Neutralizing interleukin 18 (IL-18) differentially regulates immune responses from the mesenteric lymph node compared to the lamina propria in Il-10-deficient mice

Mycobacteriumavium subsp. paratuberculosis (MAP) infection in camel requires extensive research, particularly the immune responses in the intestine. This study aimed to investigate the nature of the cellular populations that are driven by the immunopathological responses in the camel intestine infected with MAP at different ages. Immunohistochemical staining was carried out on tissues obtained from naturally infected young (5–10 years old) and older (12–15 years old) camels. The staining of the tissues, ileum, mesenteric lymph node, jejunum, and supramammary lymph nodes, with anti-CD3+, CD4+, CD8+, CD25+, CD11c+, CD14+, WC1+, CX3CR1, and Madcam-1 monoclonal antibodies revealed high expression of the molecules CD8+, CD25+, CD11c+, CD14+, WC1+, CX3CR1, and Madcam-1 in the ileum and mesenteric lymph node of the infected older camels. The results indicated the recruitment of CD8+lymphocytes, CD14+ macrophages, and CD11c+ dendritic cells to the ileal lamina propria. High expression of CX3CR1 could indicate a vital role for this special macrophage phenotype in the ileal lamina propria in maintaining intestinal homeostasis. Madcam-1 expression could have an essential role in defining the nature of the recruited cells to the site of the infection. Expression of CX3CR1 and Madcam-1 is a novel finding that merits further attention and pursuit to reveal their significance in the immune responses to MAP in the camel’s intestine.

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Lymphotoxinβ-deficient mice: Requirement of the LTα/β heterotrimers for the development of peripheral lymphoid organs, except the mesenteric lymph node

Immunology Letters ◽

10.1016/s0165-2478(97)86900-3 ◽

1997 ◽

Vol 56 (1-3) ◽

pp. 16

Author(s):

M Alimzhanov

Keyword(s):

Lymph Node ◽

Mesenteric Lymph Node ◽

Lymphoid Organs ◽

Mesenteric Lymph ◽

Deficient Mice

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Host Responses to Persistent Mycobacterium avium SubspeciesparatuberculosisInfection in Surgically Isolated Bovine Ileal Segments

Clinical and Vaccine Immunology ◽

10.1128/cvi.00496-12 ◽

2012 ◽

Vol 20 (2) ◽

pp. 156-165 ◽

Cited By ~ 21

Author(s):

Chandrashekhar Charavaryamath ◽

Patricia Gonzalez-Cano ◽

Patrick Fries ◽

Susantha Gomis ◽

Kimberley Doig ◽

...

Keyword(s):

Lymph Node ◽

T Cell ◽

Lamina Propria ◽

Mycobacterium Avium ◽

Mesenteric Lymph Node ◽

Cell Receptor ◽

Host Responses ◽

Necrosis Factor Alpha ◽

Content Type ◽

Mesenteric Lymph

ABSTRACTA lack of appropriate disease models has limited our understanding of the pathogenesis of persistent enteric infections withMycobacterium aviumsubsp.paratuberculosis. A model was developed for the controlled delivery of a defined dose ofM. aviumsubsp.paratuberculosisto surgically isolated ileal segments in newborn calves. The stable intestinal segments enabled the characterization of host responses to persistentM. aviumsubsp.paratuberculosisinfections after a 9-month period, including an analysis of local mucosal immune responses relative to an adjacent uninfected intestinal compartment.M. aviumsubsp.paratuberculosisremained localized at the initial site of intestinal infection and was not detected by PCR in the mesenteric lymph node.M. aviumsubsp.paratuberculosis-specific T cell proliferative responses included both CD4 and γδ T cell receptor (γδTcR) T cell responses in the draining mesenteric lymph node. The levels of CD8+and γδTcR+T cells increased significantly (P< 0.05) in the lamina propria, andM. aviumsubsp.paratuberculosis-specific tumor necrosis factor alpha (TNF-α) and gamma interferon secretion by lamina propria leukocytes was also significantly (P< 0.05) increased. There was a significant (P< 0.05) accumulation of macrophages and dendritic cells (DCs) in the lamina propria, but the expression of mucosal toll-like receptors 1 through 10 was not significantly changed byM. aviumsubsp.paratuberculosisinfection. In conclusion, surgically isolated ileal segments provided a model system for the establishment of a persistent and localized entericM. aviumsubsp.paratuberculosisinfection in cattle and facilitated the analysis ofM. aviumsubsp.paratuberculosis-specific changes in mucosal leukocyte phenotype and function. The accumulation of DC subpopulations in the lamina propria suggests that further investigation of mucosal DCs may provide insight into host responses toM. aviumsubsp.paratuberculosisinfection and improve vaccine strategies to preventM. aviumsubsp.paratuberculosisinfection.

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Recombinant Proteins of Cryptosporidium parvum Induce Proliferation of Mesenteric Lymph Node Cells in Infected Mice

Infection and Immunity ◽

10.1128/iai.73.8.5245-5248.2005 ◽

2005 ◽

Vol 73 (8) ◽

pp. 5245-5248 ◽

Cited By ~ 9

Author(s):

Inderpal Singh ◽

Cynthia Theodos ◽

Saul Tzipori

Keyword(s):

Lymph Node ◽

Immune Responses ◽

Recombinant Proteins ◽

Cryptosporidium Parvum ◽

Mesenteric Lymph Node ◽

Recombinant Antigens ◽

Cellular Immune Responses ◽

Mesenteric Lymph ◽

Lymph Node Cells ◽

Cellular Immune

ABSTRACT Recombinant antigens of Cryptosporidium parvum, Cp900 and Cp40 but not Cp15, stimulated C. parvum-specific proliferative immune responses of mesenteric lymph node cells in C57BL/6J mice infected with different isolates (MD, GCH1, UCP, and IOWA) of C. parvum, indicating that both Cp900 and Cp40 are immunodominant targets of cellular immune responses during C. parvum infection.

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Leptin and adiponectin supplementation modifies mesenteric lymph node lymphocyte composition and functionality in suckling rats

British Journal Of Nutrition ◽

10.1017/s0007114517003786 ◽

2018 ◽

Vol 119 (5) ◽

pp. 486-495 ◽

Cited By ~ 10

Author(s):

Blanca Grases-Pintó ◽

Mar Abril-Gil ◽

Maria J. Rodríguez-Lagunas ◽

Margarida Castell ◽

Francisco J. Pérez-Cano ◽

...

Keyword(s):

Lymph Node ◽

Immune Responses ◽

Mesenteric Lymph Node ◽

Early Life ◽

Suckling Period ◽

Mesenteric Lymph Nodes ◽

Trophic Effect ◽

Mesenteric Lymph ◽

Intestinal Immune System ◽

Intestinal Iga

AbstractAt birth, when immune responses are insufficient, there begins the development of the defence capability against pathogens. Leptin and adiponectin, adipokines that are present in breast milk, have been shown to play a role in the regulation of immune responses. We report here, for the first time, the influence of in vivo adipokine supplementation on the intestinal immune system in early life. Suckling Wistar rats were daily supplemented with leptin (0·7 μg/kg per d, n 36) or adiponectin (35 μg/kg per d, n 36) during the suckling period. The lymphocyte composition, proliferation and cytokine secretion from mesenteric lymph node lymphocytes (on days 14 and 21), as well as intestinal IgA and IgM concentration (day 21), were evaluated. At day 14, leptin supplementation significantly increased the TCRαβ+ cell proportion in mesenteric lymph nodes, in particular owing to an increase in the TCRαβ+ CD8+ cell population. Moreover, the leptin or adiponectin supplementation promoted the early development CD8+ cells, with adiponectin being the only adipokine capable of enhancing the lymphoproliferative ability at the end of the suckling period. Although leptin decreased intestinal IgA concentration, it had a trophic effect on the intestine in early life. Supplementation of both adipokines modulated the cytokine profile during (day 14) and at the end (day 21) of the suckling period. These results suggest that leptin and adiponectin during suckling play a role in the development of mucosal immunity in early life.

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Mesenteric lymph node stroma cells in the generation of intestinal immune responses

Journal of Molecular Medicine ◽

10.1007/s00109-009-0502-z ◽

2009 ◽

Vol 87 (10) ◽

pp. 945-951 ◽

Cited By ~ 11

Author(s):

Oliver Pabst ◽

Benjamin Wahl ◽

Günter Bernhardt ◽

Swantje I. Hammerschmidt

Keyword(s):

Lymph Node ◽

Immune Responses ◽

Mesenteric Lymph Node ◽

Mesenteric Lymph

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Immunity to Trichinella spiralis infection in vitamin A-deficient mice.

Journal of Experimental Medicine ◽

10.1084/jem.175.1.111 ◽

1992 ◽

Vol 175 (1) ◽

pp. 111-120 ◽

Cited By ~ 60

Author(s):

J A Carman ◽

L Pond ◽

F Nashold ◽

D L Wassom ◽

C E Hayes

Keyword(s):

Lymph Node ◽

Vitamin A ◽

Mesenteric Lymph Node ◽

Trichinella Spiralis ◽

Natural Infection ◽

Ifn Gamma ◽

Transcript Levels ◽

Mesenteric Lymph ◽

A Cells ◽

Deficient Mice

Vitamin A-deficient (A-) mice make strikingly poor IgG responses when they are immunized with purified protein antigens. Previously, we showed that A- T cells overproduce interferon gamma (IFN-gamma), which then could inhibit interleukin 4 (IL-4)-stimulated B cell IgG responses. To determine if the altered IFN-gamma regulation pattern and its immunological consequences would extend to a natural infection, we studied mice infected with the parasitic helminth Trichinella spiralis. The course of the infection was similar in A- and A-sufficient (A+) mice. These mice did not differ with respect to newborn larvae/female/hour produced in the intestine, or muscle larvae burden 5 wk postinfection. They also did not differ in the intestinal worm expulsion rate until day 15, when A- mice still harbored parasites, whereas A+ mice had cleared intestinal worms. Vitamin A deficiency reduced both the frequency of B lymphocytes secreting IgG1 antibodies to parasite antigens, and the bone marrow eosinophilia associated with helminth infection. The cytokine secretion patterns in infected mice were consistent with these observations and with previous studies. Mesenteric lymph node cells from infected A- mice secreted significantly more IFN-gamma, and significantly less IL-2, IL-4, and IL-5 than infected A+ controls. A- splenocytes secreted significantly more IFN-gamma, and equivalent amounts of IL-2, IL-4, and IL-5 compared with A+ controls. Interestingly, CD4-CD8- cells secreted the majority of the IL-4 produced in the spleen. The IL-2, IL-4, and IL-5 steady-state transcript levels correlated with secreted protein levels, but IFN-gamma transcripts did not. Although they secreted more protein, A- cells contained fewer IFN-gamma transcripts than A+ cells. These results suggest two vitamin A-mediated regulation steps in IFN-gamma gene expression: positive regulation of IFN-gamma transcript levels, and negative regulation posttranscriptionally. The essentially unaltered outcome of T. spiralis infection in vitamin A-deficient mice probably reflects a balance between cellular and humoral responses. The IFN-gamma overproduction might have a positive effect on the gut inflammatory response, but the decrease eosinophilia, cytokine production in mesenteric lymph node, and IgG1-secreting cell frequency might have a negative effect on T. spiralis immunity.

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EFFECT OF RECENT ANTIGEN PRIMING ON ADOPTIVE IMMUNE RESPONSES

Journal of Experimental Medicine ◽

10.1084/jem.139.1.1 ◽

1974 ◽

Vol 139 (1) ◽

pp. 1-12 ◽

Cited By ~ 31

Author(s):

J. Sprent ◽

J. F. A. P. Miller

Keyword(s):

Lymph Node ◽

Immune Responses ◽

Mesenteric Lymph Node ◽

Antibody Responses ◽

The Other ◽

Spleen Cells ◽

Antigen Concentration ◽

Short Term ◽

Mesenteric Lymph ◽

Circulating Lymphocytes

When thoracic duct lymphocytes (TDL) or mesenteric lymph node (MLN) cells from mice primed 1 day before with either sheep erythrocytes (SRC) or horse erythrocytes (HRC) were transferred together with both SRC and HRC to irradiated mice, antibody responses measured 7 days later could not be detected to the priming antigen but were high to the other antigen. Furthermore, this unresponsiveness of TDL and MLN to the priming antigen could not be abrogated by delaying antigen challenge of the transferred cells for 1–2 wk. Previous work had shown that short-term priming with antigen also induced specific unresponsiveness in spleen cells on adoptive transfer. Unresponsiveness in these cells, however, was only of temporary duration, full recovery in the reactivity of the cells being observed when challenge with the priming antigen on transfer was delayed for 5 or more days. Since the present work showed that such recovery from initial unresponsiveness on transfer was unique to spleen cells and did not apply to TDL or MLN, it appeared that different mechanisms were responsible for the unresponsiveness in the three populations. It is proposed that the unresponsiveness detected in TDL and MLN cells in the present study resulted from a deficiency of antigen-reactive cells, these cells having been recruited to the spleen, i.e., a region of antigen concentration. This concept of antigen-induced selective recruitment of circulating lymphocytes was supported by evidence that 51Cr-labeled heterologous erythrocytes indeed localized largely in the spleen after intravenous injection but not in MLN.

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