Skin response to lipopolysaccharide-induced sepsis based on histology

Maria Ulfa; Hotimah Masdan Salim; Winawati Eka Putri; Irmawan Farindra

doi:10.15562/bmj.v12i3.4397

Skin response to lipopolysaccharide-induced sepsis based on histology

Maria Ulfa ,

Hotimah Masdan Salim ,

Winawati Eka Putri ,

Irmawan Farindra ,

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DOI: https://doi.org/10.15562/bmj.v12i3.4397 |
Published: 2023-11-17

Abstract

Introduction: The skin is the largest organ of the human body. Sepsis is a serious disease and causes multi-organ damage, with a high cause of death. however, the mechanism by which sepsis can damage the skin structure is not clear. This study aimed to investigate skin damage in a lipopolysaccharide-induced endotoxemia (LPS) model widely used in mice.

Methods: This study used an experimental design with a control group that was randomized solely for the post-test. White mice (Mus musculus), the study's population, made up this group. LPS injection for 4 hours (LPS+4h, n=4), LPS injection for 8 hours (LPS+8h, n=4), and control group (Ctrl group, n=4) were randomly assigned to mice. The SPSS ver. 25 statistical analysis program was used. One-Way ANOVA was used to compare more than three sets of data, and Tukey's multiple comparison test was used to assess the results. The p-value of 0.05 was used to determine if the difference was significant.

Results: Based on this study, LPS injection increased the leukocyte concentration significantly (p-value<0.05) in the 4 h and 8 h vs control group. LPS-induced sepsis decreased body weight significantly (p-value<0.05). The morphology of skin thickness in the control group was normal, according to the results of the histopathologic study of the area stained with hematoxylin and eosin. However, the thickness was decreased in mice after 4 hours and 8 injections of LPS significantly (p-value<0.05).

Conclusion: LPS-induced septic mice cause damage to the skin, and changes in skin thickness due to the inflammatory process due to sepsis.

References

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Mathes SH, Ruffner H, Graf-Hausner U. The use of skin models in drug development. Adv Drug Deliv Rev. 2014;69–70:81–102. DOI: http://dx.doi.org/10.1016/j.addr.2013.12.006
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[1] Pasparakis M, Haase I, Nestle FO. Mechanisms regulating skin immunity and inflammation. Nat Rev Immunol. 2014;14(5):289–301. DOI: http://dx.doi.org/10.1038/nri3646

[2] Nedoszytko B, Sokołowska-Wojdyło M, Ruckemann-Dziurdzińska K, Roszkiewicz J, Nowicki RJ. Chemokines and cytokines network in the pathogenesis of the inflammatory skin diseases: Atopic dermatitis, psoriasis and skin mastocytosis. Postep Dermatologii i Alergol. 2014;31(2):84–91. DOI: https://doi.org/10.5114/pdia.2014.40920.

[3] Proksch E, Brandner JM, Jensen JM. The skin: An indispensable barrier. Exp Dermatol. 2008;17(12):1063–72. DOI: https://doi.org/10.1111/j.1600-0625.2008.00786.x.

[4] Semlin L, Schäfer-Korting M, Borelli C, Korting HC. In vitro models for human skin disease. Drug Discov Today. 2011;16(3–4):132–9. DOI: https://doi.org/10.1016/j.drudis.2010.12.001.

[5] Mathes SH, Ruffner H, Graf-Hausner U. The use of skin models in drug development. Adv Drug Deliv Rev. 2014;69–70:81–102. DOI: http://dx.doi.org/10.1016/j.addr.2013.12.006

[6] Corzo-León DE, Munro CA, MacCallum DM. An ex vivo human skin model to study superficial fungal infections. Front Microbiol. 2019;10(JUN):1–17. DOI: https://doi.org/10.3389/fmicb.2019.01172.

[7] Satriyasa BK, Widianti IGA, Manuaba IBGF. The potential of carrot extract as a sunscreen to prevent apoptosis in white mice (Mus musculus) fibroblast cell cultures exposed to UVB light. Bali Med J. 2022;11(2):527–30. DOI: http://dx.doi.org/10.15562/bmj.v11i2.3460.

[8] Nakayama H, Nishida K, Otsu K. Macromolecular Degradation Systems and Cardiovascular Aging. Circ Res. 2016;118(10):1577–92. DOI: https://doi.org/10.1161/circresaha.115.307495.

[9] Aubert G, Lansdorp PM. Telomeres and aging. Physiol Rev. 2008;88(2):557–79. DOI: https://doi.org/10.1152/physrev.00026.2007.

[10] Strbo N, Yin N, Stojadinovic O. Innate and Adaptive Immune Responses in Wound Epithelialization. Adv Wound Care. 2014;3(7):492–501. DOI: https://doi.org/10.1089/wound.2012.0435.

[11] Dellinger RP, Levy MM, Carlet JM, Bion J, Parker MM, Jaeschke R, et al. Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008. Intensive Care Med. 2008;34(1):17–60. DOI: https://doi.org/10.1097/01.ccm.0000298158.12101.41.

[12] Sommer K, Sander AL, Albig M, Weber R, Henrich D, Frank J, et al. Delayed Wound Repair in Sepsis Is Associated with Reduced Local Pro-Inflammatory Cytokine Expression. PLoS One. 2013;8(9). DOI: https://doi.org/10.1371/journal.pone.0073992.

[13] Xiao H, Siddiqui J, Remick DG. Mechanisms of mortality in early and late sepsis. Infect Immun. 2006;74(9):5227–35. DOI: https://doi.org/10.1128/iai.01220-05.

[14] Palomo J, Dietrich D, Martin P, Palmer G, Gabay C. The interleukin (IL)-1 cytokine family - Balance between agonists and antagonists in inflammatory diseases. Cytokine. 2015;76(1):25–37. DOI: http://dx.doi.org/10.1016/j.cyto.2015.06.017

[15] Bak RO, Mikkelsen JG. Regulation of cytokines by small RNAs during skin inflammation. J Biomed Sci. 2010;17(1):1–19. DOI: https://doi.org/10.1186%2F1423-0127-17-53.

[16] Kröller-Schön S, Knorr M, Hausding M, Oelze M, Schuff A, Schell R, et al. Glucose-independent improvement of vascular dysfunction in experimental sepsis by dipeptidyl-peptidase 4 inhibition. Cardiovasc Res. 2012;96(1):140–9. DOI: https://doi.org/10.1093/cvr/cvs246.

[17] Steven S, Dib M, Roohani S, Kashani F, Münzel T, Daiber A. Time response of oxidative/nitrosative stress and inflammation in LPS-induced endotoxaemia—a comparative study of mice and rats. Int J Mol Sci. 2017;18(10). DOI: https://doi.org/10.3390%2Fijms18102176.

Skin response to lipopolysaccharide-induced sepsis based on histology

Abstract

References

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