Mediators, initiating the inflammatory response, released in organ culture by full-thickness human skin explants exposed to the irritant, sulfur mustard

Toru Rikimaru, Masahiro Nakamura, Takafumi Yano, Gregory Beck, Gail S. Habicht, Lynda L. Rennie, Martha Widra, Carol A. Hirshman, Marc G. Boulay, Ernst W Spannhake, Gerald Sylvan Lazarus, Peggy J. Pula, Arthur M. Dannenberg

Research output: Contribution to journalArticle

Abstract

Mediators released from injured human skin that initiate the inflammatory response have not been adequately identified. Organ culture of full-thickness skin explants enables us to do so, because injury to the skin can be made in vitro, eliminating the rapid leakage of serum and infiltration of leukocytes that occur in vivo. In our studies, the military vesicant sulfur mustard (SM) (10 μl of a 0.01 to 1.0% dilution) was topically applied to injure the epidermis of the explant. Then, the explants were cultured in small Petri dishes, usually for 18 h at 36°C, and the organ-culture fluids were assayed for various inflammatory mediators. We found that the culture fluids from SM-exposed and control explants contained similar amounts of angiotensin-converting enzyme, trypsin-like and chymotrypsin-like proteases, acid phosphatase, β-glucuronidase, β-galactosidase, lysozyme, deoxyribonuclease, ribonuclease, interleukin 1, and lactic dehydrogenase. However, the culture fluids from SM-exposed explants contained increased amounts of histamine and plasminogen-activating activity, and often prostaglandin E2, when compared to culture fluids from control explants. After 3 to 4 d in culture, full-thickness human skin explants, when exposed to 0.2% SM (but not when exposed to 1.0% SM), sometimes showed separation of the epidermis and increased collagenase activity (i.e., hydroxyproline release). Thus, histamine (from local mast cells), and prostaglandin E2 and plasminogen-activating activity (probably from both mast cells and epidermal cells) are apparently involved in early mediation of the inflammatory response.

Original languageEnglish (US)
Pages (from-to)888-897
Number of pages10
JournalJournal of Investigative Dermatology
Volume96
Issue number6
StatePublished - Jun 1991

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Mustard Gas
Irritants
Organ Culture Techniques
Skin
Fluids
Plasminogen
Dinoprostone
Epidermis
Mast Cells
Histamine
Galactosidases
Chymases
Deoxyribonucleases
Glucuronidase
Hydroxyproline
Collagenases
Peptidyl-Dipeptidase A
Ribonucleases
Muramidase
Acid Phosphatase

ASJC Scopus subject areas

  • Dermatology

Cite this

Rikimaru, T., Nakamura, M., Yano, T., Beck, G., Habicht, G. S., Rennie, L. L., ... Dannenberg, A. M. (1991). Mediators, initiating the inflammatory response, released in organ culture by full-thickness human skin explants exposed to the irritant, sulfur mustard. Journal of Investigative Dermatology, 96(6), 888-897.

Mediators, initiating the inflammatory response, released in organ culture by full-thickness human skin explants exposed to the irritant, sulfur mustard. / Rikimaru, Toru; Nakamura, Masahiro; Yano, Takafumi; Beck, Gregory; Habicht, Gail S.; Rennie, Lynda L.; Widra, Martha; Hirshman, Carol A.; Boulay, Marc G.; Spannhake, Ernst W; Lazarus, Gerald Sylvan; Pula, Peggy J.; Dannenberg, Arthur M.

In: Journal of Investigative Dermatology, Vol. 96, No. 6, 06.1991, p. 888-897.

Research output: Contribution to journalArticle

Rikimaru, T, Nakamura, M, Yano, T, Beck, G, Habicht, GS, Rennie, LL, Widra, M, Hirshman, CA, Boulay, MG, Spannhake, EW, Lazarus, GS, Pula, PJ & Dannenberg, AM 1991, 'Mediators, initiating the inflammatory response, released in organ culture by full-thickness human skin explants exposed to the irritant, sulfur mustard', Journal of Investigative Dermatology, vol. 96, no. 6, pp. 888-897.
Rikimaru, Toru ; Nakamura, Masahiro ; Yano, Takafumi ; Beck, Gregory ; Habicht, Gail S. ; Rennie, Lynda L. ; Widra, Martha ; Hirshman, Carol A. ; Boulay, Marc G. ; Spannhake, Ernst W ; Lazarus, Gerald Sylvan ; Pula, Peggy J. ; Dannenberg, Arthur M. / Mediators, initiating the inflammatory response, released in organ culture by full-thickness human skin explants exposed to the irritant, sulfur mustard. In: Journal of Investigative Dermatology. 1991 ; Vol. 96, No. 6. pp. 888-897.
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abstract = "Mediators released from injured human skin that initiate the inflammatory response have not been adequately identified. Organ culture of full-thickness skin explants enables us to do so, because injury to the skin can be made in vitro, eliminating the rapid leakage of serum and infiltration of leukocytes that occur in vivo. In our studies, the military vesicant sulfur mustard (SM) (10 μl of a 0.01 to 1.0{\%} dilution) was topically applied to injure the epidermis of the explant. Then, the explants were cultured in small Petri dishes, usually for 18 h at 36°C, and the organ-culture fluids were assayed for various inflammatory mediators. We found that the culture fluids from SM-exposed and control explants contained similar amounts of angiotensin-converting enzyme, trypsin-like and chymotrypsin-like proteases, acid phosphatase, β-glucuronidase, β-galactosidase, lysozyme, deoxyribonuclease, ribonuclease, interleukin 1, and lactic dehydrogenase. However, the culture fluids from SM-exposed explants contained increased amounts of histamine and plasminogen-activating activity, and often prostaglandin E2, when compared to culture fluids from control explants. After 3 to 4 d in culture, full-thickness human skin explants, when exposed to 0.2{\%} SM (but not when exposed to 1.0{\%} SM), sometimes showed separation of the epidermis and increased collagenase activity (i.e., hydroxyproline release). Thus, histamine (from local mast cells), and prostaglandin E2 and plasminogen-activating activity (probably from both mast cells and epidermal cells) are apparently involved in early mediation of the inflammatory response.",
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AU - Rikimaru, Toru

AU - Nakamura, Masahiro

AU - Yano, Takafumi

AU - Beck, Gregory

AU - Habicht, Gail S.

AU - Rennie, Lynda L.

AU - Widra, Martha

AU - Hirshman, Carol A.

AU - Boulay, Marc G.

AU - Spannhake, Ernst W

AU - Lazarus, Gerald Sylvan

AU - Pula, Peggy J.

AU - Dannenberg, Arthur M.

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Y1 - 1991/6

N2 - Mediators released from injured human skin that initiate the inflammatory response have not been adequately identified. Organ culture of full-thickness skin explants enables us to do so, because injury to the skin can be made in vitro, eliminating the rapid leakage of serum and infiltration of leukocytes that occur in vivo. In our studies, the military vesicant sulfur mustard (SM) (10 μl of a 0.01 to 1.0% dilution) was topically applied to injure the epidermis of the explant. Then, the explants were cultured in small Petri dishes, usually for 18 h at 36°C, and the organ-culture fluids were assayed for various inflammatory mediators. We found that the culture fluids from SM-exposed and control explants contained similar amounts of angiotensin-converting enzyme, trypsin-like and chymotrypsin-like proteases, acid phosphatase, β-glucuronidase, β-galactosidase, lysozyme, deoxyribonuclease, ribonuclease, interleukin 1, and lactic dehydrogenase. However, the culture fluids from SM-exposed explants contained increased amounts of histamine and plasminogen-activating activity, and often prostaglandin E2, when compared to culture fluids from control explants. After 3 to 4 d in culture, full-thickness human skin explants, when exposed to 0.2% SM (but not when exposed to 1.0% SM), sometimes showed separation of the epidermis and increased collagenase activity (i.e., hydroxyproline release). Thus, histamine (from local mast cells), and prostaglandin E2 and plasminogen-activating activity (probably from both mast cells and epidermal cells) are apparently involved in early mediation of the inflammatory response.

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