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Pathophysiological changes induced by Pseudomonas aeruginosa infection are involved in MMP-12 and MMP-13 upregulation in human carcinoma epithelial cells and a pneumonia mouse model.

Park JW, Shin IS, Ha UH, Oh SR, Kim JH, Ahn KS - Infect. Immun. (2015)

Bottom Line: P. aeruginosa potently activates the innate immune system mostly through the recognition of pathogen-associated molecular patterns, such as flagellin.Matrix metalloproteinases 12 and 13 (MMP-12 and MMP-13, respectively) exacerbate chronic lung infection and inflammation by promoting uncontrolled tissue rearrangements and fibrosis, yet the underlying molecular mechanisms by which this occurs remain largely unknown.Moreover, we also found that the NF-κB pathway might be involved in the induction of cytokines in response to strain K infection.

View Article: PubMed Central - PubMed

Affiliation: Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Chungbuk, Republic of Korea College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.

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Proinflammatory cytokine expression in MMP-12 and MMP-13 siRNA-transfected H292 cells after P. aeruginosa strain K (PAK) infection. TNF-α (A) and IL-1β (B) protein levels were assessed by qRT-PCR and ELISA, respectively. Bars indicate the mean ± standard deviation from three independent experiments performed in duplicate. −, normal control H292 cells treated with PBS only; siNC, H292 cells treated with control siRNA; siMMP-12, H292 cells treated with MMP-12 siRNA only; siMMP-13, H292 cells treated with MMP-13 siRNA only; PAK + siNC, H292 cells treated with control siRNA plus strain K (MOI of 200); PAK + siMMP-12, H292 cells treated with MMP-12 siRNA plus strain K (MOI of 200); PAK + siMMP-13, H292 cells treated with MMP-13 siRNA plus strain K (MOI of 200). #, significantly different from normal control group; **, P < 0.01.
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Figure 8: Proinflammatory cytokine expression in MMP-12 and MMP-13 siRNA-transfected H292 cells after P. aeruginosa strain K (PAK) infection. TNF-α (A) and IL-1β (B) protein levels were assessed by qRT-PCR and ELISA, respectively. Bars indicate the mean ± standard deviation from three independent experiments performed in duplicate. −, normal control H292 cells treated with PBS only; siNC, H292 cells treated with control siRNA; siMMP-12, H292 cells treated with MMP-12 siRNA only; siMMP-13, H292 cells treated with MMP-13 siRNA only; PAK + siNC, H292 cells treated with control siRNA plus strain K (MOI of 200); PAK + siMMP-12, H292 cells treated with MMP-12 siRNA plus strain K (MOI of 200); PAK + siMMP-13, H292 cells treated with MMP-13 siRNA plus strain K (MOI of 200). #, significantly different from normal control group; **, P < 0.01.

Mentions: To determine whether MMP-12 and MMP-13 are necessary for strain K-induced proinflammatory cytokine expression, we transfected cells with siRNAs targeting either MMP-12 or MMP-13 and saw a detectable reduction in protein 24 h after transfection. We have found effects on the expression of MMP-12 and MMP-13 (data not shown). Notably, the induction of proinflammatory cytokines previously observed in response to strain K infection in normal H292 cells was absent in siRNA-transfected cells. Using an ELISA, proinflammatory cytokine expression in response to the IL-1β and TNF-α consensus sequence was also significantly reduced in the presence of proinflammatory cytokine-specific siRNAs in H292 cells (Fig. 8A and B). These data indicate that MMP-12 and MMP-13 are necessary for proinflammatory cytokine expression.


Pathophysiological changes induced by Pseudomonas aeruginosa infection are involved in MMP-12 and MMP-13 upregulation in human carcinoma epithelial cells and a pneumonia mouse model.

Park JW, Shin IS, Ha UH, Oh SR, Kim JH, Ahn KS - Infect. Immun. (2015)

Proinflammatory cytokine expression in MMP-12 and MMP-13 siRNA-transfected H292 cells after P. aeruginosa strain K (PAK) infection. TNF-α (A) and IL-1β (B) protein levels were assessed by qRT-PCR and ELISA, respectively. Bars indicate the mean ± standard deviation from three independent experiments performed in duplicate. −, normal control H292 cells treated with PBS only; siNC, H292 cells treated with control siRNA; siMMP-12, H292 cells treated with MMP-12 siRNA only; siMMP-13, H292 cells treated with MMP-13 siRNA only; PAK + siNC, H292 cells treated with control siRNA plus strain K (MOI of 200); PAK + siMMP-12, H292 cells treated with MMP-12 siRNA plus strain K (MOI of 200); PAK + siMMP-13, H292 cells treated with MMP-13 siRNA plus strain K (MOI of 200). #, significantly different from normal control group; **, P < 0.01.
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Figure 8: Proinflammatory cytokine expression in MMP-12 and MMP-13 siRNA-transfected H292 cells after P. aeruginosa strain K (PAK) infection. TNF-α (A) and IL-1β (B) protein levels were assessed by qRT-PCR and ELISA, respectively. Bars indicate the mean ± standard deviation from three independent experiments performed in duplicate. −, normal control H292 cells treated with PBS only; siNC, H292 cells treated with control siRNA; siMMP-12, H292 cells treated with MMP-12 siRNA only; siMMP-13, H292 cells treated with MMP-13 siRNA only; PAK + siNC, H292 cells treated with control siRNA plus strain K (MOI of 200); PAK + siMMP-12, H292 cells treated with MMP-12 siRNA plus strain K (MOI of 200); PAK + siMMP-13, H292 cells treated with MMP-13 siRNA plus strain K (MOI of 200). #, significantly different from normal control group; **, P < 0.01.
Mentions: To determine whether MMP-12 and MMP-13 are necessary for strain K-induced proinflammatory cytokine expression, we transfected cells with siRNAs targeting either MMP-12 or MMP-13 and saw a detectable reduction in protein 24 h after transfection. We have found effects on the expression of MMP-12 and MMP-13 (data not shown). Notably, the induction of proinflammatory cytokines previously observed in response to strain K infection in normal H292 cells was absent in siRNA-transfected cells. Using an ELISA, proinflammatory cytokine expression in response to the IL-1β and TNF-α consensus sequence was also significantly reduced in the presence of proinflammatory cytokine-specific siRNAs in H292 cells (Fig. 8A and B). These data indicate that MMP-12 and MMP-13 are necessary for proinflammatory cytokine expression.

Bottom Line: P. aeruginosa potently activates the innate immune system mostly through the recognition of pathogen-associated molecular patterns, such as flagellin.Matrix metalloproteinases 12 and 13 (MMP-12 and MMP-13, respectively) exacerbate chronic lung infection and inflammation by promoting uncontrolled tissue rearrangements and fibrosis, yet the underlying molecular mechanisms by which this occurs remain largely unknown.Moreover, we also found that the NF-κB pathway might be involved in the induction of cytokines in response to strain K infection.

View Article: PubMed Central - PubMed

Affiliation: Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Chungbuk, Republic of Korea College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.

Show MeSH
Related in: MedlinePlus