Distribution of macrophages and granulocytes expressing L1 protein (calprotectin) in human Peyer's patches compared with normal ileal lamina propria and mesenteric lymph nodes.

Bjerke, K; Halstensen, Trond S.; Jahnsen, F; Pulford, Karen; Brandtzæg, Per

doi:10.1136/gut.34.10.1357

Cited by 114 publications

(77 citation statements)

References 27 publications

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“…However, the presence of macrophages, as demonstrated by previous studies [8,46,113], as well as of cells with dendritic morphology described in several species [79,101], are suggestive of primary responses. LP macrophages bear markers associated with cell activation and may play more of a role in antigen presentation than macrophages in the PP [48,49].…”

Section: Lamina Propriasupporting

confidence: 52%

Immunology

et al. 2004

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It has been known for the past 85 years that mucosal responses can be stimulated by local presentation of antigen and that the gut immune system is capable of mounting both primary and secondary responses to potentially harmful antigens while avoiding the expression of damaging responses to harmless dietary proteins. How these types of responses are induced and regulated remains unclear. In the gut attention has for some time been focused on Peyer’s patches (PP) due to evidence that they play a vital role in the induction of humoral and cellular responses. Moreover, it has been established that MHC class II molecules are found in the gut mucosa on a variety of cell types outside PP, namely the lamina propria (LP). Fed antigens have also been detected in the LP and studies have shown that LP cells can stimulate allogeneic mixed lymphocyte responses and are capable of presenting soluble protein antigen to naïve T cells. This article reviews the present understanding of the possible roles of PP and LP in intestinal immunity in terms of induction, regulation, surveillance of immune responses and the antigen presenting cell types involved.

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Section: Lamina Propriasupporting

confidence: 52%

Immunology

et al. 2004

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“…Others [63] have demonstrated that eosinophilic granulocytes are the main cellular source of calprotectin in the normal gut mucosa. However, relatively high levels of calprotectin are found in the stools of normal individualsabout six times the plasma levels (which are about 0.…”

Section: Faecal Calprotectinmentioning

confidence: 99%

Non-invasive investigation of inflammatory bowel disease

Tibble

Bjarnason

2001

WJG

139

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“…More than 60% of the total cytosolic protein content of neutrophils is calprotectin. This calcium-and zinc-binding protein plays a regulatory role in inflammation with antimicrobial and antiproliferative properties (12). Fecal calprotectin levels correlate with fecal excretion of neutrophils (13).…”

mentioning

confidence: 99%

Colonic Immunopathogenesis of Clostridium difficile Infections

Darkoh

Turnwald

Koo

et al. 2014

Clin Vaccine Immunol

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f There are major gaps in our understanding of the immunopathogenesis of Clostridium difficile infections (CDIs). In this study, 36 different biomarkers were examined in the stools of CDI and non-CDI patients using the Proteome Profiler human cytokine array assay and quantitative enzyme-linked immunosorbent assay. Diarrheal stools from patients with CDI (CDI-positive diarrheal stools) showed higher relative amounts of the following inflammatory markers than the diarrheal stools from CDI-negative patients (CDI-negative diarrheal stools): C5a, CD40L, granulocyte colony-stimulating factor, I-309, interleukin-13 (IL-13), IL-16, IL-27, monocyte chemoattractant protein 1, tumor necrosis factor alpha, and IL-8. IL-8 and IL-23 were present in a larger number of CDI-positive diarrheal stools than CDI-negative diarrheal stools. Th1 and Th2 cytokines were not significantly different between the CDI-positive and CDI-negative diarrheal stools. Lactoferrin and calprotectin concentrations were also higher in the CDI-positive diarrheal stools. Our results demonstrate that CDI elicits a proinflammatory host response, and we report for the first time that IL-23 is a major marker in CDI-positive diarrheal stools. IL-23 may explain the lack of a robust immunological response exhibited by a proportion of CDI patients and may relate to recurrence; the IL-23 levels induced during CDI in these patients may be inadequate to sustain the cellular immunity conferred by this cytokine in promoting the induction and proliferation of effector memory T cells.

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Distribution of macrophages and granulocytes expressing L1 protein (calprotectin) in human Peyer's patches compared with normal ileal lamina propria and mesenteric lymph nodes.

Cited by 114 publications

References 27 publications

Immunology

Immunology

Non-invasive investigation of inflammatory bowel disease

Colonic Immunopathogenesis of Clostridium difficile Infections

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