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Article ; Online: Comparison of hormone-induced mRNA and protein biomarker expression changes in breast cancer cells.

Bernhardt, Sarah M / Dasari, Pallave / Glynn, Danielle J / Townsend, Amanda R / Price, Timothy J / Ingman, Wendy V

2021 Volume 187, Issue 3, Page(s) 681–693

Abstract: Purpose: Protein biomarkers estrogen receptor (ER), progesterone receptor (PR), and marker of proliferation (Ki67) are routinely assessed by immunohistochemistry to guide treatment decisions for breast cancer. Now, quantification of mRNA encoding these ... ...

Abstract	Purpose: Protein biomarkers estrogen receptor (ER), progesterone receptor (PR), and marker of proliferation (Ki67) are routinely assessed by immunohistochemistry to guide treatment decisions for breast cancer. Now, quantification of mRNA encoding these proteins is being adopted in the clinic. However, mRNA and protein biomarkers may be differentially regulated by fluctuations in estrogen and progesterone that occur across the menstrual cycle in premenopausal breast cancer patients. This study aimed to compare how estrogen and progesterone affect mRNA and protein biomarker expression in hormone-responsive breast cancer cells. Methods: Hormone-responsive ZR-75-1 and T-47D human breast cancer cell lines were xenografted into the mammary fat pad of BALB/c nude mice supplemented with estrogen. Progesterone or vehicle was administered prior to dissection of tumors. Protein expression of ER, PR and Ki67 was quantified by immunohistochemistry, and mRNA encoding these proteins, ESR1, PGR and KI67, respectively, was quantified by real-time PCR. mRNA expression was also quantified in breast cancer cell lines treated with estrogen and progesterone in vitro. Results: In T-47D-xenografted tumors, estrogen and progesterone treatment reduced PGR and KI67 mRNA expression, and reduced PR and Ki67 protein positivity, compared to estrogen treatment alone. In ZR-75-1 xenografted tumors, no significant differences in protein or mRNA biomarker expression were observed. In vitro, estrogen and progesterone co-treatment significantly reduced ESR1 and PGR mRNA expression in both T-47D and ZR-75-1 cell lines. Conclusions: Estrogen and progesterone similarly affect mRNA and protein biomarker expression in hormone-responsive breast cancer xenografts. Further research is needed to investigate concordance between protein and mRNA biomarkers in premenopausal breast cancer.
MeSH term(s)	Animals ; Biomarkers ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Female ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Progesterone ; RNA, Messenger/genetics ; Receptors, Progesterone/genetics
Chemical Substances	Biomarkers ; RNA, Messenger ; Receptors, Progesterone ; Progesterone (4G7DS2Q64Y)
Language	English
Publishing date	2021-05-31
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	604563-7
ISSN	1573-7217 ; 0167-6806
ISSN (online)	1573-7217
ISSN	0167-6806
DOI	10.1007/s10549-021-06254-z
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Zs.A 1655: Show issues

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Article ; Online: Erratum to 'Involvement of Adenosine 5'-Triphosphate in Ultrasound-Induced Fracture Repair' [Ultrasound Med Biol 31 (2005) 1131-1138].

Hayton, Michael J / Parmar, Kat L / Dillon, Jane P / Glynn, Danielle / Curran, Judith M / Gallagher, James A / Buckley, Katherine A

Ultrasound in medicine & biology

2019 Volume 45, Issue 9, Page(s) 2586

Language	English
Publishing date	2019-06-05
Publishing country	England
Document type	Published Erratum
ZDB-ID	186150-5
ISSN	1879-291X ; 0301-5629
ISSN (online)	1879-291X
ISSN	0301-5629
DOI	10.1016/j.ultrasmedbio.2019.05.006
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Zs.A 963: Show issues

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Article: Mouse models of mastitis - how physiological are they?

Ingman, Wendy V / Glynn, Danielle J / Hutchinson, Mark R

International breastfeeding journal

2015 Volume 10, Page(s) 12

Abstract: Lactation mastitis is a common, but poorly understood, inflammatory breast disease that is a significant health burden. A better understanding of the aetiology of mastitis is urgently required, and will assist in the development of improved prevention ... ...

Abstract	Lactation mastitis is a common, but poorly understood, inflammatory breast disease that is a significant health burden. A better understanding of the aetiology of mastitis is urgently required, and will assist in the development of improved prevention and treatment strategies in both human and animal species. Studies in mice have the potential to greatly assist in identifying new drug candidates for clinical trials, and in developing a better understanding of the disease. Mouse models of mastitis involve administration of a mastitis-inducing agent to the mammary gland usually during lactation to examine the host immune response, and progression through to resolution of the disease. There are important variations in the protocols of these mouse models that critically affect the conclusions that can be drawn from the research. Some protocols involve weaning of offspring at the time of mastitis induction, and there are variations in the mastitis-inducing agent and its carrier. Induction of mammary gland involution through weaning of offspring limits the capacity to study the disease in the context of a lactating mammary gland. Administration of live bacteria in an aqueous carrier can cause sepsis, restricting the physiological relevance of the model. Mouse model research should employ appropriately designed controls and closely monitor the health of the mice. In this commentary, we discuss the advantages and study design limitations of each mouse model, and highlight the potential for further development of physiologically relevant mouse models of mastitis.
Language	English
Publishing date	2015
Publishing country	England
Document type	Journal Article
ISSN	1746-4358
ISSN	1746-4358
DOI	10.1186/s13006-015-0038-5
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Article ; Online: Interferon-gamma inhibits seminal plasma induction of colony-stimulating factor 2 in mouse and human reproductive tract epithelial cells.

Sharkey, David J / Glynn, Danielle J / Schjenken, John E / Tremellen, Kelton P / Robertson, Sarah A

Biology of reproduction

2018 Volume 99, Issue 3, Page(s) 514–526

Abstract: Seminal fluid interacts with the female reproductive tract to initiate a permissive immune response that facilitates embryo implantation and pregnancy success. The immune-regulatory cytokine interferon-γ (IFNG), which can be elevated in seminal plasma, ... ...

Abstract	Seminal fluid interacts with the female reproductive tract to initiate a permissive immune response that facilitates embryo implantation and pregnancy success. The immune-regulatory cytokine interferon-γ (IFNG), which can be elevated in seminal plasma, is associated with reduced fertility. Here, we investigated how IFNG influences the female immune response to seminal fluid. In human Ect1 cervical epithelial cells, IFNG added at physiologically relevant concentrations substantially impaired seminal plasma-induced synthesis of key cytokines colony-stimulating factor 2 (CSF2) and interleukin-6 (IL6). Seminal fluid-induced CSF2 synthesis was also suppressed in the uterus of mice in vivo, when IFNG was delivered transcervically 12 h after mating. Transforming growth factor B1 (TGFB1) is the major seminal fluid signaling factor which elicits CSF2 induction, and IFNG exhibited potent dose-dependent suppression of CSF2 synthesis induced by TGFB1 in murine uterine epithelial cells in vitro. Similarly, IFNG suppressed TGFB1-mediated CSF2 induction in Ect1 cells and human primary cervical epithelial cells; however, IL6 regulation by IFNG was independent of TGFB1. Quantitative PCR confirmed that CSF2 regulation by IFNG in Ect1 cells occurs at the gene transcription level, secondary to IFNG suppression of TGFBR2 encoding TGFB receptor 2. Conversely, TGFB1 suppressed IFNG receptor 1 and 2 genes IFNGR1 and IFNGR2. These data identify IFNG as a potent inhibitor of the TGFB-mediated seminal fluid interaction with relevant reproductive tract epithelia in mice and human. These findings raise the prospect that IFNG in the male partner's seminal fluid impairs immune adaptation for pregnancy following coitus in women.
MeSH term(s)	Animals ; Cells, Cultured ; Cervix Uteri/metabolism ; Cytokines/biosynthesis ; Cytokines/genetics ; Epithelial Cells/chemistry ; Epithelial Cells/metabolism ; Female ; Granulocyte-Macrophage Colony-Stimulating Factor/biosynthesis ; Humans ; Immune Tolerance/drug effects ; Immunity/drug effects ; Interferon-gamma/pharmacology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Pregnancy ; RNA, Messenger/analysis ; Reproduction/immunology ; Semen/immunology ; Semen/physiology ; Transforming Growth Factor beta1/pharmacology ; Uterus/metabolism
Chemical Substances	Cytokines ; RNA, Messenger ; Transforming Growth Factor beta1 ; Interferon-gamma (82115-62-6) ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1)
Language	English
Publishing date	2018-04-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1118-6
ISSN	1529-7268 ; 0006-3363
ISSN (online)	1529-7268
ISSN	0006-3363
DOI	10.1093/biolre/ioy071
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Zs.A 551: Show issues

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Article ; Online: Important food sources of fructose-containing sugars and adiposity: A systematic review and meta-analysis of controlled feeding trials.

The American journal of clinical nutrition

2023 Volume 117, Issue 4, Page(s) 741–765

Abstract: Background: Sugar-sweetened beverages (SSBs) providing excess energy increase adiposity. The effect of other food sources of sugars at different energy control levels is unclear.: Objectives: To determine the effect of food sources of fructose- ... ...

Abstract	Background: Sugar-sweetened beverages (SSBs) providing excess energy increase adiposity. The effect of other food sources of sugars at different energy control levels is unclear. Objectives: To determine the effect of food sources of fructose-containing sugars by energy control on adiposity. Methods: In this systematic review and meta-analysis, MEDLINE, Embase, and Cochrane Library were searched through April 2022 for controlled trials ≥2 wk. We prespecified 4 trial designs by energy control: substitution (energy-matched replacement of sugars), addition (energy from sugars added), subtraction (energy from sugars subtracted), and ad libitum (energy from sugars freely replaced). Independent authors extracted data. The primary outcome was body weight. Secondary outcomes included other adiposity measures. Grading of Recommendations Assessment, Development, and Evaluation (GRADE) was used to assess the certainty of evidence. Results: We included 169 trials (255 trial comparisons, n = 10,357) assessing 14 food sources at 4 energy control levels over a median 12 wk. Total fructose-containing sugars increased body weight (MD: 0.28 kg; 95% CI: 0.06, 0.50 kg; P Conclusions: Energy control and food sources mediate the effect of fructose-containing sugars on adiposity. The evidence provides a good indication that excess energy from sugars (particularly SSBs at high doses ≥20%E or 100 g/d) increase adiposity, whereas their removal decrease adiposity. Most other food sources had no effect, with some showing decreases (particularly fruits at lower doses ≤10%E or 50 g/d). This trial was registered at clinicaltrials.gov as NCT02558920 (https://clinicaltrials.gov/ct2/show/NCT02558920).
MeSH term(s)	Humans ; Fructose ; Adiposity ; Obesity ; Body Weight ; Fruit ; Beverages
Chemical Substances	Fructose (30237-26-4)
Language	English
Publishing date	2023-02-23
Publishing country	United States
Document type	Meta-Analysis ; Systematic Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	280048-2
ISSN	1938-3207 ; 0002-9165
ISSN (online)	1938-3207
ISSN	0002-9165
DOI	10.1016/j.ajcnut.2023.01.023
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Ue I Zs.208: Show issues

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Article ; Online: Ovarian cycle stage critically affects 21-gene recurrence scores in Mmtv-Pymt mouse mammary tumours.

Bernhardt, Sarah M / Dasari, Pallave / Glynn, Danielle J / Woolford, Lucy / Moldenhauer, Lachlan M / Walsh, David / Townsend, Amanda R / Price, Timothy J / Ingman, Wendy V

BMC cancer

2021 Volume 21, Issue 1, Page(s) 736

Abstract: Background: The Oncotype DX 21-gene Recurrence Score is predictive of adjuvant chemotherapy benefit for women with early-stage, estrogen receptor (ER)-positive, HER2-negative breast cancer. In premenopausal women, fluctuations in estrogen and ... ...

Abstract	Background: The Oncotype DX 21-gene Recurrence Score is predictive of adjuvant chemotherapy benefit for women with early-stage, estrogen receptor (ER)-positive, HER2-negative breast cancer. In premenopausal women, fluctuations in estrogen and progesterone during the menstrual cycle impact gene expression in hormone-responsive cancers. However, the extent to which menstrual cycling affects the Oncotype DX 21-gene signature remains unclear. Here, we investigate the impact of ovarian cycle stage on the 21-gene signature using a naturally cycling mouse model of breast cancer. Methods: ER-positive mammary tumours were dissected from naturally cycling Mmtv-Pymt mice at either the estrus or diestrus phase of the ovarian cycle. The Oncotype DX 21-gene signature was assessed through quantitative real time-PCR, and a 21-gene experimental recurrence score analogous to the Oncotype DX Recurrence Score was calculated. Results: Tumours collected at diestrus exhibited significant differences in expression of 6 Oncotype DX signature genes (Ki67, Ccnb1, Esr1, Erbb2, Grb7, Bag1; p ≤ 0.05) and a significant increase in 21-gene recurrence score (21.8 ± 2.4; mean ± SEM) compared to tumours dissected at estrus (15.5 ± 1.9; p = 0.03). Clustering analysis revealed a subgroup of tumours collected at diestrus characterised by increased expression of proliferation- (p < 0.001) and invasion-group (p = 0.01) genes, and increased 21-gene recurrence score (p = 0.01). No correlation between ER, PR, HER2, and KI67 protein abundance measured by Western blot and abundance of mRNA for the corresponding gene was observed, suggesting that gene expression is more susceptible to hormone-induced fluctuation compared to protein expression. Conclusions: Ovarian cycle stage at the time of tissue collection critically affects the 21-gene signature in Mmtv-Pymt murine mammary tumours. Further studies are required to determine whether Oncotype DX Recurrence Scores in women are similarly affected by menstrual cycle stage.
MeSH term(s)	Animals ; Female ; Gene Expression Profiling/methods ; Genomics/methods ; Mammary Neoplasms, Animal ; Menstrual Cycle/genetics ; Mice ; Mice, Transgenic ; Neoplasm Recurrence, Local
Language	English
Publishing date	2021-06-26
Publishing country	England
Document type	Journal Article
ZDB-ID	2041352-X
ISSN	1471-2407 ; 1471-2407
ISSN (online)	1471-2407
ISSN	1471-2407
DOI	10.1186/s12885-021-08496-y
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Article ; Online: Attenuated TGFB signalling in macrophages decreases susceptibility to DMBA-induced mammary cancer in mice.

Sun, Xuan / Bernhardt, Sarah M / Glynn, Danielle J / Hodson, Leigh J / Woolford, Lucy / Evdokiou, Andreas / Yan, Cong / Du, Hong / Robertson, Sarah A / Ingman, Wendy V

Breast cancer research : BCR

2021 Volume 23, Issue 1, Page(s) 39

Abstract: Background: Transforming growth factor beta1 (TGFB1) is a multi-functional cytokine that regulates mammary gland development and cancer progression through endocrine, paracrine and autocrine mechanisms. TGFB1 also plays roles in tumour development and ... ...

Abstract	Background: Transforming growth factor beta1 (TGFB1) is a multi-functional cytokine that regulates mammary gland development and cancer progression through endocrine, paracrine and autocrine mechanisms. TGFB1 also plays roles in tumour development and progression, and its increased expression is associated with an increased breast cancer risk. Macrophages are key target cells for TGFB1 action, also playing crucial roles in tumourigenesis. However, the precise role of TGFB-regulated macrophages in the mammary gland is unclear. This study investigated the effect of attenuated TGFB signalling in macrophages on mammary gland development and mammary cancer susceptibility in mice. Methods: A transgenic mouse model was generated, wherein a dominant negative TGFB receptor is activated in macrophages, in turn attenuating the TGFB signalling pathway specifically in the macrophage population. The mammary glands were assessed for morphological changes through wholemount and H&E analysis, and the abundance and phenotype of macrophages were analysed through immunohistochemistry. Another cohort of mice received carcinogen 7,12-dimethylbenz(a)anthracene (DMBA), and tumour development was monitored weekly. Human non-neoplastic breast tissue was also immunohistochemically assessed for latent TGFB1 and macrophage marker CD68. Results: Attenuation of TGFB signalling resulted in an increase in the percentage of alveolar epithelium in the mammary gland at dioestrus and an increase in macrophage abundance. The phenotype of macrophages was also altered, with inflammatory macrophage markers iNOS and CCR7 increased by 110% and 40%, respectively. A significant decrease in DMBA-induced mammary tumour incidence and prolonged tumour-free survival in mice with attenuated TGFB signalling were observed. In human non-neoplastic breast tissue, there was a significant inverse relationship between latent TGFB1 protein and CD68-positive macrophages. Conclusions: TGFB acts on macrophage populations in the mammary gland to reduce their abundance and dampen the inflammatory phenotype. TGFB signalling in macrophages increases mammary cancer susceptibility potentially through suppression of immune surveillance activities of macrophages.
MeSH term(s)	9,10-Dimethyl-1,2-benzanthracene/adverse effects ; Animals ; Disease Susceptibility ; Disease-Free Survival ; Epithelial Cells/metabolism ; Estrous Cycle ; Female ; Humans ; Inflammation ; Macrophages/metabolism ; Mammary Glands, Animal/growth & development ; Mammary Glands, Animal/metabolism ; Mammary Glands, Animal/pathology ; Mammary Glands, Human/growth & development ; Mammary Glands, Human/metabolism ; Mammary Glands, Human/pathology ; Mammary Neoplasms, Experimental/chemically induced ; Mammary Neoplasms, Experimental/metabolism ; Mammary Neoplasms, Experimental/pathology ; Mice ; Mice, Transgenic ; Receptor, Transforming Growth Factor-beta Type I/genetics ; Receptor, Transforming Growth Factor-beta Type I/metabolism ; Signal Transduction ; Smad2 Protein/metabolism ; Transforming Growth Factor beta1/metabolism
Chemical Substances	Smad2 Protein ; Smad2 protein, mouse ; Tgfb1 protein, mouse ; Transforming Growth Factor beta1 ; 9,10-Dimethyl-1,2-benzanthracene (57-97-6) ; Receptor, Transforming Growth Factor-beta Type I (EC 2.7.11.30) ; Tgfbr1 protein, mouse (EC 2.7.11.30)
Language	English
Publishing date	2021-03-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2015059-3
ISSN	1465-542X ; 1465-5411
ISSN (online)	1465-542X
ISSN	1465-5411
DOI	10.1186/s13058-021-01417-8
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Zs.A 5494: Show issues

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Article ; Online: Inflammatory mediators in mastitis and lactation insufficiency.

Ingman, Wendy V / Glynn, Danielle J / Hutchinson, Mark R

Journal of mammary gland biology and neoplasia

2014 Volume 19, Issue 2, Page(s) 161–167

Abstract: Mastitis is a common inflammatory disease during lactation that causes reduced milk supply. A growing body of evidence challenges the central role of pathogenic bacteria in mastitis, with disease severity associated with markers of inflammation rather ... ...

Abstract	Mastitis is a common inflammatory disease during lactation that causes reduced milk supply. A growing body of evidence challenges the central role of pathogenic bacteria in mastitis, with disease severity associated with markers of inflammation rather than infection. Inflammation in the mammary gland may be triggered by microbe-associated molecular patterns (MAMPs) as well as danger-associated molecular patterns (DAMPs) binding to pattern recognition receptors such as the toll-like receptors (TLRs) on the surface of mammary epithelial cells and local immune cell populations. Activation of the TLR4 signalling pathway and downstream nuclear factor kappa B (NFkB) is critical to mediating local mammary gland inflammation and systemic immune responses in mouse models of mastitis. However, activation of NFkB also induces epithelial cell apoptosis and reduced milk protein synthesis, suggesting that inflammatory mediators activated during mastitis promote partial involution. Perturbed milk flow, maternal stress and genetic predisposition are significant risk factors for mastitis, and could lead to a heightened TLR4-mediated inflammatory response, resulting in increased susceptibility and severity of mastitis disease in the context of low MAMP abundance. Therefore, heightened host inflammatory signalling may act in concert with pathogenic or commensal bacterial species to cause both the inflammation associated with mastitis and lactation insufficiency. Here, we present an alternate paradigm to the widely held notion that breast inflammation is driven principally by infectious bacterial pathogens, and suggest there may be other therapeutic strategies, apart from the currently utilised antimicrobial agents, that could be employed to prevent and treat mastitis in women.
MeSH term(s)	Animals ; Breast/metabolism ; Female ; Humans ; Inflammation/metabolism ; Inflammation Mediators/metabolism ; Lactation/metabolism ; Lactation Disorders/metabolism ; Mammary Glands, Animal/metabolism ; Mastitis/metabolism ; Signal Transduction/physiology
Chemical Substances	Inflammation Mediators
Language	English
Publishing date	2014-06-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1327345-0
ISSN	1573-7039 ; 1083-3021
ISSN (online)	1573-7039
ISSN	1083-3021
DOI	10.1007/s10911-014-9325-9
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Zs.A 4478: Show issues

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Article ; Online: Rationale, Design and Participants Baseline Characteristics of a Crossover Randomized Controlled Trial of the Effect of Replacing SSBs with NSBs versus Water on Glucose Tolerance, Gut Microbiome and Cardiometabolic Risk in Overweight or Obese Adult SSB Consumer: Strategies to Oppose SUGARS with Non-Nutritive Sweeteners or Water (STOP Sugars NOW) Trial and Ectopic Fat Sub-Study.

Nutrients

2023 Volume 15, Issue 5

Abstract: Background: Health authorities are near universal in their recommendation to replace sugar-sweetened beverages (SSBs) with water. Non-nutritive sweetened beverages (NSBs) are not as widely recommended as a replacement strategy due to a lack of ... ...

Abstract	Background: Health authorities are near universal in their recommendation to replace sugar-sweetened beverages (SSBs) with water. Non-nutritive sweetened beverages (NSBs) are not as widely recommended as a replacement strategy due to a lack of established benefits and concerns they may induce glucose intolerance through changes in the gut microbiome. The STOP Sugars NOW trial aims to assess the effect of the substitution of NSBs (the "intended substitution") versus water (the "standard of care substitution") for SSBs on glucose tolerance and microbiota diversity. Design and methods: The STOP Sugars NOW trial (NCT03543644) is a pragmatic, "head-to-head", open-label, crossover, randomized controlled trial conducted in an outpatient setting. Participants were overweight or obese adults with a high waist circumference who regularly consumed ≥1 SSBs daily. Each participant completed three 4-week treatment phases (usual SSBs, matched NSBs, or water) in random order, which were separated by ≥4-week washout. Blocked randomization was performed centrally by computer with allocation concealment. Outcome assessment was blinded; however, blinding of participants and trial personnel was not possible. The two primary outcomes are oral glucose tolerance (incremental area under the curve) and gut microbiota beta-diversity (weighted UniFrac distance). Secondary outcomes include related markers of adiposity and glucose and insulin regulation. Adherence was assessed by objective biomarkers of added sugars and non-nutritive sweeteners and self-report intake. A subset of participants was included in an Ectopic Fat sub-study in which the primary outcome is intrahepatocellular lipid (IHCL) by 1H-MRS. Analyses will be according to the intention to treat principle. Baseline results: Recruitment began on 1 June 2018, and the last participant completed the trial on 15 October 2020. We screened 1086 participants, of whom 80 were enrolled and randomized in the main trial and 32 of these were enrolled and randomized in the Ectopic Fat sub-study. The participants were predominantly middle-aged (mean age 41.8 ± SD 13.0 y) and had obesity (BMI of 33.7 ± 6.8 kg/m Conclusions: Baseline characteristics for both the main and Ectopic Fat sub-study meet our inclusion criteria and represent a group with overweight or obesity, with characteristics putting them at risk for type 2 diabetes. Findings will be published in peer-reviewed open-access medical journals and provide high-level evidence to inform clinical practice guidelines and public health policy for the use NSBs in sugars reduction strategies. Trial registration: ClinicalTrials.gov identifier, NCT03543644.
MeSH term(s)	Middle Aged ; Humans ; Adult ; Male ; Female ; Overweight ; Non-Nutritive Sweeteners ; Sugar-Sweetened Beverages ; Gastrointestinal Microbiome ; Water ; Sugars ; Diabetes Mellitus, Type 2 ; Obesity ; Glucose ; Cardiovascular Diseases ; Beverages
Chemical Substances	Non-Nutritive Sweeteners ; Water (059QF0KO0R) ; Sugars ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-02-28
Publishing country	Switzerland
Document type	Randomized Controlled Trial ; Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu15051238
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Article ; Online: Toll-like receptor 4 regulates lipopolysaccharide-induced inflammation and lactation insufficiency in a mouse model of mastitis.

Glynn, Danielle J / Hutchinson, Mark R / Ingman, Wendy V

Biology of reproduction

2014 Volume 90, Issue 5, Page(s) 91

Abstract: Lactation mastitis is a debilitating inflammatory breast disease in postpartum women. Disease severity is associated with markers of inflammation rather than bacterial load, suggesting that immune-signaling pathways activated in the host are important in ...

Abstract	Lactation mastitis is a debilitating inflammatory breast disease in postpartum women. Disease severity is associated with markers of inflammation rather than bacterial load, suggesting that immune-signaling pathways activated in the host are important in the disease pathology. The role of the innate pattern recognition receptor toll-like receptor 4 (TLR4) in progression and resolution of mastitislike disease was investigated in a mouse model. Lipopolysaccharide in Matrigel (10 μg/10 μl) was administered into the teat canal of lactating Tlr4 null mutant and wild-type mice to induce a localized area of inflammation. Mastitis induction resulted in a marked influx of RB6-positive neutrophils and F4/80-positive macrophages, which was higher in Tlr4(-/-) mice compared to wild-type mice. Tlr4 null mutation resulted in an altered immune-signaling fingerprint following induction of mastitis, with attenuated serum cytokines, including CXCL1, CCL2, interleukin 1 beta, and tumor necrosis factor alpha compared to wild-type mice. In both genotypes, the localized area of inflammation had resolved after 7 days, and milk protein was evident. However, the mammary glands of wild-type mice exhibited reduced capacity for milk production, with decreased percent area populated with glandular epithelium and decreased abundance of nuclear phosphorylated signal transducer and activator of transcription 5 compared to Tlr4 null mice. This study demonstrates that inflammatory pathways activated in the host are critically important in mastitis disease progression and suggests that lactation insufficiency associated with mastitis may be a consequence of TLR4-mediated inflammation, rather than the bacterial infection itself.
MeSH term(s)	Animals ; Animals, Newborn ; Chi-Square Distribution ; Cytokines/blood ; Cytokines/immunology ; Disease Models, Animal ; Female ; Genotype ; Immunity, Innate/immunology ; Immunohistochemistry ; Lactation/immunology ; Lipopolysaccharides/immunology ; Mastitis/genetics ; Mastitis/immunology ; Mice, Inbred BALB C ; Mice, Knockout ; Signal Transduction ; Specific Pathogen-Free Organisms ; Toll-Like Receptor 4/immunology
Chemical Substances	Cytokines ; Lipopolysaccharides ; Toll-Like Receptor 4
Language	English
Publishing date	2014-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1118-6
ISSN	1529-7268 ; 0006-3363
ISSN (online)	1529-7268
ISSN	0006-3363
DOI	10.1095/biolreprod.114.117663
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