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Article ; Online: Interaction effect of systemic inflammation and modifiable rheumatoid cachexia risk factors on resting energy expenditure in patients with rheumatoid arthritis.

Hanaoka, Beatriz Y / Zhao, Jing / Heitman, Kristen / Khan, Fahad / Jarjour, Wael / Volek, Jeff / Brock, Guy / Gower, Barbara A

JCSM clinical reports

2022 Volume 7, Issue 1, Page(s) 12–23

Abstract: Background: In rheumatoid cachexia (RC), high resting energy expenditure (REE) is associated with loss of muscle mass driven by proinflammatory cytokines. The objectives of this study were to investigate parameters associated with RC, and the ... ...

Abstract	Background: In rheumatoid cachexia (RC), high resting energy expenditure (REE) is associated with loss of muscle mass driven by proinflammatory cytokines. The objectives of this study were to investigate parameters associated with RC, and the interaction between systemic inflammation and modifiable risk factors for RC on REE. Methods: Thirty-five rheumatoid arthritis (RA) and nineteen non-RA controls comparable in age, sex, race and BMI underwent measures of REE by indirect calorimetry. Clinical, dietary, body composition and physical function data were collected. Homeostasis model assessment for insulin resistance (HOMA-IR) and serum interleukin-6 (IL-6) were used as parameters of IR and systemic inflammation, respectively. Regression models tested association between REE and dependent variables, including pre-specified interaction tests involving HOMA-IR and IL-6 and dietary intake of protein per weight (PPW) and IL-6. Results: RA subjects were mostly women (94%) and had a median age of 54 years (50.5, 70) and BMI of 30.5 kg/m Conclusions: While IR can lead to muscle catabolism, IR was not significantly associated with REE in RA individuals. Higher dietary protein intake could attenuate the effect of systemic inflammation on REE in RA patients.
Language	English
Publishing date	2022-01-07
Publishing country	Germany
Document type	Journal Article
ISSN	2521-3555
ISSN (online)	2521-3555
DOI	10.1002/crt2.45
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Differentially co-expressed myofibre transcripts associated with abnormal myofibre proportion in chronic obstructive pulmonary disease.

Chiles, Joe W / Wilson, Ava C / Tindal, Rachel / Lavin, Kaleen / Windham, Samuel / Rossiter, Harry B / Casaburi, Richard / Thalacker-Mercer, Anna / Buford, Thomas W / Patel, Rakesh / Wells, J Michael / Bamman, Marcas M / Hanaoka, Beatriz Y / Dransfield, Mark / McDonald, Merry-Lynn N

Journal of cachexia, sarcopenia and muscle

2024

Abstract: Background: Skeletal muscle dysfunction is a common extrapulmonary manifestation of chronic obstructive pulmonary disease (COPD). Alterations in skeletal muscle myosin heavy chain expression, with reduced type I and increased type II myosin heavy chain ... ...

Abstract	Background: Skeletal muscle dysfunction is a common extrapulmonary manifestation of chronic obstructive pulmonary disease (COPD). Alterations in skeletal muscle myosin heavy chain expression, with reduced type I and increased type II myosin heavy chain expression, are associated with COPD severity when studied in largely male cohorts. The objectives of this study were (1) to define an abnormal myofibre proportion phenotype in both males and females with COPD and (2) to identify transcripts and transcriptional networks associated with abnormal myofibre proportion in COPD. Methods: Forty-six participants with COPD were assessed for body composition, strength, endurance and pulmonary function. Skeletal muscle biopsies from the vastus lateralis were assayed for fibre-type distribution and cross-sectional area via immunofluorescence microscopy and RNA-sequenced to generate transcriptome-wide gene expression data. Sex-stratified k-means clustering of type I and IIx/IIax fibre proportions was used to define abnormal myofibre proportion in participants with COPD and contrasted with previously defined criteria. Single transcripts and weighted co-expression network analysis modules were tested for correlation with the abnormal myofibre proportion phenotype. Results: Abnormal myofibre proportion was defined in males with COPD (n = 29) as <18% type I and/or >22% type IIx/IIax fibres and in females with COPD (n = 17) as <36% type I and/or >12% type IIx/IIax fibres. Half of the participants with COPD were classified as having an abnormal myofibre proportion. Participants with COPD and an abnormal myofibre proportion had lower median handgrip strength (26.1 vs. 34.0 kg, P = 0.022), 6-min walk distance (300 vs. 353 m, P = 0.039) and forced expiratory volume in 1 s-to-forced vital capacity ratio (0.42 vs. 0.48, P = 0.041) compared with participants with COPD and normal myofibre proportions. Twenty-nine transcripts were associated with abnormal myofibre proportions in participants with COPD, with the upregulated NEB, TPM1 and TPM2 genes having the largest fold differences. Co-expression network analysis revealed that two transcript modules were significantly positively associated with the presence of abnormal myofibre proportions. One of these co-expression modules contained genes classically associated with muscle atrophy, as well as transcripts associated with both type I and type II myofibres, and was enriched for genetic loci associated with bone mineral density. Conclusions: Our findings indicate that there are significant transcriptional alterations associated with abnormal myofibre proportions in participants with COPD. Transcripts canonically associated with both type I and type IIa fibres were enriched in a co-expression network associated with abnormal myofibre proportion, suggesting altered transcriptional regulation across multiple fibre types.
Language	English
Publishing date	2024-04-22
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2586864-0
ISSN	2190-6009 ; 2190-5991
ISSN (online)	2190-6009
ISSN	2190-5991
DOI	10.1002/jcsm.13473
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Article ; Online: Association between skeletal muscle mitochondrial dysfunction and insulin resistance in patients with rheumatoid arthritis: a case-control study.

Moellering, Douglas R / Smith-Johnston, Kelley / Kelley, Christian / Sammy, Melissa J / Benedict, Jason / Brock, Guy / Johnson, Jillian / Baskin, Kedryn K / Jarjour, Wael N / Belury, Martha A / Reiser, Peter J / Nagareddy, Prabhakara R / Hanaoka, Beatriz Y

Arthritis research & therapy

2023 Volume 25, Issue 1, Page(s) 85

Abstract: Background: Insulin resistance affects a substantial proportion of patients with rheumatoid arthritis (RA). Skeletal muscle mitochondrial dysfunction results in the accumulation of lipid intermediates that interfere with insulin signaling. We therefore ... ...

Abstract	Background: Insulin resistance affects a substantial proportion of patients with rheumatoid arthritis (RA). Skeletal muscle mitochondrial dysfunction results in the accumulation of lipid intermediates that interfere with insulin signaling. We therefore sought to determine if lower oxidative phosphorylation and muscle mitochondrial content are associated with insulin resistance in patients with RA. Methods: This was a cross-sectional prospective study of RA patients. Matsuda index from the glucose tolerance test was used to estimate insulin sensitivity. Mitochondrial content was measured by citrate synthase (CS) activity in snap-frozen muscle samples. Mitochondrial function was measured by using high-resolution respirometry of permeabilized muscle fibers and electron transport chain complex IV enzyme kinetics in isolated mitochondrial subpopulations. Results: RA participants demonstrated lower insulin sensitivity as measured by the Matsuda index compared to controls [median 3.95 IQR (2.33, 5.64) vs. 7.17 (5.83, 7.75), p = 0.02]. There was lower muscle mitochondrial content among RA vs. controls [median 60 mU/mg IQR (45, 80) vs. 79 mU/mg (65, 97), p = 0.03]. Notably, OxPhos normalized to mitochondrial content was higher among RA vs. controls [mean difference (95% CI) = 0.14 (0.02, 0.26), p = 0.03], indicating a possible compensatory mechanism for lower mitochondrial content or lipid overload. Among RA participants, the activity of muscle CS activity was not correlated with the Matsuda index (ρ = - 0.05, p = 0.84), but it was positively correlated with self-reported (IPAQ) total MET-minutes/week (ρ = 0.44, p = 0.03) and Actigraph-measured time on physical activity (MET rate) (ρ = 0.47, p = 0.03). Conclusions: Mitochondrial content and function were not associated with insulin sensitivity among participants with RA. However, our study demonstrates a significant association between muscle mitochondrial content and physical activity level, highlighting the potential for future exercise interventions that enhance mitochondrial efficiency in RA patients.
MeSH term(s)	Humans ; Insulin Resistance/physiology ; Case-Control Studies ; Cross-Sectional Studies ; Prospective Studies ; Muscle, Skeletal ; Mitochondria ; Arthritis, Rheumatoid/metabolism ; Lipids ; Mitochondria, Muscle/metabolism
Chemical Substances	Lipids
Language	English
Publishing date	2023-05-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2107602-9
ISSN	1478-6362 ; 1478-6354
ISSN (online)	1478-6362
ISSN	1478-6354
DOI	10.1186/s13075-023-03065-z
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Article ; Online: Interaction effect of systemic inflammation and modifiable rheumatoid cachexia risk factors on resting energy expenditure in patients with rheumatoid arthritis

Beatriz Y. Hanaoka / Jing Zhao / Kristen Heitman / Fahad Khan / Wael Jarjour / Jeff Volek / Guy Brock / Barbara A. Gower

JCSM Clinical Reports, Vol 7, Iss 1, Pp 12-

2022 Volume 23

Abstract: Abstract Background In rheumatoid cachexia (RC), high resting energy expenditure (REE) is associated with loss of muscle mass driven by proinflammatory cytokines. The objectives of this study were to investigate parameters associated with RC and the ... ...

Abstract	Abstract Background In rheumatoid cachexia (RC), high resting energy expenditure (REE) is associated with loss of muscle mass driven by proinflammatory cytokines. The objectives of this study were to investigate parameters associated with RC and the interaction between systemic inflammation and modifiable risk factors for RC on REE. Methods Thirty‐five rheumatoid arthritis (RA) and 19 non‐RA controls comparable in age/sex/race/body mass index (BMI) underwent measures of REE by indirect calorimetry. Homeostasis model assessment for insulin resistance (HOMA‐IR) and serum interleukin‐6 (IL‐6) were used as parameters of IR and systemic inflammation, respectively. Regression models tested association between REE and dependent variables, including pre‐specified interaction tests involving HOMA‐IR and IL‐6 and dietary intake of protein per weight (PPW) and IL‐6. Results Rheumatoid arthritis subjects were mostly women (94%) and had a median age of 54 years (50.5, 70) and BMI of 30.5 kg/m2 (26.1, 36.9). Approximately two‐thirds of RA participants were seropositive, with median disease duration [interquartile range (IQR)] and a DAS‐28 C‐reactive protein [IQR] of 7.83 years [4.89, 18.14] and 1.7 mg/day [1.21, 2.78], respectively. RA participants demonstrated significantly higher levels of HOMA‐IR compared with non‐RA controls (P = 0.006). Fat‐free mass index (FFMI, P = 0.33), REE (P = 0.68), IL‐6 (P = 0.13), and estimates of dietary intake including PPW tertiles (P = 0.83) were not significantly different between RA and non‐RA. In univariate analyses, REE was positively associated with BMI (P = <0.001), FFMI and FMI (P = <0.001), and HOMA‐IR (P = 0.001), but not with PPW (P = 0.10). After adjustment for age and FFMI, we did not observe significant associations of HOMA‐IR [β = 4.66, 95% confidence interval (CI) [−33.16, 42.48], P = 0.80], IL‐6 (β = −9.45, 95% CI [−25.61, 6.72], P = 0.24), or the interaction between HOMA‐IR and IL‐6 (β = 6.00, 95% CI [−5.47, 17.46], P = 0.29) with REE. In multiple regression models ...
Keywords	Rheumatoid arthritis ; Rheumatoid cachexia ; Resting energy expenditure ; Insulin resistance ; Systemic inflammation ; Dietary protein ; Internal medicine ; RC31-1245
Subject code	610
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Wiley
Document type	Article ; Online
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Article: Administration of an LXR agonist promotes atherosclerotic lesion remodelling in murine inflammatory arthritis.

Dragoljevic, Dragana / Lee, Man Kit Sam / Pernes, Gerard / Morgan, Pooranee K / Louis, Cynthia / Shihata, Waled / Huynh, Kevin / Kochetkova, Arina A / Bell, Patrick W / Mellett, Natalie A / Meikle, Peter J / Lancaster, Graeme I / Kraakman, Michael J / Nagareddy, Prabhakara R / Hanaoka, Beatriz Y / Wicks, Ian P / Murphy, Andrew J

Clinical & translational immunology

2023 Volume 12, Issue 4, Page(s) e1446

Abstract: Objectives: The leading cause of mortality in patients with rheumatoid arthritis is atherosclerotic cardiovascular disease (CVD). We have shown that murine arthritis impairs atherosclerotic lesion regression, because of cellular cholesterol efflux ... ...

Abstract	Objectives: The leading cause of mortality in patients with rheumatoid arthritis is atherosclerotic cardiovascular disease (CVD). We have shown that murine arthritis impairs atherosclerotic lesion regression, because of cellular cholesterol efflux defects in haematopoietic stem and progenitor cells (HSPCs), causing monocytosis and impaired atherosclerotic regression. Therefore, we hypothesised that improving cholesterol efflux using a Liver X Receptor (LXR) agonist would improve cholesterol efflux and improve atherosclerotic lesion regression in arthritis. Methods: Ldlr Results: LXR activation during murine inflammatory arthritis completely restored atherosclerotic lesion regression in arthritic mice, evidenced by reduced lesion size, macrophage abundance and lipid content. Mechanistically, serum from arthritic mice promoted foam cell formation, demonstrated by increased cellular lipid accumulation in macrophages and paralleled by a reduction in mRNA of the cholesterol efflux transporters Conclusion: Taken together, we show that the LXR agonist T0901317 rescues impaired atherosclerotic lesion regression in murine arthritis because of enhanced cholesterol efflux transporter expression and reduced foam cell development in atherosclerotic lesions.
Language	English
Publishing date	2023-04-18
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2694482-0
ISSN	2050-0068
ISSN	2050-0068
DOI	10.1002/cti2.1446
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Article: Neutrophil Migratory Patterns: Implications for Cardiovascular Disease.

Dahdah, Albert / Johnson, Jillian / Gopalkrishna, Sreejit / Jaggers, Robert M / Webb, Darren / Murphy, Andrew J / Hanssen, Nordin M J / Hanaoka, Beatriz Y / Nagareddy, Prabhakara R

Frontiers in cell and developmental biology

2022 Volume 10, Page(s) 795784

Abstract: The body's inflammatory response involves a series of processes that are necessary for the immune system to mitigate threats from invading pathogens. Leukocyte migration is a crucial process in both homeostatic and inflammatory states. The mechanisms ... ...

Abstract	The body's inflammatory response involves a series of processes that are necessary for the immune system to mitigate threats from invading pathogens. Leukocyte migration is a crucial process in both homeostatic and inflammatory states. The mechanisms involved in immune cell recruitment to the site of inflammation are numerous and require several cascades and cues of activation. Immune cells have multiple origins and can be recruited from primary and secondary lymphoid, as well as reservoir organs within the body to generate an immune response to certain stimuli. However, no matter the origin, an important aspect of any inflammatory response is the web of networks that facilitates immune cell trafficking. The vasculature is an important organ for this trafficking, especially during an inflammatory response, mainly because it allows cells to migrate towards the source of insult/injury and serves as a reservoir for leukocytes and granulocytes under steady state conditions. One of the most active and vital leukocytes in the immune system's arsenal are neutrophils. Neutrophils exist under two forms in the vasculature: a marginated pool that is attached to the vessel walls, and a demarginated pool that freely circulates within the blood stream. In this review, we seek to present the current consensus on the mechanisms involved in leukocyte margination and demargination, with a focus on the role of neutrophil migration patterns during physio-pathological conditions, in particular diabetes and cardiovascular disease.
Language	English
Publishing date	2022-03-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2022.795784
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Article ; Online: Neutrophil Migratory Patterns

Albert Dahdah / Jillian Johnson / Sreejit Gopalkrishna / Robert M. Jaggers / Darren Webb / Andrew J. Murphy / Nordin M. J. Hanssen / Beatriz Y. Hanaoka / Prabhakara R. Nagareddy

Frontiers in Cell and Developmental Biology, Vol

Implications for Cardiovascular Disease

2022 Volume 10

Abstract: The body’s inflammatory response involves a series of processes that are necessary for the immune system to mitigate threats from invading pathogens. Leukocyte migration is a crucial process in both homeostatic and inflammatory states. The mechanisms ... ...

Abstract	The body’s inflammatory response involves a series of processes that are necessary for the immune system to mitigate threats from invading pathogens. Leukocyte migration is a crucial process in both homeostatic and inflammatory states. The mechanisms involved in immune cell recruitment to the site of inflammation are numerous and require several cascades and cues of activation. Immune cells have multiple origins and can be recruited from primary and secondary lymphoid, as well as reservoir organs within the body to generate an immune response to certain stimuli. However, no matter the origin, an important aspect of any inflammatory response is the web of networks that facilitates immune cell trafficking. The vasculature is an important organ for this trafficking, especially during an inflammatory response, mainly because it allows cells to migrate towards the source of insult/injury and serves as a reservoir for leukocytes and granulocytes under steady state conditions. One of the most active and vital leukocytes in the immune system’s arsenal are neutrophils. Neutrophils exist under two forms in the vasculature: a marginated pool that is attached to the vessel walls, and a demarginated pool that freely circulates within the blood stream. In this review, we seek to present the current consensus on the mechanisms involved in leukocyte margination and demargination, with a focus on the role of neutrophil migration patterns during physio-pathological conditions, in particular diabetes and cardiovascular disease.
Keywords	neutrophils ; margination ; demargination ; migration ; cardiovasclar disease ; catecholamine stress ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2022-03-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article ; Online: Chronic Inflammation in Rheumatoid Arthritis and Mediators of Skeletal Muscle Pathology and Physical Impairment: A Review.

Hanaoka, Beatriz Y / Ithurburn, Matthew P / Rigsbee, Cody A / Bridges, S Louis / Moellering, Douglas R / Gower, Barbara / Bamman, Marcas

Arthritis care & research

2019 Volume 71, Issue 2, Page(s) 173–177

MeSH term(s)	Antirheumatic Agents/pharmacology ; Antirheumatic Agents/therapeutic use ; Arthritis, Rheumatoid/diagnosis ; Arthritis, Rheumatoid/physiopathology ; Arthritis, Rheumatoid/therapy ; Chronic Disease ; Exercise/physiology ; Humans ; Inflammation/diagnosis ; Inflammation/physiopathology ; Inflammation/therapy ; Insulin Resistance/physiology ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/pathology ; Muscle, Skeletal/physiology ; Muscular Atrophy/blood ; Muscular Atrophy/epidemiology ; Muscular Atrophy/therapy
Chemical Substances	Antirheumatic Agents
Language	English
Publishing date	2019-01-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	645059-3
ISSN	2151-4658 ; 0893-7524 ; 2151-464X
ISSN (online)	2151-4658
ISSN	0893-7524 ; 2151-464X
DOI	10.1002/acr.23775
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Zs.A 2446: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.A 24: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Glucocorticoid effects on skeletal muscle: benefit and risk in patients with autoimmune inflammatory rheumatoid diseases.

Hanaoka, Beatriz Y / Peterson, Charlotte A / Crofford, Leslie J

Expert review of clinical immunology

2012 Volume 8, Issue 8, Page(s) 695–697

MeSH term(s)	Anti-Inflammatory Agents/adverse effects ; Anti-Inflammatory Agents/therapeutic use ; Arthritis, Rheumatoid/drug therapy ; Arthritis, Rheumatoid/genetics ; Arthritis, Rheumatoid/immunology ; Autoimmunity/drug effects ; Genetic Predisposition to Disease ; Glucocorticoids/adverse effects ; Glucocorticoids/therapeutic use ; Homeostasis/drug effects ; Humans ; Immunosuppression ; Muscle, Skeletal/drug effects ; Polymorphism, Genetic ; Precision Medicine ; Receptors, Glucocorticoid/genetics ; Risk ; Treatment Outcome ; Wound Healing/drug effects
Chemical Substances	Anti-Inflammatory Agents ; Glucocorticoids ; Receptors, Glucocorticoid
Language	English
Publishing date	2012-11
Publishing country	England
Document type	Editorial
ZDB-ID	2274260-8
ISSN	1744-8409 ; 1744-666X
ISSN (online)	1744-8409
ISSN	1744-666X
DOI	10.1586/eci.12.76
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Zs.A 6661: Show issues

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Article: Inhibition of interleukin-1β signalling promotes atherosclerotic lesion remodelling in mice with inflammatory arthritis.

Dragoljevic, Dragana / Lee, Man Kit Sam / Louis, Cynthia / Shihata, Waled / Kraakman, Michael J / Hansen, Jacinta / Masters, Seth L / Hanaoka, Beatriz Y / Nagareddy, Prabhakara R / Lancaster, Graeme I / Wicks, Ian P / Murphy, Andrew J

Clinical & translational immunology

2020 Volume 9, Issue 11, Page(s) e1206

Abstract: Objectives: Rheumatoid arthritis (RA), an inflammatory joint disorder, independently increases the risk of cardiovascular disease (CVD). IL-1β contributes to both RA and CVD. We hypothesised that inhibiting IL-1 signalling with the IL-1R antagonist, ... ...

Abstract	Objectives: Rheumatoid arthritis (RA), an inflammatory joint disorder, independently increases the risk of cardiovascular disease (CVD). IL-1β contributes to both RA and CVD. We hypothesised that inhibiting IL-1 signalling with the IL-1R antagonist, anakinra, would dampen inflammation and promote resolution of atherosclerosis in arthritic mice. Methods: Low-density lipoprotein receptor (Ldlr)-deficient mice were fed a Western-type diet for 14 weeks to develop atherosclerotic plaques. Mice were then switched to a chow diet, promoting lesion regression, and randomised to a control group or into groups where arthritis was induced by passive transfer of K/BxN arthritogenic serum. The arthritic mice were further randomised to vehicle or anakinra. Results: Arthritis impaired atherosclerotic lesion regression when cholesterol was lowered. This was associated with a higher burden of plaque macrophages, likely due to monocytosis, driven by myelopoiesis in the bone marrow and spleen. Interestingly, delayed intervention with anakinra had no effect on arthritis in these mice. However, a significant improvement in atherosclerotic plaque remodelling to a more stable phenotype was observed. This was associated with fewer circulating monocytes, caused by a reduction in splenic extramedullary myelopoiesis. Conclusion: We show that inhibiting IL-1 signalling in arthritic mice with pre-existing atherosclerosis promotes lesion remodelling to a more stable phenotype, that is less likely to rupture and cause ischemic events such as myocardial infarction. This suggests that IL-1R antagonism may suppress CVD complications in patients with RA. Furthermore, inhibiting IL-1β signalling in other patients with inflammatory diseases that also predispose to CVD may also benefit from anti-IL-1 therapy.
Language	English
Publishing date	2020-11-09
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2694482-0
ISSN	2050-0068
ISSN	2050-0068
DOI	10.1002/cti2.1206
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