A new model of outbred genetically selected mice which present a strong acute inflammatory response in the absence of complement component C5

Amano, Mariane Tami; Carneiro, Adriana S.; Ribeiro, Orlando; Cabrera, Wafa K.; Franco, Marcelo De; Ibañez, Olga M.; Isaac, Lourdes; Starobinas, Nancy

doi:10.1007/s00011-008-8132-4

Cited by 7 publications

(5 citation statements)

References 30 publications

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“…Ribeiro and coworkers [32] detected high concentrations of C5a fragment in the Biogel-induced inflammatory exudate of AIRmax animals when compared to AIRmin. Consistent with these results, AIRmax sublines homozygous for the Slc11a1 gene R allele, which lack C5a, are more resistant to arthritis than the homozygous mice for the S alleles [33]. Expression of these genes in the PIA-resistant AIRmin line was unaffected by pristane.…”

Section: Discussionmentioning

confidence: 55%

miRNA Expression and Interaction with Genes Involved in Susceptibility to Pristane-Induced Arthritis

Fernandes

Borrego

Jensen

et al. 2018

Journal of Immunology Research

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Pristane-induced arthritis (PIA) in mice is an experimental model that resembles human rheumatoid arthritis, a chronic autoimmune disease that affects joints and is characterized by synovial inflammation and articular cartilage and bone destruction. AIRmax and AIRmin mouse lines differ in their susceptibility to PIA, and linkage analysis in this model mapped arthritis severity QTLs in chromosomes 5 and 8. miRNAs are a class of small RNA molecules that have been extensively studied in the development of arthritis. We analyzed miRNA and gene expression profiles in peritoneal cells of AIRmax and AIRmin lines, in order to evaluate the genetic architecture in this model. Susceptible AIRmax mice showed higher gene (2025 vs 1043) and miRNA (240 vs 59) modulation than resistant AIRmin mice at the onset of disease symptoms. miR-132-3p/212-3p, miR-106-5p, miR-27b-3p, and miR-25-3p were among the miRNAs with the highest expression in susceptible animals, showing a negative correlation with the expression of predicted target genes (Il10, Cd69, and Sp1r1). Our study showed that global gene and miRNA expression profiles in peritoneal cells of susceptible AIRmax and resistant AIRmin lines during pristane-induced arthritis are distinct, evidencing interesting targets for further validation.

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Section: Discussionmentioning

confidence: 55%

miRNA Expression and Interaction with Genes Involved in Susceptibility to Pristane-Induced Arthritis

Fernandes

Borrego

Jensen

et al. 2018

Journal of Immunology Research

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“…The differences in inflammatory cell population between the model described by Medicherla et al, and the one reported here is interesting, but may merely reflect that in Medicherla et al, A/J mice were used, while we used BALB/c mice. A/J mice lack part of the complement system [14] and perhaps would not be able to promote a full anti-inflammatory response to the TS challenge. In fact, many other studies assessing acute TS exposure in mice with fully intact complement systems show that acute TS exposure leads to an inflammatory infiltrate dominated by neutrophils [15, 16] and not by macrophages.…”

Section: Discussionmentioning

confidence: 99%

The role of the CCR1 receptor in the inflammatory response to tobacco smoke in a mouse model

et al. 2010

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ObjectiveThe aim was to create pathological changes in mice relevant to human smoke exposure that can be used to further understand the mechanisms and pathology of smoke-induced inflammatory disease.MethodsMice were exposed to tobacco smoke or lipopolysaccharide (LPS) to generate an inflammatory infiltrate within the lungs.ResultsTobacco smoke exposure over a 4 day period led to neutrophilia in the lungs of BALB/c mice. Within the inflammatory exudates, significant changes were also seen in protein levels of IL-1B, IL-6, MIP-2, KC (IL-8) and TIMP-1 as measured by ELISA. Further protein changes, as measured via multiplex analysis revealed increased levels of MMP-9, MDC, LIF and MCP-1, amongst other mediators. Major changes in whole lung tissue gene expression patterns were observed. The neutrophilia seen after smoke exposure was steroid-insensitive, relative to doses of steroid needed to reduce LPS-driven neutrophilia in controls. This exposes pathological switches that are changed upon exposure to tobacco smoke, rendering steroids less effective under these conditions. Challenge of chemokine receptor type 1 (CCR1) KO mice in the tobacco smoke model showed that lack of this gene protected the mice from smoke-induced inflammation.ConclusionsThis suggests the CCR1 receptor has a key role in the pathogenesis of smoke-induced inflammation.

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“…Nas articulações dos animais AIRmax SS (score 12), após 180 dias do tratamento com pristane, foi observado um infiltrado inflamatório com predomínio de células mononucleares (AMANO et al, 2009). Nossos experimentos neste projeto reproduziram os dados de incidência/severidade publicados anteriormente pelo nosso grupo.…”

Section: Análise Da Articulação Da Pataunclassified

Participação do gene Slc11a1 na modulação da resposta imune na artrite induzida por pristane em camundongos selecionados para resposta inflamatória aguda.

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A new model of outbred genetically selected mice which present a strong acute inflammatory response in the absence of complement component C5

Abstract: The AIRmax(RR) line is a new experimental mouse model in which a strong inflammatory response can be triggered in vivo in the absence of C5.

Cited by 7 publications

References 30 publications

miRNA Expression and Interaction with Genes Involved in Susceptibility to Pristane-Induced Arthritis

miRNA Expression and Interaction with Genes Involved in Susceptibility to Pristane-Induced Arthritis

The role of the CCR1 receptor in the inflammatory response to tobacco smoke in a mouse model

Participação do gene Slc11a1 na modulação da resposta imune na artrite induzida por pristane em camundongos selecionados para resposta inflamatória aguda.

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