Spatial distribution of LTi-like cells in intestinal mucosa regulates type 3 innate immunity

Lymphoid tissue inducer (LTi)-like cells are tissue resident innate lymphocytes that rapidly secrete cytokines that promote gut epithelial integrity and protect against extracellular bacterial infections.Here, we report that the retention of LTi-like cells in conventional solitary intestinal lymphoid tissue (SILT) is essential for controlling LTi-like cell function and is maintained by expression of the chemokine receptor CXCR5. Deletion of Cxcr5 functionally unleashed LTi-like cells in a cell intrinsic manner, leading to uncontrolled IL-17 and IL-22 production. The elevated production of IL-22 in Cxcr5-deficient mice improved gut barrier integrity and protected mice during infection with the opportunistic pathogen Clostridium difficile. Interestingly, Cxcr5−/− mice developed LTi-like cell aggregates that were displaced from their typical niche at the intestinal crypt, and LTi-like cell hyperresponsiveness was associated with the local formation of this unconventional SILT. Thus, LTi-like cell positioning within mucosa controls their activity via niche-specific signals that temper cytokine production during homeostasis.

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2351-PUB: Influence of Short-Term Improvements in Glycemic Control with Intensive Insulin Therapy on Pancreatic a-Cell Function and the Relationship between Concurrent SGLT2 Inhibitor Therapy and Insulin Withdrawal

Diabetes ◽

10.2337/db19-2351-pub ◽

2019 ◽

Vol 68 (Supplement 1) ◽

pp. 2351-PUB

Author(s):

MAKIKO MATSUI ◽

HIROSHI TAKAHASHI ◽

SHOUKO SAWANO ◽

YUTAKA MORI ◽

KAZUNORI UTSUNOMIYA

Keyword(s):

Glycemic Control ◽

Insulin Therapy ◽

Intensive Insulin Therapy ◽

Cell Function ◽

Sglt2 Inhibitor ◽

Inhibitor Therapy ◽

Short Term ◽

Insulin Withdrawal ◽

A Cell ◽

The Relationship

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Effect of RIP Overexpression on Abiotic Stress Tolerance and Development of Rice

International Journal of Molecular Sciences ◽

10.3390/ijms22031434 ◽

2021 ◽

Vol 22 (3) ◽

pp. 1434

Author(s):

Pieter Wytynck ◽

Jeroen Lambin ◽

Simin Chen ◽

Sinem Demirel Asci ◽

Isabel Verbeke ◽

...

Keyword(s):

Methyl Jasmonate ◽

Stress Responses ◽

Abiotic Stress Tolerance ◽

Protein Translation ◽

Ribosome Inactivating Proteins ◽

Close Proximity ◽

Inhibit Protein Translation ◽

Plant Ribosomes ◽

A Cell ◽

Type 3

Ribosome-inactivating proteins (RIPs) are a class of cytotoxic enzymes that can inhibit protein translation by depurinating rRNA. Most plant RIPs are synthesized with a leader sequence that sequesters the proteins to a cell compartment away from the host ribosomes. However, several rice RIPs lack these signal peptides suggesting they reside in the cytosol in close proximity to the plant ribosomes. This paper aims to elucidate the physiological function of two nucleocytoplasmic RIPs from rice, in particular, the type 1 RIP referred to as OsRIP1 and a presumed type 3 RIP called nuRIP. Transgenic rice lines overexpressing these RIPs were constructed and studied for developmental effects resulting from this overexpression under greenhouse conditions. In addition, the performance of transgenic seedlings in response to drought, salt, abscisic acid and methyl jasmonate treatment was investigated. Results suggest that both RIPs can affect methyl jasmonate mediated stress responses.

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Studies of intestinal lymphoid tissue

Virchows Archiv A Pathological Anatomy and Histopathology ◽

10.1007/bf00750263 ◽

1988 ◽

Vol 412 (4) ◽

pp. 365-370 ◽

Cited By ~ 5

Author(s):

M. N. Marsh ◽

R. J. Leigh ◽

D. E. Loft ◽

G. V. Garner ◽

D. B. Gordon

Keyword(s):

Lymphoid Tissue ◽

Intestinal Lymphoid Tissue

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Jinx, an MCMV susceptibility phenotype caused by disruption of Unc13d: a mouse model of type 3 familial hemophagocytic lymphohistiocytosis

Journal of Experimental Medicine ◽

10.1084/jem.20062447 ◽

2007 ◽

Vol 204 (4) ◽

pp. 853-863 ◽

Cited By ~ 115

Author(s):

Karine Crozat ◽

Kasper Hoebe ◽

Sophie Ugolini ◽

Nancy A. Hong ◽

Edith Janssen ◽

...

Keyword(s):

Hemophagocytic Lymphohistiocytosis ◽

Cell Function ◽

Nk Cell ◽

Lymphocytic Choriomeningitis ◽

Chromosome 11 ◽

Familial Hemophagocytic Lymphohistiocytosis ◽

Cytokine Levels ◽

Antigen Presenting ◽

Type 3 ◽

Mouse Chromosome 11

Mouse cytomegalovirus (MCMV) susceptibility often results from defects of natural killer (NK) cell function. Here we describe Jinx, an N-ethyl-N-nitrosourea–induced MCMV susceptibility mutation that permits unchecked proliferation of the virus, causing death. In Jinx homozygotes, activated NK cells and cytotoxic T lymphocytes (CTLs) fail to degranulate, although they retain the ability to produce cytokines, and cytokine levels are markedly elevated in the blood of infected mutant mice. Jinx was mapped to mouse chromosome 11 on a total of 246 meioses and confined to a 4.60–million basepair critical region encompassing 122 annotated genes. The phenotype was ascribed to the creation of a novel donor splice site in Unc13d, the mouse orthologue of human MUNC13-4, in which mutations cause type 3 familial hemophagocytic lymphohistiocytosis (FHL3), a fatal disease marked by massive hepatosplenomegaly, anemia, and thrombocytopenia. Jinx mice do not spontaneously develop clinical features of hemophagocytic lymphohistiocytosis (HLH), but do so when infected with lymphocytic choriomeningitis virus, exhibiting hyperactivation of CTLs and antigen-presenting cells, and inadequate restriction of viral proliferation. In contrast, neither Listeria monocytogenes nor MCMV induces the syndrome. In mice, the HLH phenotype is conditional, which suggests the existence of a specific infectious trigger of FHL3 in humans.

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Solubility and Bioactivity of the Pseudomonas Quinolone Signal Are Increased by a Pseudomonas aeruginosa-Produced Surfactant

Infection and Immunity ◽

10.1128/iai.73.2.878-882.2005 ◽

2005 ◽

Vol 73 (2) ◽

pp. 878-882 ◽

Cited By ~ 60

Author(s):

M. Worth Calfee ◽

John G. Shelton ◽

James A. McCubrey ◽

Everett C. Pesci

Keyword(s):

Pseudomonas Aeruginosa ◽

Aqueous Solutions ◽

Opportunistic Pathogen ◽

Homoserine Lactone ◽

Cellular Functions ◽

Pseudomonas Quinolone Signal ◽

Serious Infections ◽

Enhanced Solubility ◽

Apoptosis Assay ◽

A Cell

ABSTRACT Pseudomonas aeruginosa is a gram-negative bacterium that causes serious infections in immunocompromised individuals and cystic fibrosis patients. This opportunistic pathogen controls many of its virulence factors and cellular functions through the activity of three cell-to-cell signals, N-(3-oxododecanoyl)-l-homoserine lactone, N-butyryl-l-homoserine lactone, and the Pseudomonas quinolone signal (PQS). The activity of these signals is dependent upon their ability to dissolve in and freely diffuse through the aqueous solution in which P. aeruginosa happens to reside. Despite this, our data indicated that PQS was relatively insoluble in aqueous solutions, which led us to postulate that P. aeruginosa could be producing a PQS-solubilizing factor. In this report, we show that the P. aeruginosa-produced biosurfactant rhamnolipid greatly enhances the solubility of PQS in aqueous solutions. The enhanced solubility of PQS led to an increase in PQS bioactivity, as measured by both a gene induction assay and an apoptosis assay. This is the first demonstration of the importance of a bacterial surfactant in the solubilization and bioactivity of a cell-to-cell signal.

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Decreased Glibenclamide Uptake in Hepatocytes of Hepatocyte Nuclear Factor-1 -Deficient Mice: A Mechanism for Hypersensitivity to Sulfonylurea Therapy in Patients With Maturity-Onset Diabetes of the Young, Type 3 (MODY3)

Diabetes ◽

10.2337/diabetes.51.2007.s343 ◽

2002 ◽

Vol 51 (Supplement 3) ◽

pp. S343-S348 ◽

Cited By ~ 24

Author(s):

P. Boileau ◽

C. Wolfrum ◽

D. Q. Shih ◽

T.-A. Yang ◽

A. W. Wolkoff ◽

...

Keyword(s):

Nuclear Factor ◽

Maturity Onset Diabetes ◽

Hepatocyte Nuclear Factor ◽

Onset Diabetes ◽

Nuclear Factor 1 ◽

Type 3 ◽

Deficient Mice

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AN OVERVIEW: INVESTIGATION OF ELECTROPORATION TECHNIQUE ON CELL PROPERTIES CULTURED ON MICROPATTERNED SURFACE.

Jurnal Teknologi ◽

10.11113/jt.v77.6228 ◽

2015 ◽

Vol 77 (6) ◽

Cited By ~ 2

Author(s):

Nur Adilah Abd Rahman ◽

Mamman Hassan Buhari ◽

M. Mahadi Abdul Jamil

Keyword(s):

Wound Healing ◽

Cell Function ◽

Microcontact Printing ◽

Healing Process ◽

Wound Healing Process ◽

Medical Applications ◽

Electrical Fields ◽

A Cell ◽

Basic Concepts ◽

A New Technique

Electroporation (EP) is a method of controlling cell function by using pulses of electrical fields to create pore through a cell membrane and causes other substance around it to be absorbed into the cell. Where This method had been led to variety of medical applications. While, microcontact printing (μCP) is a quite useful technique for patterning extracellular matrix as an adhesion molecule for cells that works for controlling the cell growth. This study focuses on reviewing the basic concepts and techniques of electroporation and Microcontact printing, as applied to molecular biology & cancer treatment. The combination of these two technique might be a new technique for wound healing process treatment.

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Adaptation of B and A cell function during prolonged glucose infusion in human subjects

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1984.246.5.e405 ◽

1984 ◽

Vol 246 (5) ◽

pp. E405-E411 ◽

Cited By ~ 7

Author(s):

W. K. Ward ◽

J. B. Halter ◽

J. C. Beard ◽

D. Porte

Keyword(s):

Cell Function ◽

Human Subjects ◽

Glucose Infusion ◽

Healthy Men ◽

Before And After ◽

Mild Hyperglycemia ◽

A Cell ◽

Per Se ◽

Insulin Responses ◽

The Relationship

States of insulin resistance are characterized by hyperinsulinemia that often appears to be out of proportion to the minimal degree of hyperglycemia. One possible explanation for these findings is that mild hyperglycemia per se can cause an adaptive increase in islet sensitivity to glucose, leading to increased insulin output at a given glucose level. To test this hypothesis, we compared acute insulin responses (AIR) and acute glucagon responses (AGR) to 5-g arginine injections before and after 20-h glucose infusions (200 mg X m-2 X min-1) in 11 healthy men of varying age and degree of adiposity. The 20-h glucose infusion caused an increase in fasting plasma glucose (PG) in all subjects (95 +/- 2 vs. 130 +/- 3 mg/dl). PG was clamped at three levels (approximately 95, 165, and 235 mg/dl) before and after the 20-h glucose infusion. Despite matching of PG levels, consistent increases of AIR were observed after the 20-h glucose infusion: 86 +/- 10 vs. 57 +/- 8 at PG = 95 (P = 0.002); 241 +/- 20 vs. 192 +/- 22 at PG = 165 (P = 0.02); and 508 +/- 59 vs. 380 +/- 50 microU/ml at PG = 235 mg/dl (P = 0.009). In addition, the slope of the relationship between AIR and PG level (potentiation slope), a measure of B cell sensitivity to glucose, increased consistently from 2.28 +/- 0.35 (control) to 3.07 +/- 0.45 (P = 0.004) after the 20-h infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

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Amelioration of Congenital Tufting Enteropathy in EpCAM (TROP1)-Deficient Mice via Heterotopic Expression of TROP2 in Intestinal Epithelial Cells

Cells ◽

10.3390/cells9081847 ◽

2020 ◽

Vol 9 (8) ◽

pp. 1847

Author(s):

Gaku Nakato ◽

Sohshi Morimura ◽

Michael Lu ◽

Xu Feng ◽

Chuanjin Wu ◽

...

Keyword(s):

Stem Cell ◽

Epithelial Cells ◽

Cell Function ◽

Intestinal Epithelial Cells ◽

Surface Proteins ◽

Stem Cell Markers ◽

Intestinal Epithelial ◽

Mesenteric Lymph Nodes ◽

Function Expression ◽

Deficient Mice

TROP1 (EpCAM) and TROP2 are homologous cell surface proteins that are widely expressed, and often co-expressed, in developing and adult epithelia. Various functions have been ascribed to EpCAM and TROP2, but responsible mechanisms are incompletely characterized and functional equivalence has not been examined. Adult intestinal epithelial cells (IEC) express high levels of EpCAM, while TROP2 is not expressed. EpCAM deficiency causes congenital tufting enteropathy (CTE) in humans and a corresponding lethal condition in mice. We expressed TROP2 and EpCAM in the IEC of EpCAM-deficient mice utilizing a villin promoter to assess EpCAM and TROP2 function. Expression of EpCAM or TROP2 in the IEC of EpCAM knockout mice prevented CTE. TROP2 rescue (T2R) mice were smaller than controls, while EpCAM rescue (EpR) mice were not. Abnormalities were observed in the diameters and histology of T2R small intestine, and Paneth and stem cell markers were decreased. T2R mice also exhibited enlarged mesenteric lymph nodes, enhanced permeability to 4 kDa FITC-dextran and increased sensitivity to detergent-induced colitis, consistent with compromised barrier function. Studies of IEC organoids and spheroids revealed that stem cell function was also compromised in T2R mice. We conclude that EpCAM and TROP2 exhibit functional redundancy, but they are not equivalent.

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