A functional polymorphism in <i>MMP1</i> could influence osteomyelitis development

Montes, A. Hugo; Valle-Garay, Eulalia; Álvarez, Victoria; Pevida, Marta; Pérez, Eugenio Sanz; Paz, Jose; Meana, Álvaro; Asensi, Vı́ctor

doi:10.1359/jbmr.091013

Cited by 27 publications

(27 citation statements)

References 33 publications

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“…Tubes were centrifuged for 5 minutes at 1,800 g and serum was removed and frozen at −80°C until use. Plasma levels of MMPs-1, -2, -3, -8, - 9, -10 and -13 and TIMP -1, -2, and -4 were measured using the Quantibody TM Human MMP Array 1 from Raybiotech (Raybiotech, Parkway Lane, Norcross, GA, USA) according to the manufacturer's instructions26.…”

Section: Methodsmentioning

confidence: 99%

“…The following SNPs of MMPs were genotyped by PCR: MMP-1 (−1607 1G/2G , rs 11292517), MMP-3 (−1612 5A/6A , rs35068180), MMP-8 (−799 C/T, rs 11225395), MMP-9 (−1562 C/T , rs 34016235), and MMP-13 (−77 A/G , rs 2252070). Oligonucleotide primer sequences, PCR conditions and restriction enzymes used for genotyping and sequencing the different matrix metalloproteases ( MMPs ) polymorphisms studied are described elsewhere16222426.…”

Section: Methodsmentioning

confidence: 99%

“…These functional MMPs SNPs are associated mostly with cardiovascular disease susceptibility, but also with cancer, rheumatic diseases and other conditions, such as endometriosis161718192021222324. To our knowledge, only two papers on MMPs SNPs and infection have been published, one reporting an association of a MMP9 SNP with periodontitis susceptibility25 and a second, from our group, of a MMP1 SNP with bacterial osteomyelitis26. Very recently an association between a TIMP1 SNP and sepsis mortality has been published27.…”

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confidence: 99%

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Role of plasma matrix-metalloproteases (MMPs) and their polymorphisms (SNPs) in sepsis development and outcome in ICU patients

Martin

Asensi

Montes

et al. 2014

Sci Rep

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Matrix-metalloproteases (MMPs) and their tissue-inhibitors (TIMPs), modulated by different single nucleotide polymorphisms (SNPs), are critical in sepsis development. Ninety ICU severely septic and 91 ICU uninfected patients were prospectively studied. MMP-1 (−1607 1G/2G), MMP-3 (−1612 5A/6A), MMP-8 (−799 C/T), MMP-9 (−1562 C/T), and MMP-13 (−77A/G) SNPs were genotyped. Plasma MMPs (-1, -2, -3, -8, -9, -10, -13) and TIMPs (-1,-2,-4) were measured. AA homozygotes and A allele carriers of MMP-13 (−77 A/G) and 1G2G carriers of the MMP-1 (−1607 1G/2G) SNPs frequencies were different between septic and uninfected patients (p < 0.05), as well as plasma MMP-3, -8, -9 -10 and TIMP-2 levels (p < 0.04). No differences in MMPs levels among MMP-13 or MMP-1 SNPs genotypes carriers were observed. The area under the ROC curve for MMP-8 in the diagnosis of sepsis was 0.87 (95% CI 0.82–0.92), and that of CRP was 0.98 (0.94–0.998), whereas the area of MMP-9 in the detection of non-septic state was 0.73 (0.65–0.80), p < 0.0001 for all curves. Sepsis associated with increased MMP-8 and decreased MMP-9 levels in multivariate analysis (p < 0.0002). We report for the first time an association between MMP-13 and MMP-1 SNPs and sepsis. An independent association of MMP-8 and MMP-9 levels with sepsis was also observed.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Role of plasma matrix-metalloproteases (MMPs) and their polymorphisms (SNPs) in sepsis development and outcome in ICU patients

Martin

Asensi

Montes

et al. 2014

Sci Rep

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“…It is clear that it is multifactorial and influenced mainly by local factors related to the bone lesion and microorganisms inoculated into the bone, but inherited factors and cell immunity dysfunctions could play some role as well [14][15][16][17][18][19][20][21][22][23][24][25][26].…”

Section: Editorialmentioning

confidence: 99%

Role of Neutrophils Apoptosis in Osteomyelitis Pathogenesis

Asensi¹,

Collazos²,

Valle-Garay³

2017

Clin Microbiol

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EditorialOsteomyelitis is a bone infection characterized by progressive inflammatory destruction of the infected bone and new apposition of bone at the site of infection. In adults, osteomyelitis is usually a complication of open wounds due to fractures, surgery, or both, with or without the presence of foreign bodies such as prosthetic devices. In fact, it is estimated that about 0.4 to 7% of trauma and orthopaedic interventions are complicated by osteomyelitis [1][2][3][4][5][6].Bone infections can also be the result of bacteraemia, mostly in children and in elderly patients, in whom the infection involves mainly the axial skeleton. The microorganism most frequently isolated in both post-traumatic and haematogenous cases is Staphylococcus aureus.Osteomyelitis constitutes a difficult-to-treat infection, with high rates of recurrence of about 20-30% despite appropriate medical and surgical therapies, causing significant morbidity and mortality [7][8][9][10][11][12][13].Much attention has been dedicated to improving the medical and surgical treatments of osteomyelitis, but little progress has been made toward understanding its pathogenesis. It is clear that it is multifactorial and influenced mainly by local factors related to the bone lesion and microorganisms inoculated into the bone, but inherited factors and cell immunity dysfunctions could play some role as well [14][15][16][17][18][19][20][21][22][23][24][25][26].

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“…Multiple genetic differences have been identified between patients with osteomyelitis and control subjects, indicating possible hereditary susceptibilities. A recent study identified polymorphisms resulting in upregulation of MMPs with significantly higher frequency in patients with osteomyelitis than in healthy controls (Angel Hugo Montes et al, 2010). The mutation may cause an increase in osteoblast MMP1 production, which has been linked to osteodestructive activity in metastasis (Lu et al, 2009) and inflammatory arthropathy (Neidhart et al, 2009).…”

Section: Geneticsmentioning

confidence: 99%