPs (MCP-1, -2, and -3; MIM# 158105, MIM# 602283, and MIM# 158106, respectively) share 51%-78% amino acid homology and activate monocytes via the chemotactic cytokine (CC) β chemokine receptor (CCR) 2.…”

Section: Introductionmentioning

confidence: 99%

“…The three MCPs (MCP-1, -2, and -3; MIM# 158105, MIM# 602283, and MIM# 158106, respectively) share 51%-78% amino acid homology and activate monocytes via the chemotactic cytokine (CC) β chemokine receptor (CCR) 2. MCP-3 activates both CCR1 and CCR3, while MCP-2 activates CCR5 3,4…”

Section: Introductionmentioning

confidence: 99%

Gene - Gene Interactions AmongMCPGenes Polymorphisms in Asthma

Lee

Park

2014

Allergy Asthma Immunol Res

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PurposeMonocyte chemoattractant proteins (MCPs) are important cytokines that involved in cellular activation and releasing of inflammatoy mediators by basophils and eosinophils in allergic disease. Some MCP gene variants implicate in asthma and monoclonal antibody for MCP-3 blocks allergic inflammations in the patients with asthma. Detection of interactions between gene and environment or between genes for complex disease such as asthma is important. We searched for an evidence of genetic effect of single nucleotide polymorphisms (SNPs) of MCP genes as well as gene - gene interactions involved in asthma.MethodsFour hundreds asthmatics and four hundreds normal controls were enrolled. Asthma was defined as a positive bronchodilator response or positive methacholine provocation test with compatible clinical symptoms. Seven MCP gene SNPs (2 SNPs in MCP-1, 1 in MCP-2, and 4 in MCP-3) were included. Association analyses between SNP and asthma, and the tests for gene - gene interaction were performed.ResultsStrong linkage disequilibria were found among 7 MCP gene polymorphisms. There was no SNP that showed a significant association with asthma among 7 SNPs of 3 MCP genes. No haplotype was associated with asthma, either. The combination of MCP1-2518G>A, MCP2+46A>C, and MCP3+563C>T was the best predictive model for asthma as compared to the control in tests for gene - gene interaction. The MCP1-2518G>A and MCP2+46A>C was the second best predictive combination and this had the highest synergistic interaction effect on the subject's status than any other combination of polymorphisms. Complete linkages were not associated with the gene - gene interactions models.ConclusionsMCP gene polymorphisms probably interact with each other; thus, these findings may help in developing a possible genetic marker to predict asthma.

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Role of monocyte chemotactic protein-3 and -4 in children with virus exacerbation of asthma

Cited by 25 publications

References 20 publications

CCL7 and IRF-7 Mediate Hallmark Inflammatory and IFN Responses following Rhinovirus 1B Infection

CCL7 and IRF-7 Mediate Hallmark Inflammatory and IFN Responses following Rhinovirus 1B Infection

Host Regulatory Network Response to Infection with Highly Pathogenic H5N1 Avian Influenza Virus

Gene - Gene Interactions AmongMCPGenes Polymorphisms in Asthma

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