Lymphocyte Homing and Ig Secretion in the Murine Mammary Gland

Feltz, M. J. M. van der; Groot, Nanda de; Bayley, J-P; Lee, S. H.; Verbeet, Martin Ph.; Boer, H. H.

doi:10.1046/j.1365-3083.2001.00933.x

Cited by 35 publications

(24 citation statements)

References 37 publications

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“…Immediately postpartum, this is achieved by seconding IgA at mucosal surfaces into the serum, which results in a rapid increase in circulating polymeric IgA that permits loading of IgA into the milk via the blood, such that all IgA in milk from 4-day lactating dams is serum derived (26,27). By around day 8 of lactation, substantial numbers of mucosally derived IgA plasma cells have migrated to the mammary glands to establish local production, such that the proportion of serum-derived IgA decreases to below 25% of the total milk IgA (57,60,61). The density of IgA plasma cells in the mammary glands continues to increase up to day 18 of lactation in concert with increased expression of polymeric immunoglobulin receptor and SC (57,60).…”

Section: Discussionmentioning

confidence: 99%

Antibody-Mediated Protection against Infection withHelicobacter pyloriin a Suckling Mouse Model of Passive Immunity

Gorrell

Robins-Browne

2009

Infect Immun

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Studies of active immunization againstHelicobacter pylori indicate that antibodies play a minor role in immunity. There is also evidence, however, that the translocation of antibodies in the stomach may be insufficient to achieve functional antibody levels in the gastric lumen. We have used a suckling mouse model of passive immunity to determine if perorally delivered antibodies can protect against infection with H. pylori. Female C57BL/6 mice were immunized parenterally with formalin-fixed cells of three clinical isolates of H. pylori (3HP) or the mouse-adapted H. pylori strain SS1 before mating. Their pups were challenged with the SS1 strain at 4 days of age and left to suckle before determination of bacterial loads 14 days later. Compared to age-matched controls, pups suckled by 3HP-vaccinated dams were significantly protected against infection (>95% reduction in median bacterial load; P < 0.0001). Pups suckled by SS1-vaccinated dams were also significantly protected in terms of both median bacterial load (>99.5% reduction; P < 0.0001) and the number of culture-negative pups (28% versus 2% for immune and nonimmune cohorts, respectively; P < 0.0001). Similar results were obtained with pups suckled by dams immunized with a urease-deficient mutant of SS1. Fostering experiments demonstrated that protection was entirely attributable to suckling from an immunized dam, and antibody isotype analysis suggested that protection was mediated by the immunoglobulin G fraction of immune milk. Analysis of the bacterial loads in pups sampled before and after weaning confirmed that infection had been prevented in culture-negative animals. These data indicate that antibodies can prevent colonization by H. pylori and suppress the bacterial loads in animals that are colonized.

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Section: Discussionmentioning

confidence: 99%

Antibody-Mediated Protection against Infection withHelicobacter pyloriin a Suckling Mouse Model of Passive Immunity

Gorrell

Robins-Browne

2009

Infect Immun

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“…Unfortunately, we could not shed light on the mechanism responsible for the suggested PRL modulation of T-cell homing to MG as no major changes in the mRNA expression of CCR1, CCR2, CCR7, CXCR3, and CXCR5 chemokine receptors were found. To support this notion, reports indicate that at least two adhesion molecules, MadCam and a4 b7, are involved in MG homing during pregnancy and lactation (Tanneau et al 1999, van der Feltz et al 2001, Nishimura 2003, Bourges et al 2008. The possibility cannot be excluded that additional changes may occur during T-cell recruitment and maintenance in MG, involving addressins, integrins, and chemokine receptors' expression on T cells as well as chemokine production by mammary epithelial cells under hormone/cytokine stimulation.…”

Section: Discussionmentioning

confidence: 99%

“…It has been known since the 1970s that plasma cells from gut-associated lymphoid tissue are recruited to MG expressing specific adhesion molecules such as CD44 and CD62L and produce mainly IgA to be secreted to milk, transferring immune protection to neonates . Mammary IgA-secreting cell numbers increase during pregnancy in parallel with mammary lobulo-alveolar compartment expansion, reaching maximal levels post partum (Parmely & Manning 1983, Tanneau et al 1999, van der Feltz et al 2001. Lymphocyte homing is an extremely highly regulated mechanism modulated by chemokines, cytokines, integrins, and addressins (Kunkel & Butcher 2002).…”

Section: Introductionmentioning

confidence: 99%

Impaired mammary gland T cell population during early lactation in hypoprolactinemic lactation-deficient rats

Mackern-Oberti¹,

Valdéz²,

Vargas–Roig³

et al. 2013

Reproduction

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Mammary stroma is composed of various cell types, including migratory leukocytes. Although mammary antibody-secreting cells have been extensively studied, reports focusing on mammary T cells are scarce. It is thought that the recruitment mechanism of leukocytes to the mammary gland (MG) is controlled by pregnancy-and lactation-specific stimuli. But whether prolactin (PRL) modulates the T-cell population in MG is still unknown. Our aim was to study the relationship between PRL levels and T and B cells during early lactation (L2, day 2 post partum) and mid-lactation (L12, day 12 of lactation). In order to investigate whether PRL is associated with homing events to MG, female Sprague Dawley (SD) and SD-derived desmoglein 4 K/K hairless (phenotype with lactation deficit, OFA hr/hr) rats were killed during estrus, pregnancy, and post partum, and blood, MG, and corpora lutea were obtained to perform fluorescent-activated cell sorting (FACS), real-time PCR, and histological and RIA studies. Serum PRL levels were lower in OFA hr/hr rats than in SD rats during early lactation. MG of OFA hr/hr rats showed less secretory material compared with SD rats. FACS analysis showed lower percentage of MG CD3C cells in OFA hr/hr rats compared with SD rats on L2 and L12. OFA hr/hr rats showed higher absolute numbers of circulating CD3C cells compared with SD rats on L2 but not on L12. These results show that T-cell population in MG is affected in early lactating OFA hr/hr rats and strongly suggest that serum PRL levels may be involved in the homing events to MG, probably helping antibody-secreting cells and protecting the gland during lactation development.

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“…The MAd-CAM-1 staining area increases during pregnancy and then decreases during lactation; however there is no change in the number of ß 7 + /c-IgA + cells during pregnancy, and they increase during lactation. Another investigation [49] has also showed that IgA-producing plasma cell numbers and MAdCAM-1 expression are not related. These results invoke the involvement of other factors in the mediation of lymphocyte migration in the lactating mammary gland.…”

Section: Other Potential Lymphocyte Trafficking Mediator Molecules Inmentioning

confidence: 97%

“…Adhesion molecules [14,29] belong to one of these families that mediate lymphocyte trafficking, and chemokines [3,41] are the others. Nishimura et al [34][35][36] and other investigators [42,49] found that some of these molecules are expressed in the mammary gland. This review is focused on these molecules, especially glycosylation-dependent cell adhesion molecule-1 (GlyCAM-1) and mucosal addressin cell adhesion molecule-1 (MAdCAM-1) in the mammary gland.…”

Section: Introductionmentioning

confidence: 93%

Expression of potential lymphocyte trafficking mediator molecules in the mammary gland

Nishimura

2003

Vet. Res.

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-The mammary gland performs a variety of immunological functions, including protecting itself from mastitis and protecting neonates from infectious agents. Several molecules that mediate lymphocyte trafficking in the immune system are also expressed in the mammary gland. This review is focused on the immunological function of these molecules, especially glycosylation-dependent cell adhesion molecule-1 (GlyCAM-1) and mucosal addressin cell adhesion molecule-1 (MAdCAM-1) in the mammary gland. GlyCAM-1 is expressed in the lactating mouse mammary gland. Endothelial cells produce this protein and secrete it into milk. The glycosylated modification of mammary gland GlyCAM-1 is different from that of the lymph nodes, and lacks the binding ability for L-selectin on lymphocytes. GlyCAM-1 in the mammary gland is not involved in lymphocyte migration, and probably has another function besides that of the lymph nodes. MAdCAM-1 is expressed on endothelial cells of small venules around mouse mammary lobules during lactation. This molecule has the ability to interact with α 4 ß 7 integrin on lymphocytes and mediates lymphocyte recruitment to the mammary gland. The density of ß 7 + /CD3 + T-cells is correlated with the density of the MAdCAM-1-stained area, suggesting that MAdCAM-1 may mediate the migration of these cells. In contrast, there is no relationship between MAdCAM-1 expression and the number of ß 7 + /c-IgA + B-cells, implying that some other factor is involved in lymphocyte migration to the mammary gland. Chemokines, such as IL-8, GRO-α, MCP-1, RANTES and MEC, have been detected in human and mouse mammary glands. Although little information is available, these molecules may contribute to lymphocyte migration to the mammary gland. mammary gland / mucosal-associated lymphoid tissue (MALT) / glycosylation-dependent cell adhesion molecule-1 (GlyCAM-1) / mucosal addressin cell adhesion molecule-1 (MAdCAM-1)

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Lymphocyte Homing and Ig Secretion in the Murine Mammary Gland

Cited by 35 publications

References 37 publications

Antibody-Mediated Protection against Infection withHelicobacter pyloriin a Suckling Mouse Model of Passive Immunity

Antibody-Mediated Protection against Infection withHelicobacter pyloriin a Suckling Mouse Model of Passive Immunity

Impaired mammary gland T cell population during early lactation in hypoprolactinemic lactation-deficient rats

Expression of potential lymphocyte trafficking mediator molecules in the mammary gland

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