scholarly journals Induction of Serum Amyloid A Genes Is Associated with Growth and Apoptosis of HC11 Mammary Epithelial Cells

2008 ◽  
Vol 72 (1) ◽  
pp. 70-81 ◽  
Author(s):  
Yoonjung KHO ◽  
Sungchan KIM ◽  
Byung Sun YOON ◽  
Jai-Hee MOON ◽  
Bona KIM ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Serum Amyloid A ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Serum Amyloid ◽  
Amyloid A

scholarly journals Induction of Serum Amyloid A3 in Mouse Mammary Epithelial Cells Stimulated with Lipopolysaccharide and Lipoteichoic Acid

Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1548
Author(s):  
Sato Kamiya ◽  
Kaori Shimizu ◽  
Ayaka Okada ◽  
Yasuo Inoshima
Keyword(s):  
Epithelial Cells ◽  
Protein Expression ◽  
Bacterial Infection ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelium ◽  
Lipoteichoic Acid ◽  
Mammary Epithelial ◽  
Serum Amyloid ◽  
Amyloid A ◽  
Mouse Mammary Epithelium

In this study, to establish whether serum amyloid A (SAA) 3 plays a role in the defense against bacterial infection in mouse mammary epithelium, normal murine mammary gland (NMuMG) epithelial cells were stimulated with lipopolysaccharide (LPS) and lipoteichoic acid (LTA). LPS and LTA significantly enhanced mRNA expression level of the Saa3 gene, whereas no significant change was observed in the Saa1 mRNA level. Furthermore, LPS induced SAA3 protein expression more strongly than LTA, whereas neither LPS nor LTA significantly affected SAA1 protein expression. These data indicate that the expression of SAA3 in mouse mammary epithelial cells was increased by the stimulation with bacterial antigens. SAA3 has been reported to stimulate neutrophils in the intestinal epithelium and increase interleukin-22 expression, which induces activation of the innate immune system and production of antibacterial proteins, such as antimicrobial peptides. Therefore, collectively, these data suggest that SAA3 is involved in the defense against bacterial infection in mouse mammary epithelium.

scholarly journals Immune relevant gene expression of mammary epithelial cells and their influence on leukocyte chemotaxis in response to different mastitis pathogens

2012 ◽  
Vol 51 (No. 4) ◽  
pp. 125-132 ◽  
Author(s):  
O. Wellnitz ◽  
P. Reith ◽  
Haas SC ◽  
Meyer HHD
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Mrna Expression ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
E Coli ◽  
Amyloid A ◽  
Streptococcus Uberis ◽  
Leukocyte Chemotaxis ◽  
Mastitis Pathogens

Different mastitis pathogens induce different courses of infection, i.e. more or less severe. Mammary epithelial cells play an important role in the initial combat against microorganisms by expression of cytokines and acute phase proteins that regulate the immune response. The objective of the present study was to investigate the involvement of the epithelial cells into the outcome of mastitis induced by different pathogens. Primary epithelial cell cultures isolated from milk were used to test the immune response by measuring the mRNA expression of immunomodulators and their influence on polymorph nuclear chemotaxis. Because the cells showed different responses to isolated bacterial endotoxins (lipopolysaccharide, lipoteichoic acid, and peptidoglycans) compared to whole bacteria, they were treated with heat inactivated (10 MOI) gram-negative Escherichia coli, a very common pathogen causing acute intra-mammary infections, with Staphylococcus aureus, a prevalent cause of chronic, and, Streptococcus uberis, an inducer of acute and chronic mastitis. E. coli induced an increased mRNA expression of interleukin (IL)-8 within a 1 h treatment. A treatment for 6 h with E. coli and S. aureus induced increased mRNA expression of IL-6, IL-8, TNF-&aacute; and serum amyloid A (SAA). After a 24 h treatment the expression of these immunomodulators was still elevated, except in the E. coli treatment the SAA expression showed no differences to control cells anymore. Interestingly, Str. uberis in the same concentration did only induce the expression of IL-8 after a 6 h treatment but had no influence on other immunomodulator mRNA expression. Cell culture supernatants of E. coli and S. aureus treated cells for 12 h increased leukocyte chemotaxis in a 96-well MultiScreen<sup>TM</sup>MIC-plate. S. aureus seemed to induce increased chemotaxis after shorter treatments than E. coli. In conclusion, mammary epithelial cells are involved in the different immune response to various mastitis pathogens, and the induction of chemotaxis of leukocytes from blood to milk during mastitis. Therefore, most likely epithelial cells play a role in the differential pattern of immunomediators stimulated by different pathogens.

Molecular and immunohistochemical studies on epidermal responses in Atlantic salmon Salmo salar L. induced by Gyrodactylus salaris Malmberg, 1957

2009 ◽  
Vol 84 (2) ◽  
pp. 166-172 ◽  
Author(s):  
P. W. Kania ◽  
O. Evensen ◽  
T. B. Larsen ◽  
K. Buchmann
Keyword(s):  
Epithelial Cells ◽  
Atlantic Salmon ◽  
Serum Amyloid A ◽  
Initial Response ◽  
Interferon Γ ◽  
Serum Amyloid ◽  
Amyloid A ◽  
Genes Encoding ◽  
Immunohistochemical Studies ◽  
Differential Ability

AbstractVarious strains of Atlantic salmon exhibit different levels of susceptibility to infections with the ectoparasitic monogenean Gyrodactylus salaris. The basic mechanisms involved in this differential ability to respond to this monogenean were elucidated using controlled and duplicated challenge experiments. Highly susceptible East Atlantic salmon allowed parasite populations to reach up to 3000 parasites per host within 6 weeks, whereas less susceptible Baltic salmon never reached larger parasite burdens than 122 parasites per host during the same period. The present study, comprising immunohistochemistry and gene expression analyses, showed that highly susceptible salmon erected a response mainly associated with an increased expression of interleukin-1β (IL-1β), interferon-γ (IFN-γ), IL-10 and infiltration of CD3-positive cells in the epidermis of infected fins. Less susceptible salmon showed no initial response in fins but 3–6 weeks post-infection a number of other genes (encoding the immune-regulating cytokine IL-10, cell marker MHC II and the pathogen-binding protein serum amyloid A) were found to be up-regulated. No proliferation of epithelial cells was seen in the skin of less susceptible salmon, and IL-10 may play a role in this regard. It can be hypothesized that resistant salmon regulate the parasite population by restricting nutrients (sloughed epithelial cells and associated material) and thereby starve the parasites. In association with this ‘scorched-earth strategy’, the production of pathogen-binding effector molecules such as serum amyloid A (SAA) (or others still not detected) may contribute to the resistance status of the fish during the later infection phases.

scholarly journals Mammary Defences and Immunity against Mastitis in Sheep

Animals ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. 726 ◽  
Author(s):  
Angeliki I. Katsafadou ◽  
Antonis P. Politis ◽  
Vasia S. Mavrogianni ◽  
Mariana S. Barbagianni ◽  
Natalia G. C. Vasileiou ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Complement System ◽  
Management Practices ◽  
Acute Phase Proteins ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Amyloid A ◽  
Wide Range ◽  
The Complement System

The objectives of this review paper are to present udder defences, including teat of the udder, mammary epithelial cells, leucocytes, immunoglobulins, complement system and chemical antibacterial agents, to describe cooperation and interactions between them and to elaborate on potentials regarding their significance in mammary immunisation strategies. The teat of the udder provides initial protection to the mammary gland. The mammary epithelial cells synthesise antibacterial proteins and the leucocytes produce various inflammation mediators (cytokines or chemokines), phagocytose bacteria and recognise antigenic structures. In the mammary gland, four immunoglobulins (IgG1, IgG2, IgM and IgA) have important roles against bacterial pathogens. The complement system is a collection of proteins, participating in the inflammatory process through various pathways. Other components contributing to humoral mammary defence include lactoferrin, lysozyme and the lactoperoxidase/myeloperoxidase systems, as well as oligosaccharides, gangliosides, reactive oxygen species, acute phase proteins (e.g., haptoglobin and serum amyloid A), ribonucleases and a wide range of antimicrobial peptides. Management practices, genetic variations and nutrition can influence mammary defences and should be taken into account in the formulation of prevention strategies against ovine mastitis.

scholarly journals Epithelial retinoic acid receptor β regulates serum amyloid A expression and vitamin A-dependent intestinal immunity

2019 ◽  
Author(s):  
Sureka Gattu ◽  
Ye-Ji Bang ◽  
Mihir Pendse ◽  
Chaitanya Dende ◽  
Andrew L. Chara ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Epithelial Cells ◽  
Vitamin A ◽  
Serum Amyloid A ◽  
Retinoic Acid Receptor ◽  
Immunoglobulin A ◽  
Serum Amyloid ◽  
Intestinal Immunity ◽  
Acid Receptor ◽  
Amyloid A

AbstractVitamin A is a dietary component that is essential for the development of intestinal immunity. Vitamin A is absorbed and converted to its bioactive derivatives retinol and retinoic acid by the intestinal epithelium, yet little is known about how epithelial cells regulate vitamin A-dependent intestinal immunity. Here we show that epithelial cell expression of the transcription factor retinoic acid receptor β (RARβ) is essential for vitamin A-dependent intestinal immunity. Epithelial RARβ activated vitamin A-dependent expression of serum amyloid A (SAA) proteins by binding directly to Saa promoters. In accordance with the known role of SAAs in regulating Th17 cell effector function, epithelial RARβ promoted IL-17 production by intestinal Th17 cells. More broadly, epithelial RARβ was required for the development of key vitamin A-dependent adaptive immune responses, including CD4+ T cell homing to the intestine and the development of immunoglobulin A-producing intestinal B cells. Our findings provide insight into how the intestinal epithelium senses dietary vitamin A status to regulate adaptive immunity and highlight the role of epithelial cells in regulating intestinal immunity in response to diet.Significance StatementVitamin A is a nutrient that is essential for the development of intestinal immunity. It is absorbed by gut epithelial cells which convert it to retinol and retinoic acid. Here we show that the transcription factor retinoic acid receptor β (RARβ) allows epithelial cells to sense vitamin A in the diet and regulate vitamin A-dependent immunity in the intestine. We find that epithelial RARβ regulates several intestinal immune responses, including production of the immunomodulatory protein serum amyloid A, T cell homing to the intestine, and B cell production of immunoglobulin A. Our findings provide new insight into how epithelial cells sense vitamin A to regulate intestinal immunity and highlight why vitamin A is so important for immunity to infection.

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