Systemic and intestinal levels of factor XIII-A: the impact of inflammation on expression in macrophage subtypes

Soendergaard, Christoffer; Kvist, Peter Helding; Seidelin, Jakob Benedict; Pelzer, H.; Nielsen, Ole Haagen

doi:10.1007/s00535-015-1152-2

Cited by 13 publications

(10 citation statements)

References 49 publications

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“…Linking mucosal immunity to coagulation, mucosal M2 macrophages have been recently shown to contain intracellular FXIII stores. The cell number of this subtype is decreased in inflamed mucosa in the setting of ulcerative colitis (110). Previously, macrophage procoagulant activity was found to be increased in rats with depleted intestinal microflora and orally fed with streptomycin-resistant E. coli , implying that the gut is a focal point from which systemic inflammation arises (111).…”

Section: Introductionmentioning

confidence: 99%

Challenge to the Intestinal Mucosa During Sepsis

et al. 2019

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Sepsis is a complex of life-threating organ dysfunction in critically ill patients, with a primary infectious cause or through secondary infection of damaged tissues. The systemic consequences of sepsis have been intensively examined and evidences of local alterations and repercussions in the intestinal mucosal compartment is gradually defining gut-associated changes during sepsis. In the present review, we focus on sepsis-induced dysfunction of the intestinal barrier, consisting of an increased permeability of the epithelial lining, which may facilitate bacterial translocation. We discuss disturbances in intestinal vascular tonus and perfusion and coagulopathies with respect to their proposed underlying molecular mechanisms. The consequences of enzymatic responses by pancreatic proteases, intestinal alkaline phosphatases, and several matrix metalloproteases are also described. We conclude our insight with a discussion on novel therapeutic interventions derived from crucial aspects of the gut mucosal dynamics during sepsis.

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Section: Introductionmentioning

confidence: 99%

Challenge to the Intestinal Mucosa During Sepsis

et al. 2019

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“…BAFF is also produced by adipocytes [76]. The role of F13A1 in inflammation in many tissues is supported by vast literature and it is expressed by macrophages and dendritic cells [51,52,[77][78][79][80][81][82]. The mechanisms by which FXIII-A contributes to inflammation involve its fibrin-stabilizing function [83,84] and monocyte/macrophage adhesion [79,85].…”

Section: Discussionmentioning

confidence: 99%

Transglutaminases and Obesity in Humans: Association of F13A1 to Adipocyte Hypertrophy and Adipose Tissue Immune Response

Kaartinen

Arora

Heinonen

et al. 2020

IJMS

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Transglutaminases TG2 and FXIII-A have recently been linked to adipose tissue biology and obesity, however, human studies for TG family members in adipocytes have not been conducted. In this study, we investigated the association of TGM family members to acquired weight gain in a rare set of monozygotic (MZ) twins discordant for body weight, i.e., heavy–lean twin pairs. We report that F13A1 is the only TGM family member showing significantly altered, higher expression in adipose tissue of the heavier twin. Our previous work linked adipocyte F13A1 to increased weight, body fat mass, adipocyte size, and pro-inflammatory pathways. Here, we explored further the link of F13A1 to adipocyte size in the MZ twins via a previously conducted TWA study that was further mined for genes that specifically associate to hypertrophic adipocytes. We report that differential expression of F13A1 (ΔHeavy–Lean) associated with 47 genes which were linked via gene enrichment analysis to immune response, leucocyte and neutrophil activation, as well as cytokine response and signaling. Our work brings further support to the role of F13A1 in the human adipose tissue pathology, suggesting a role in the cascade that links hypertrophic adipocytes with inflammation.

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“…Healthy volunteers consisted of patients with irritable bowel syndrome [ 57 ] or patients undergoing a scheduled control visit following a previous polypectomy. Demographics and clinical characteristics are described in details in Table 1 and have also been described previously [ 58 , 59 ]. Multiple intestinal biopsies were sampled from each patient within a 5 cm radius.…”

Section: Methodsmentioning

confidence: 99%

Characterization of Growth Hormone Resistance in Experimental and Ulcerative Colitis

Soendergaard

Kvist

Thygesen

et al. 2017

IJMS

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Growth hormone (GH) resistance may develop as a consequence of inflammation during conditions such as inflammatory bowel disease, encompassing ulcerative colitis (UC). However, the specific role of the GH–insulin growth factor (IGF)-1-axis and/or the functional consequences of GH resistance in this condition are unclear. In situ hybridization targeting the GH receptor (GHR) and relevant transcriptional analyses were performed in patients with UC and in IL-10 knock-out mice with piroxicam accelerated colitis (PAC). Using cultured primary epithelial cells, the effects of inflammation on the molecular mechanisms governing GH resistance was verified. Also, the therapeutic potential of GH on mucosal healing was tested in the PAC model. Inflammation induced intestinal GH resistance in UC and experimental colitis by down-regulating GHR expression and up-regulating suppressor of cytokine signalling (SOCS) proteins. These effects are driven by pro-inflammatory mediators (tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6) as confirmed using primary epithelial cells. Treatment of experimental colitis with GH increased IGF-1 and body weight of the mice, but had no effects on colonic inflammation or mucosal healing. The high transcriptional similarity between UC and experimental colitis accentuates the formation of intestinal GH resistance during inflammation. Inflammation-induced GH resistance not only impairs general growth but induces a state of local resistance, which potentially impairs the actions of GH on mucosal healing during colitis when using long-acting GH therapy.

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Systemic and intestinal levels of factor XIII-A: the impact of inflammation on expression in macrophage subtypes

Abstract: Intestinal inflammation in UC induces loss of M2 macrophages with subsequent loss of FXIII-A synthesis. The loss of cellular FXIII-A may impact migration and phagocytosis, and hence limit pathogen eradication in UC.

Cited by 13 publications

References 49 publications

Challenge to the Intestinal Mucosa During Sepsis

Challenge to the Intestinal Mucosa During Sepsis

Transglutaminases and Obesity in Humans: Association of F13A1 to Adipocyte Hypertrophy and Adipose Tissue Immune Response

Characterization of Growth Hormone Resistance in Experimental and Ulcerative Colitis

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