Effect of Bacterial Exposure on Acellular Human Dermis in a Rat Ventral Hernia Model

Jennifer E. Keller, Charles J. Dolce, Kenneth C Walters, Jessica J. Heath, Richard D. Peindl, Kent W. Kercher, Amy E. Lincourt, B. Todd Heniford, David A. Iannitti

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Background: Effectiveness of acellular human dermis (AHD) as an alternative to synthetic mesh in contaminated fields has been described. Cellular migration after implantation and corresponding strength of attachment is not well documented. Our aim is to correlate AHD vascularization, fibroblast migration, and strength of attachment with presence of inflammatory cells in clean and contaminated fields. Materials and Methods: Lewis rats were randomized to a control and three experimental groups. AHD was placed as an onlay over the intact abdominal wall. Experimental groups (n = 72) were exposed to Staphilococcus aureus at 1 × 104, 1 × 105, or 1 × 106 by direct application; controls (n = 12) were not exposed. At 5 and 28 d, abdominal walls were explanted and tissue ingrowth assessed via tensiometry measuring energy (E) and max stress (MS) at the AHD-tissue interface. Vascularity, fibroblast migration, and inflammatory cell migration were compared using light microscopy. Results: Shear strength reported as energy and max stress were significantly greater at 28 versus 5 d in all experimental groups, remaining unchanged in controls. Plasma cells and histiocytes significantly increased in all groups; macrophages increased in experimental groups only. Vascular ingrowth increased significantly in all groups; fibroblast migration was greater in controls and 1 × 106 exposed group only. Conclusions: Contamination of AHD results in inflammatory cell influx and a surprising increase in shear strength. Interestingly, shear strength does not increase without contamination. Inflammation stimulates vascular ingrowth, but not equally significant fibroblast migration. Longer survivals are required to determine if energy and max stress of controls increase, and fibroblast migration follows vascular ingrowth.

Original languageEnglish (US)
Pages (from-to)148-152
Number of pages5
JournalJournal of Surgical Research
Volume162
Issue number1
DOIs
StatePublished - Jul 1 2010

Fingerprint

Acellular Dermis
Ventral Hernia
Shear Strength
Fibroblasts
Blood Vessels
Abdominal Wall
Inlays
Histiocytes
Plasma Cells
Cell Movement
Microscopy
Macrophages
Inflammation
Light
Survival

Keywords

  • acellular human dermis
  • bacterial contamination
  • biologics
  • inflammation
  • ingrowth
  • shear strength

ASJC Scopus subject areas

  • Surgery

Cite this

Keller, J. E., Dolce, C. J., Walters, K. C., Heath, J. J., Peindl, R. D., Kercher, K. W., ... Iannitti, D. A. (2010). Effect of Bacterial Exposure on Acellular Human Dermis in a Rat Ventral Hernia Model. Journal of Surgical Research, 162(1), 148-152. https://doi.org/10.1016/j.jss.2009.03.083

Effect of Bacterial Exposure on Acellular Human Dermis in a Rat Ventral Hernia Model. / Keller, Jennifer E.; Dolce, Charles J.; Walters, Kenneth C; Heath, Jessica J.; Peindl, Richard D.; Kercher, Kent W.; Lincourt, Amy E.; Heniford, B. Todd; Iannitti, David A.

In: Journal of Surgical Research, Vol. 162, No. 1, 01.07.2010, p. 148-152.

Research output: Contribution to journalArticle

Keller, JE, Dolce, CJ, Walters, KC, Heath, JJ, Peindl, RD, Kercher, KW, Lincourt, AE, Heniford, BT & Iannitti, DA 2010, 'Effect of Bacterial Exposure on Acellular Human Dermis in a Rat Ventral Hernia Model', Journal of Surgical Research, vol. 162, no. 1, pp. 148-152. https://doi.org/10.1016/j.jss.2009.03.083
Keller, Jennifer E. ; Dolce, Charles J. ; Walters, Kenneth C ; Heath, Jessica J. ; Peindl, Richard D. ; Kercher, Kent W. ; Lincourt, Amy E. ; Heniford, B. Todd ; Iannitti, David A. / Effect of Bacterial Exposure on Acellular Human Dermis in a Rat Ventral Hernia Model. In: Journal of Surgical Research. 2010 ; Vol. 162, No. 1. pp. 148-152.
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abstract = "Background: Effectiveness of acellular human dermis (AHD) as an alternative to synthetic mesh in contaminated fields has been described. Cellular migration after implantation and corresponding strength of attachment is not well documented. Our aim is to correlate AHD vascularization, fibroblast migration, and strength of attachment with presence of inflammatory cells in clean and contaminated fields. Materials and Methods: Lewis rats were randomized to a control and three experimental groups. AHD was placed as an onlay over the intact abdominal wall. Experimental groups (n = 72) were exposed to Staphilococcus aureus at 1 × 104, 1 × 105, or 1 × 106 by direct application; controls (n = 12) were not exposed. At 5 and 28 d, abdominal walls were explanted and tissue ingrowth assessed via tensiometry measuring energy (E) and max stress (MS) at the AHD-tissue interface. Vascularity, fibroblast migration, and inflammatory cell migration were compared using light microscopy. Results: Shear strength reported as energy and max stress were significantly greater at 28 versus 5 d in all experimental groups, remaining unchanged in controls. Plasma cells and histiocytes significantly increased in all groups; macrophages increased in experimental groups only. Vascular ingrowth increased significantly in all groups; fibroblast migration was greater in controls and 1 × 106 exposed group only. Conclusions: Contamination of AHD results in inflammatory cell influx and a surprising increase in shear strength. Interestingly, shear strength does not increase without contamination. Inflammation stimulates vascular ingrowth, but not equally significant fibroblast migration. Longer survivals are required to determine if energy and max stress of controls increase, and fibroblast migration follows vascular ingrowth.",
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AU - Peindl, Richard D.

AU - Kercher, Kent W.

AU - Lincourt, Amy E.

AU - Heniford, B. Todd

AU - Iannitti, David A.

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N2 - Background: Effectiveness of acellular human dermis (AHD) as an alternative to synthetic mesh in contaminated fields has been described. Cellular migration after implantation and corresponding strength of attachment is not well documented. Our aim is to correlate AHD vascularization, fibroblast migration, and strength of attachment with presence of inflammatory cells in clean and contaminated fields. Materials and Methods: Lewis rats were randomized to a control and three experimental groups. AHD was placed as an onlay over the intact abdominal wall. Experimental groups (n = 72) were exposed to Staphilococcus aureus at 1 × 104, 1 × 105, or 1 × 106 by direct application; controls (n = 12) were not exposed. At 5 and 28 d, abdominal walls were explanted and tissue ingrowth assessed via tensiometry measuring energy (E) and max stress (MS) at the AHD-tissue interface. Vascularity, fibroblast migration, and inflammatory cell migration were compared using light microscopy. Results: Shear strength reported as energy and max stress were significantly greater at 28 versus 5 d in all experimental groups, remaining unchanged in controls. Plasma cells and histiocytes significantly increased in all groups; macrophages increased in experimental groups only. Vascular ingrowth increased significantly in all groups; fibroblast migration was greater in controls and 1 × 106 exposed group only. Conclusions: Contamination of AHD results in inflammatory cell influx and a surprising increase in shear strength. Interestingly, shear strength does not increase without contamination. Inflammation stimulates vascular ingrowth, but not equally significant fibroblast migration. Longer survivals are required to determine if energy and max stress of controls increase, and fibroblast migration follows vascular ingrowth.

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