Heterogeneity of HLA-DR-positive histiocytes in human intestinal lamina propria: a combined histochemical and immunohistological analysis.

Selby, Warwick; Poulter, L W; Hobbs, Steve; Jewell, D P; Jánossy, G.

doi:10.1136/jcp.36.4.379

Cited by 119 publications

(61 citation statements)

References 28 publications

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“…TNF-a acts in an autocrine fashion, being secreted by activated maerophages, and inducing other maerophages to differentiate into epithelioid cells. A macrophage influx is a feature of Crohn's disease and to a lesser extent ulcerative colitis (Selby et at., 1983b;Allison et al, 1988;Seldenrijk et al, 1989;Mahida et al, 1989b); however, it is still unknown why granulomas are seen only in Crohn's disease.…”

Section: Discussionmentioning

confidence: 99%

“…In IBD the density of the infiltrate of all of these cell types is increased (reviewed by Brandtzaeg, 1987). There have been numerous immunohistochemical studies on the changes of plasma cell isotype, T cell populations, macrophages and dendritic cells in IBD (Selby et al, 1983a(Selby et al, , 1983b(Selby et al, , 1984MacDermott,era/., 1986;Brandtzaeg, 1987;Allison era/., 1988;Seldenrijk et al, 1989;Mahida et al, 1989b). There have also been several studies on local T cell immunoregulation and immunoglobulin production in IBD but these have been uninformative (Fiocchi, Youngman & Farmer, 1983;Elson, Machelski & Weiserbs, 1985;James et al, 1985).…”

Section: Introductionmentioning

confidence: 99%

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Tumour necrosis factor-alpha and interferon-gamma production measured at the single cell level in normal and inflamed human intestine

MacDonald

Hutchings

Choy

et al. 1990

Clinical and Experimental Immunology

433

110

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SUMMARY The spot‐ELISA technique has been used to enumerate the frequency of cells secreting tumor necrosis factor‐alpha (TNF‐α) and interferon‐γ (IFN‐γ), isolated from biopsies of normal intestine and from biopsies of children with inflammatory bowel disease. TNF‐α production was undetectable in six out of 12 biopsies from normal intestine and in the other six biopsies it ranged from 60 to 580 TNF‐α‐secreting cells/106 isolated intestinal cells. In contrast, cells isolated from biopsies of children with Crohn's disease (n= 9) all showed elevated frequencies of TNF‐á‐secreting cells (500–12 000 secreting cells/106 cells). In ulcerative colitis, four out of eight children had increased production of TNF‐α and in children with indeterminate colitis two out of three had elevated levels. There was no correlation between plasma TNF‐α levels and the number of intestinal cells secreting TNF‐α. In controls and all groups of patients IFN‐γ‐secreting cells were uncommon. These results suggest that TNF‐α is an important mediator of inflammation in the human gut, and, furthermore, may play a role in the growth failure frequently seen in children with inflammatory bowel disease.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Tumour necrosis factor-alpha and interferon-gamma production measured at the single cell level in normal and inflamed human intestine

MacDonald

Hutchings

Choy

et al. 1990

Clinical and Experimental Immunology

433

110

View full text Add to dashboard Cite

show abstract

“…In Crohn's disease, there is an increased density of mucosal macrophages (Thyberg, Graf & Klingenstrom, 1981), and granuloma formation is commonly observed. In recent years it has become clear that a heterogeneous population of macrophage-like cells exists within these infiltrates in Crohn's colitis and in ulcerative colitis, and that this heterogeneity is more marked than in uninflamed colonic mucosa (Selby et al, 1983;Wilders et al, 1984;Mahida et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Changes in phenotypically distinct mucosal macrophage populations may be a prerequisite for the development of inflammatory bowel disease

Allison

Poulter

1991

Clinical and Experimental Immunology

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SUMMARYPrevious studies have demonstrated the presence ofmuch more marked macrophage heterogeneity in colonic mucosa affected by the idiopathic inflammatory bowel diseases (ulcerative colitis and Crohn's disease) than in normal mucosa. This study examines the morphology, distribution and phenotypic expression of mucosal macrophage-like cells in biopsies from patients with idiopathic inflammatory bowel disease in comparison with disease control samples from patients with colonic infection or ischaemia. Approximately 80% of macrophage-like cells in histologically normal mucosa co-express the antigens recognized by the monoclonal antibodies RFD1 (an interdigitating cell marker) and RFD7 (a marker for mature tissue macrophages). In idiopathic inflammatory bowel disease, the normal colonic macrophage population is partly replaced by cells staining positively with RFD7 alone, and, to a lesser extent, with RFD1 + dendritic cells. Sections from patients with infections and ischaemia exhibited epithelial HLA-DR positivity and infiltration of the lamina propria by a more heterogeneous population of macrophages than that seen in histologically normal mucosa. However, the displacement of the normal colonic macrophage phenotype by RFD7+ tissue macrophages occurred to a significantly greater extent in idiopathic inflammatory bowel disease than in disease control mucosa. A pathognomonic feature of the ulcerative colitis and Crohn's colitis sections was the clustering of RFD9+ epithelioid cells at the bases of disrupted crypts and adjacent to areas of mucosal damage. It is concluded that a degree of macrophage heterogeneity and macrophage infiltration can occur as a non-specific response to colonic mucosal damage. The distinctive feature of idiopathic inflammatory bowel disease mucosa is the almost complete replacement of the normal colonic mucosal macrophage population by tissue macrophages and epithelioid cells, and this phenomenon may be important in promoting the development of a chronic inflammatory state.

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“…We hypothesize that chemokinetic agents in human milk may aid in recruiting macrophages to mucosal sites of the recipient's alimentary tract (45,46). It may be particularly important for the infant to receive these chemokinetic agents because of the developmental delay in the motility of blood monocytes in early life (47)(48)(49)(50).…”

Section: Discussionmentioning

confidence: 99%

Chemokinetic Agents for Monocytes in Human Milk: Possible Role of Tumor Necrosis Factor-α

et al. 1989

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ABSTRACT. Human milk was found to contain chemokinetic agents for human blood monocytes. The chemokinetic agents were whey proteins that were inactivated by heating at 56" C for 20 min or treatment with trypsin. Three peaks of chemokinetic activity less than 60 kD in size were found by gel filtration chromatography. The chemokinetic activity of each peak obtained by gel filtration was partially blocked by polyclonal rabbit antibodies to recombinant human tumor necrosis factor-a (TNF-a). TNF-a, or a protein that immunologically cross-reacted with it, was also detected in human milk by blockage of the cytotoxicity of human milk by anti-TNF-a. Such proteins or others that elicit the release of TNF-a from the target cells may be responsible for the enhanced motility of human milk macrophages, and it is possible that they may alter the immunologic or metabolic activities of the alimentary tract of the recipient infant. (Pediatu Res 25:629-633) Abbreviations mammary gland or that blood monocytes are modified in the mammary gland or by factors in human milk. Additional experimental observations supported those possibilities. In contrast to the lack of movement of neutrophils in human milk (12)(13)(14), it was discovered that HMM spontaneously moved more rapidly than blood monocytes in a three-dimensional, type I collagen matrix (1 5).In this study, the genesis of the increased motility of human milk macrophages was investigated. We tested whether circulating systemic factors produced early in lactation, mammary gland tissue factors, or constituents in human milk up-regulated the motility of blood monocytes. The investigations revealed that human milk contains chemokinetic agents for blood monocytes and that one of those chemokinetic agents may be TNF-a or a protein that immunologically cross-reacts with it. MATERIALS AND METHODSResearch subjects-leukocyte preparations. The use of human subjects in this iesearch was ~p p~o v e d by the Institutional Review HML, human milk leukocytes HMM, human milk macrophages Board of the Medical School. Donors were healthy adults or MEME, minimum essential medium, Eagle-modified healthy women who delivered full-term, normal infants vaginally PBML, peripheral blood mononuclear leukocytes 2 to 3 days before the collections (16). Milk was collected into sterile polypropylene tubes by a low pressure electric pump TNF-a, tumor necrosis factor-a (Egnell, Inc., Cary, IL). Unfractionated HML were prepared as follows. Human colostrum was diluted 1 :4 in RMPI 1640 (Whittaker M.A. Bioproducts, Walkersville, MD) and centrifuged at 4000 x g for 10 min at 4" C. The cellular pellets were then Neutrophils, macrophages, and lymphocytes are found in hu-resuspended in RPMI 1640 to achieve a final concentration of 1 man milk during the first few months of lactation and the X lo7 leukocytes/ml. Heparinized venous blood was subjected numbers of macrophages in milk are particularly high as com-to Ficoll-Hypaque (Sigma Chemical Co., St. Louis, MO) density pared to the numbers of monocytes in human blood (1, ...

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Heterogeneity of HLA-DR-positive histiocytes in human intestinal lamina propria: a combined histochemical and immunohistological analysis.

Cited by 119 publications

References 28 publications

Tumour necrosis factor-alpha and interferon-gamma production measured at the single cell level in normal and inflamed human intestine

Tumour necrosis factor-alpha and interferon-gamma production measured at the single cell level in normal and inflamed human intestine

Changes in phenotypically distinct mucosal macrophage populations may be a prerequisite for the development of inflammatory bowel disease

Chemokinetic Agents for Monocytes in Human Milk: Possible Role of Tumor Necrosis Factor-α

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