Expression of antimicrobial peptides in diabetic foot ulcer

Rivas-Santiago, Bruno; Trujillo, Valentín; Montoya, Alejandra; González-Curiel, Irma; Castañeda-Delgado, Julio Enrique; Cardenas, Albertina; Rincon, Kublai; Hernández, Medardo; Hernández-Pando, Rogelio

doi:10.1016/j.jdermsci.2011.09.013

Cited by 62 publications

(60 citation statements)

References 27 publications

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“…It was discovered that b-defensins were overexpressed in diabetic foot ulcers. This suggested that b-defensins could promote wound healing (24). These findings seem to indicate that b-defensins play a crucial role in the development and healing of mucosal damage and inflammation in UC.…”

mentioning

confidence: 69%

Porcine β-Defensin 2 Attenuates Inflammation and Mucosal Lesions in Dextran Sodium Sulfate–Induced Colitis

Han¹,

Zhang

Xia

et al. 2015

The Journal of Immunology

140

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Intestinal permeability plays a critical role in the etiopathogenesis of ulcerative colitis. Defensins, including porcine β-defensin (pBD)2, are crucial antimicrobial peptides for gut protection owing to their antibacterial and immunomodulatory activities. The purpose of this study was to investigate the protective effects of pBD2 on mucosal injury and the disruption of the epithelial barrier during the pathological process of dextran sodium sulfate (DSS)–induced colitis. The effects and mechanism of pBD2 were evaluated both using a DSS-induced C57BL/6 mouse model and, in vitro, using Caco-2 and RAW264.7 cells. DSS-induced colitis was characterized by higher disease activity index, shortened colon length, elevated activities of myeloperoxidase and eosinophil peroxidase, histologic evidence of inflammation, and increased expression levels of TNF-α, IL-6, and IL-8. pBD2 increased the expression of zonula occludens-1, zonula occludens-2, claudin-1, mucin-1, and mucin-2 mRNA and proteins, and it decreased permeability to FITC-D, as well as apoptosis, in DSS-treated mice. pBD2 also decreased inflammatory infiltrates of the colon epithelium. In Caco-2 cells, pBD2 increased transepithelial electrical resistance and mucin mRNA expression, and it decreased the permeability of FITC-D while preserving the structural integrity of the tight junctions. The effects of pBD2 appeared to be through upregulation of the expression of genes associated with tight junctions and mucins, and by suppressing DSS-induced increases in inflammation, inducible NO synthase, cyclooxygenase-2, and apoptosis. These results show that pBD2 improves DSS-induced changes in mucosal lesions and paracellular permeability, possibly by affecting the activation of NF-κB signaling. The present study demonstrates that intrarectal administration of pBD2 may be a novel preventive option for ulcerative colitis.

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mentioning

confidence: 69%

Porcine β-Defensin 2 Attenuates Inflammation and Mucosal Lesions in Dextran Sodium Sulfate–Induced Colitis

Han¹,

Zhang

Xia

et al. 2015

The Journal of Immunology

140

View full text Add to dashboard Cite

show abstract

“…Diabetes, a common comorbidity of obesity, is a well-known risk factor for pneumococcal infections, and poor glucose control in diabetes is known to increase the risk of pneumococcal pneumonia [44], [45]. Hyperglycemia in type II diabetes is known to compromise host defense against cutaneous infections by impairing wound healing, antimicrobial peptide (LL-37)(cathelicidin) production, and epithelial cell proliferation following tissue injury [15], [46], [47]. Therefore, the combination of obesity and diabetes may be required to impair host defense during bacterial pneumonia.…”

Section: Discussionmentioning

confidence: 99%

No Impairment in Host Defense against Streptococcus pneumoniae in Obese CPEfat/fat Mice

et al. 2014

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In the US and globally, dramatic increases in the prevalence of adult and childhood obesity have been reported during the last 30 years. In addition to cardiovascular disease, type II diabetes, and liver disease, obesity has recently been recognized as an important risk factor for influenza pneumonia. During the influenza pandemic of 2009, obese individuals experienced a greater severity of illness from the H1N1 virus. In addition, obese mice have also been shown to exhibit increased lethality and aberrant pulmonary inflammatory responses following influenza infection. In contrast to influenza, the impact of obesity on bacterial pneumonia in human patients is controversial. In this report, we compared the responses of lean WT and obese CPEfat/fat mice following an intratracheal infection with Streptococcus pneumoniae, the leading cause of community-acquired pneumonia. At 16 weeks of age, CPEfat/fat mice develop severe obesity, hyperglycemia, elevated serum triglycerides and leptin, and increased blood neutrophil counts. There were no differences between lean WT and obese CPEfat/fat mice in survival or lung and spleen bacterial burdens following intratracheal infection with S. pneumoniae. Besides a modest increase in TNF-α levels and increased peripheral blood neutrophil counts in CPEfat/fat mice, there were not differences in lung or serum cytokines after infection. These results suggest that obesity, accompanied by hyperglycemia and modestly elevated triglycerides, at least in the case of CPEfat/fat mice, does not impair innate immunity against pneumococcal pneumonia.

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“…Some peptides were also reported to be decreased in diabetic foot ulcer. Expression of antimicrobial peptides, LL-37, is decreased in diabetic ulcer [25]. Besides their antimicrobial effect, LL-37 supported the process of wound healing by increasing keratinocyte proliferation and migration and by promoting angiogenesis.…”

Section: Altered Wound Healing In Diseasesmentioning

confidence: 99%