Roles of the ERK MAPK in the regulation of proinflammatory and apoptotic responses in chicken macrophages infected with H9N2 avian influenza virus

Xing, Zheng; Cardona, Carol J.; Anunciacion, Jerome; Adams, Sean; Dao, Nguyet

doi:10.1099/vir.0.015578-0

Cited by 64 publications

(52 citation statements)

References 36 publications

(40 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…P38 MAPK activation controls the expression of cytokines like RANTES, IL-8 and TNF-alpha in different types of cultured cells [35][36][37][38][39] and has been identified as a key factor for the hyperinduction of TNFalpha expression in human macrophages due to H5N1 but not H1N1 infection [37,40]. Moreover, all three MAPK signalling pathways are involved in influenza A virusinduced cytokine production in cultured human lung tissues [41].…”

Section: Discussionmentioning

confidence: 99%

Comparison of pro-inflammatory cytokine expression and cellular signal transduction in human macrophages infected with different influenza A viruses

Geiler

Michaelis

Sithisarn

et al. 2010

Med Microbiol Immunol

View full text Add to dashboard Cite

Influenza A virus infection of macrophages and virus-induced pro-inflammatory gene expression are regarded to contribute to severity of influenza A virus-caused diseases. Although some data are available on cytokine production by influenza A virus-infected macrophages, systematic comparisons of the virus types are currently considered to be of high relevance in humans (pandemic H1N1/2009, seasonal H1N1, seasonal H3N2, highly pathogenic avian influenza H5N1) on pro-inflammatory potential, and relevant underlying cellular signalling events are missing. Here, we show that the infection of human monocyte-derived macrophages with pandemic H1N1/2009 (A/HH/01/2009), seasonal H1N1/1999 (A/New Caledonia/20/99), seasonal H3N2/2004 (A/California/7/2004) or highly pathogenic H5N1/2004 (A/Thailand/1(Kan-1)/04) results in similar infection rates. However, the investigated H1N1 strains caused delayed and decreased apoptosis in comparison with H3N2/2004 or H5N1/2004. Moreover, human macrophage infection with H3N2/2004 or H5N1/2004 but not with H1N1 viruses was associated with pronounced pro-inflammatory cytokine production and activation of relevant mitogen-activated protein kinase pathways as indicated by phosphorylation of p38, JNK and ERK 1/2. These findings are in line with clinical observations indicating enhanced disease severity in H3N2- or H5N1-infected patients compared to individuals infected with pandemic H1N1/2009 or seasonal H1N1.

show abstract

Section: Discussionmentioning

confidence: 99%

Comparison of pro-inflammatory cytokine expression and cellular signal transduction in human macrophages infected with different influenza A viruses

Geiler

Michaelis

Sithisarn

et al. 2010

Med Microbiol Immunol

View full text Add to dashboard Cite

show abstract

“…A minimum of 12 mutations can be observed for chickens with severe inflammatory cardiomyopathy. These mutations can skew coding regions of chromosomes, with subsequent functional alterations such as cell cycle regulation, clonal proliferation of immune system cells, and tissue injury (72,185,196,205,455). The complex intragenomic interactions affecting immune effectors and target cells may explain the variegated pathology in Chagas' disease.…”

Section: Use Of Tptail-pcr To Map Kdna Mutations In the Chicken Genomementioning

confidence: 99%

Pathogenesis of Chagas' Disease: Parasite Persistence and Autoimmunity

et al. 2011

View full text Add to dashboard Cite

SUMMARY Acute Trypanosoma cruzi infections can be asymptomatic, but chronically infected individuals can die of Chagas' disease. The transfer of the parasite mitochondrial kinetoplast DNA (kDNA) minicircle to the genome of chagasic patients can explain the pathogenesis of the disease; in cases of Chagas' disease with evident cardiomyopathy, the kDNA minicircles integrate mainly into retrotransposons at several chromosomes, but the minicircles are also detected in coding regions of genes that regulate cell growth, differentiation, and immune responses. An accurate evaluation of the role played by the genotype alterations in the autoimmune rejection of self-tissues in Chagas' disease is achieved with the cross-kingdom chicken model system, which is refractory to T. cruzi infections. The inoculation of T. cruzi into embryonated eggs prior to incubation generates parasite-free chicks, which retain the kDNA minicircle sequence mainly in the macrochromosome coding genes. Crossbreeding transfers the kDNA mutations to the chicken progeny. The kDNA-mutated chickens develop severe cardiomyopathy in adult life and die of heart failure. The phenotyping of the lesions revealed that cytotoxic CD45, CD8 + γδ, and CD8α + T lymphocytes carry out the rejection of the chicken heart. These results suggest that the inflammatory cardiomyopathy of Chagas' disease is a genetically driven autoimmune disease.

show abstract

“…We observed no difference in the abilities of the insNA and wt viruses to induce cytokine transcription upon infection of the chicken lung epithelial cell line CLEC213 (6) (data not shown). Therefore, the differences observed in vivo could involve other cell types from the inflammatory response, including cells of myeloid origin and lymphocytes, activated or recruited locally in response to infection (22,28).…”

mentioning

confidence: 99%

Length Variations in the NA Stalk of an H7N1 Influenza Virus Have Opposite Effects on Viral Excretion in Chickens and Ducks

Hoffmann

Munier

Larcher

et al. 2012

J Virol

View full text Add to dashboard Cite

A deletion of ϳ20 amino acids in the stalk of neuraminidase is frequently observed upon transmission of influenza A viruses from waterfowl to domestic poultry. A pair of recombinant H7N1 viruses bearing either a short-or long-stalk neuraminidase was genetically engineered. Inoculation of the long-stalk-neuraminidase virus resulted in a higher cloacal excretion in ducks and led conversely to lower-level oropharyngeal excretion in chickens, associated with a higher-level local immune response and better survival. Therefore, a short-stalk neuraminidase is a determinant of viral adaptation and virulence in chickens but is detrimental to virus replication and shedding in ducks.

show abstract

Roles of the ERK MAPK in the regulation of proinflammatory and apoptotic responses in chicken macrophages infected with H9N2 avian influenza virus

Cited by 64 publications

References 36 publications

Comparison of pro-inflammatory cytokine expression and cellular signal transduction in human macrophages infected with different influenza A viruses

Comparison of pro-inflammatory cytokine expression and cellular signal transduction in human macrophages infected with different influenza A viruses

Pathogenesis of Chagas' Disease: Parasite Persistence and Autoimmunity

Length Variations in the NA Stalk of an H7N1 Influenza Virus Have Opposite Effects on Viral Excretion in Chickens and Ducks

Contact Info

Product

Resources

About