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Although intensive care treatment is life-saving, it also brings with it a number of undesirable events. Skin rash is not uncommon in a patient whose condition is critical, but treatment should be evaluated quickly and planning should be made to prevent it. If a drug reaction is suspected, all medications that may be relevant should be reevaluated. © 2023 Anestezi Dergisi. All rights reserved.

Although intensive care treatment is life-saving, it also brings with it a number of undesirable events. Skin rash is not uncommon in a patient whose condition is critical, but treatment should be evaluated quickly and planning should be made to prevent it. If a drug reaction is suspected, all medications that may be relevant should be reevaluated. © 2023 Anestezi Dergisi. All rights reserved.

Annexin A1 (AnxA1) is recognized as an endogenous anti-inflammatory molecule. However, its effects on the adaptive immune response and, in particular, on T cells remain unclear. In this study, we investigated the actions of AnxA1 in three distinct models of T cell-mediated inflammation. In contact hypersensitivity, collagen-induced arthritis, and inflammation induced by OT-II TCR transgenic T cells responding to OVA, AnxA1 deficiency significantly increased Ag-induced T cell proliferation and the resultant level of inflammation. In the contact hypersensitivity model, this was associated with increased adhesion of CD4+ T cells, CD8+ T cells, and neutrophils in the dermal microvasculature, as well as increased T cell expression of RORgt and IL-17A. In collageninduced arthritis, deficiency of endogenous AnxA1 increased susceptibility to arthritis and Ag-specific T cell activation. Deficiency of AnxA1 also increased OVA-induced cutaneous delayed-type hypersensitivity and IFN-g and IL-17 release. Transfer experiments using CD4+ T cells from AnxA12/2 mice demonstrated that the absence of AnxA1 solely in T cells resulted in increased inflammatory responses in wild-type recipients. Similarly, experiments using AnxA12/2 OT-II CD4+ T cells demonstrated that the absence of AnxA1 in T cells was sufficient to induce increased Ag-specific CD4+ T cell proliferation in vivo, augment T cell production of IFN-g, IL-17, TNF, and IL-6, and increase Akt, ERK, and p38 activation. Together, these findings indicate that T cell-expressed AnxA1 functions to attenuate T cell-driven inflammatory responses via T cell-intrinsic effects on intracellular signaling, proliferation, and Th1/Th17 cytokine release. Copyright © 2013 by The American Association of Immunologists, Inc.

Annexin A1 (AnxA1) is recognized as an endogenous anti-inflammatory molecule. However, its effects on the adaptive immune response and, in particular, on T cells remain unclear. In this study, we investigated the actions of AnxA1 in three distinct models of T cell-mediated inflammation. In contact hypersensitivity, collagen-induced arthritis, and inflammation induced by OT-II TCR transgenic T cells responding to OVA, AnxA1 deficiency significantly increased Ag-induced T cell proliferation and the resultant level of inflammation. In the contact hypersensitivity model, this was associated with increased adhesion of CD4+ T cells, CD8+ T cells, and neutrophils in the dermal microvasculature, as well as increased T cell expression of RORgt and IL-17A. In collageninduced arthritis, deficiency of endogenous AnxA1 increased susceptibility to arthritis and Ag-specific T cell activation. Deficiency of AnxA1 also increased OVA-induced cutaneous delayed-type hypersensitivity and IFN-g and IL-17 release. Transfer experiments using CD4+ T cells from AnxA12/2 mice demonstrated that the absence of AnxA1 solely in T cells resulted in increased inflammatory responses in wild-type recipients. Similarly, experiments using AnxA12/2 OT-II CD4+ T cells demonstrated that the absence of AnxA1 in T cells was sufficient to induce increased Ag-specific CD4+ T cell proliferation in vivo, augment T cell production of IFN-g, IL-17, TNF, and IL-6, and increase Akt, ERK, and p38 activation. Together, these findings indicate that T cell-expressed AnxA1 functions to attenuate T cell-driven inflammatory responses via T cell-intrinsic effects on intracellular signaling, proliferation, and Th1/Th17 cytokine release. Copyright © 2013 by The American Association of Immunologists, Inc.

Aim: The aim of the present study was to demonstrate acute, local vasodilatatory effects of insulin and C-peptide on cutaneous microvascular function in Type 1 diabetic subjects. There are no published data available examining physiological effects of C-peptide delivered in this way. Method(s): The study included 20 participants with C-peptide-deficient Type 1 diabetes mellitus. Cutaneous microvascular function was assessed on the forearm using laser Doppler velocimetry. Insulin, C-peptide, acetylcholine (ACh), sodium nitroprusside (SNP) and saline were delivered through the skin using iontophoresis. The response was measured as percentage increase in flux above baseline. Result(s): C-peptide delivered by iontophoresis produced a vasodilatatory response greater than the response to saline (289.5 +/- 265.9% vs. 105.1 +/- 163.6%, P = 0.003). The response to C-peptide was also shown to be dose dependent. Further, the size of the response to C-peptide correlated well with the size of the response to the endothelium-dependent vasodilatator ACh (r = 0.666, P = 0.001) but not with the size of the response to the endothelium-independent vasodilator SNP (r = 0.345, P > 0.05). Conclusion(s): Physiological effects of C-peptide on cutaneous microvascular function could be demonstrated in individuals with Type 1 diabetes. The results support both physiological activity of C-peptide and an endothelium-dependent mechanism similar to that of ACh. The technique reported may be useful in investigating vasoactive actions of C-peptide in a safe and non-invasive way.

Aim: The aim of the present study was to demonstrate acute, local vasodilatatory effects of insulin and C-peptide on cutaneous microvascular function in Type 1 diabetic subjects. There are no published data available examining physiological effects of C-peptide delivered in this way. Method(s): The study included 20 participants with C-peptide-deficient Type 1 diabetes mellitus. Cutaneous microvascular function was assessed on the forearm using laser Doppler velocimetry. Insulin, C-peptide, acetylcholine (ACh), sodium nitroprusside (SNP) and saline were delivered through the skin using iontophoresis. The response was measured as percentage increase in flux above baseline. Result(s): C-peptide delivered by iontophoresis produced a vasodilatatory response greater than the response to saline (289.5 +/- 265.9% vs. 105.1 +/- 163.6%, P = 0.003). The response to C-peptide was also shown to be dose dependent. Further, the size of the response to C-peptide correlated well with the size of the response to the endothelium-dependent vasodilatator ACh (r = 0.666, P = 0.001) but not with the size of the response to the endothelium-independent vasodilator SNP (r = 0.345, P > 0.05). Conclusion(s): Physiological effects of C-peptide on cutaneous microvascular function could be demonstrated in individuals with Type 1 diabetes. The results support both physiological activity of C-peptide and an endothelium-dependent mechanism similar to that of ACh. The technique reported may be useful in investigating vasoactive actions of C-peptide in a safe and non-invasive way.