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Article: Disparate Recruitment and Retention of Plasmacytoid Dendritic Cells to The Small Intestinal Mucosa between Young and Aged Mice.

Hoffman, Rosemary A / Huang, Sulan / Chalasani, Geetha / Vallejo, Abbe N

2021 Volume 12, Issue 5, Page(s) 1183–1196

Abstract: Plasmacytoid dendritic cells (pDC), a highly specialized class of innate immune cells that serve as rapid sensors of danger signals in circulation or in lymphoid tissue are well studied. However, there remains knowledge gaps about age-dependent changes ... ...

Abstract	Plasmacytoid dendritic cells (pDC), a highly specialized class of innate immune cells that serve as rapid sensors of danger signals in circulation or in lymphoid tissue are well studied. However, there remains knowledge gaps about age-dependent changes of pDC function in the intestinal mucosa. Here, we report that under homeostatic conditions, the proportion of pDC expressing C-C chemokine receptor 9 (CCR9) in the intestinal intraepithelial cell (iIEC) population is comparable between young (2-4 months) and aged (18-24 months) mice, but the absolute numbers of iIEC and pDC are significantly lower in aged mice. Employing the classic model of acute endotoxemia induced by lipopolysaccharide (LPS), we found a decrease in the proportion and absolute number of intraepithelial pDC in both young and aged mice despite the LPS-induced increased expression of the chemokine C-C ligand 25 (CCL25), the ligand of CCR9, in the intestinal mucosa of young mice. In adoptive transfer experiments, a significantly lower number of pDC was retained into the intestinal layer of aged host mice after LPS administration. This was associated with recoverable pDC numbers in the intestinal lumen. Furthermore, co-adoptive transfer of young and aged pDC into young hosts also showed significantly lower retention of aged pDC in the epithelial layer compared to the co-transferred young pDC. Collectively, these data show age-associated changes in mucosal CCL25 gene expression and in pDC number. These may underlie the reported inadequate responses to gastrointestinal pathogens during chronologic aging.
Language	English
Publishing date	2021-08-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2625789-0
ISSN	2152-5250
ISSN	2152-5250
DOI	10.14336/AD.2021.0119
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Article ; Online: Innate-Like Lymphocytes Are Immediate Participants in the Hyper-Acute Immune Response to Trauma and Hemorrhagic Shock.

Manson, Joanna / Hoffman, Rosemary / Chen, Shuhua / Ramadan, Mostafa H / Billiar, Timothy R

Frontiers in immunology

2019 Volume 10, Page(s) 1501

Abstract: Adverse outcomes following severe traumatic injury are frequently attributed to a state of immunological dysfunction acquired during treatment and recovery. Recent genomic evidence however, suggests that the trajectory toward development of multiple ... ...

Abstract	Adverse outcomes following severe traumatic injury are frequently attributed to a state of immunological dysfunction acquired during treatment and recovery. Recent genomic evidence however, suggests that the trajectory toward development of multiple organ dysfunction syndrome (MODS) is already in play at admission (<2 h following injury). Improved understanding of the molecular events during the hyper-acute immunological response to trauma, <2 h following injury, may reveal opportunities to ameliorate organ injury and expedite recovery. Lymphocytes have not previously been considered key participants in this early response; however, two observations in human trauma patients namely, raised populations of circulating NKT and NK cells during the hyper-acute phase and persistent lymphopenia beyond 48 h show association with the development of MODS during recovery. These highlight the need for greater understanding of lymphocyte function in the hyper-acute phase of inflammation. An exploratory study was therefore conducted in a well-established murine model of trauma and hemorrhagic shock (T&HS) to investigate (1) the development of lymphopenia in the murine model and (2) the phenotypic and functional changes of three innate-like lymphocyte subsets, NK1.1+ CD3-, NK1.1+ CD3+, γδTCR+ CD3+ cells, focusing on the first 6 h following injury. Rapid changes in phenotype and function were demonstrated in these cells within blood and spleen, but responses in lung tissue lagged behind. This study describes the immediacy of the innate-like lymphocyte response to trauma in different body compartments and considers new lines for further investigation to develop our understanding of MODS pathogenesis.
MeSH term(s)	Animals ; Immunity, Innate/immunology ; Killer Cells, Natural/immunology ; Lymphocyte Count ; Lymphocyte Subsets/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Models, Animal ; Multiple Organ Failure/immunology ; Multiple Organ Failure/pathology ; Natural Killer T-Cells/immunology ; Shock, Hemorrhagic/immunology ; Shock, Hemorrhagic/pathology ; Wounds and Injuries/immunology ; Wounds and Injuries/pathology
Language	English
Publishing date	2019-07-11
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.01501
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Article ; Online: Role of the IL-33-ST2 axis in sepsis.

Xu, Hui / Turnquist, Heth R / Hoffman, Rosemary / Billiar, Timothy R

Military Medical Research

2017 Volume 4, Page(s) 3

Abstract: Sepsis remains a major clinical problem with high morbidity and mortality. As new inflammatory mediators are characterized, it is important to understand their roles in sepsis. Interleukin 33 (IL-33) is a recently described member of the IL-1 family that ...

Abstract	Sepsis remains a major clinical problem with high morbidity and mortality. As new inflammatory mediators are characterized, it is important to understand their roles in sepsis. Interleukin 33 (IL-33) is a recently described member of the IL-1 family that is widely expressed in cells of barrier tissues. Upon tissue damage, IL-33 is released as an alarmin and activates various types of cells of both the innate and adaptive immune system through binding to the ST2/IL-1 receptor accessory protein complex. IL-33 has apparent pleiotropic functions in many disease models, with its actions strongly shaped by the local microenvironment. Recent studies have established a role for the IL-33-ST2 axis in the initiation and perpetuation of inflammation during endotoxemia, but its roles in sepsis appear to be organism and model dependent. In this review, we focus on the recent advances in understanding the role of the IL-33/ST2 axis in sepsis.
MeSH term(s)	Biomarkers/analysis ; Biomarkers/blood ; Humans ; Inflammation/diagnosis ; Inflammation/physiopathology ; Interleukin-33/analysis ; Interleukin-33/blood ; Interleukins/metabolism ; Sepsis/diagnosis ; Sepsis/mortality ; Sepsis/physiopathology ; Signal Transduction/physiology
Chemical Substances	Biomarkers ; IL33 protein, human ; Interleukin-33 ; Interleukins
Language	English
Publishing date	2017
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2768940-2
ISSN	2054-9369 ; 2095-7467
ISSN (online)	2054-9369
ISSN	2095-7467
DOI	10.1186/s40779-017-0115-8
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Article ; Online: Choosing and remaining in mental health nursing: perceptions of Western Australian nurses.

Harrison, Carole A / Hauck, Yvonne / Hoffman, Rosemary

International journal of mental health nursing

2014 Volume 23, Issue 6, Page(s) 561–569

Abstract: Mental health nursing has an ageing workforce with a critical shortage of nurses in Western Australia. Additionally, mental health is not the preferred career for many graduate nurses. Current challenges with recruitment and retention suggest that ... ...

Abstract	Mental health nursing has an ageing workforce with a critical shortage of nurses in Western Australia. Additionally, mental health is not the preferred career for many graduate nurses. Current challenges with recruitment and retention suggest that strategies are needed to address this issue. This research project adopted a novel approach that focused on exploring the positive aspects of why mental health nurses remain, rather than why they leave. A cross-sectional design was employed comprising a brief interview survey, and nurses working within one public mental health service in Western Australia were invited to participate. A total of 192 nurses participated across 5 months, from adult, older adult, forensic, and education/research programmes. Thematic analysis was conducted from five key questions, and responses from questions one and two are discussed in this paper: 'Why did you choose mental health nursing?' and 'Why do you remain in mental health nursing?'. The main themes extracted in response to choosing mental health nursing were wanting to make a difference, mental health captured my interest, encouraged by others, and opportunities. Subsequent themes extracted from responses to remaining in mental health nursing were facing reality, passion for mental health nursing, patient-centred caring, and workplace conditions. Findings will be utilized to inform strategies for recruitment and retention of graduate nurses; further development of support systems, such as preceptorship training and improving student clinical experiences; as well as improving professional development opportunities for existing mental health nurses.
MeSH term(s)	Adult ; Career Choice ; Cross-Sectional Studies ; Female ; Humans ; Male ; Middle Aged ; Personnel Turnover/statistics & numerical data ; Psychiatric Nursing/manpower ; Psychiatric Nursing/statistics & numerical data ; Surveys and Questionnaires ; Western Australia ; Young Adult
Language	English
Publishing date	2014-12
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2076760-2
ISSN	1447-0349 ; 1445-8330
ISSN (online)	1447-0349
ISSN	1445-8330
DOI	10.1111/inm.12094
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Article ; Online: TLR9 signaling in fibroblastic reticular cells regulates peritoneal immunity.

Xu, Li / Li, Yiming / Yang, Chenxuan / Loughran, Patricia / Liao, Hong / Hoffman, Rosemary / Billiar, Timothy R / Deng, Meihong

The Journal of clinical investigation

2019 Volume 129, Issue 9, Page(s) 3657–3669

Abstract: Fibroblastic reticular cells (FRCs), a subpopulation of stromal cells in lymphoid organs and fat-associated lymphoid clusters (FALCs) in adipose tissue, play immune-regulatory roles in the host response to infection and may be useful as a form of cell ... ...

Abstract	Fibroblastic reticular cells (FRCs), a subpopulation of stromal cells in lymphoid organs and fat-associated lymphoid clusters (FALCs) in adipose tissue, play immune-regulatory roles in the host response to infection and may be useful as a form of cell therapy in sepsis. Here, we found an unexpected major role of TLR9 in controlling peritoneal immune cell recruitment and FALC formation at baseline and after sepsis induced by cecal ligation and puncture (CLP). TLR9 regulated peritoneal immunity via suppression of chemokine production by FRCs. Adoptive transfer of TLR9-deficient FRCs more effectively decreased mortality, bacterial load, and systemic inflammation after CLP than WT FRCs. Importantly, we found that activation of TLR9 signaling suppressed chemokine production by human adipose tissue-derived FRCs. Together, our results indicate that TLR9 plays critical roles in regulating peritoneal immunity via suppression of chemokine production by FRCs. These data form a knowledge basis upon which to design new therapeutic strategies to improve the therapeutic efficacy of FRC-based treatments for sepsis and immune dysregulation diseases.
MeSH term(s)	Adipose Tissue/metabolism ; Animals ; B-Lymphocytes/metabolism ; Chemokine CXCL13/metabolism ; Chemokines/metabolism ; Cytokines/metabolism ; Female ; Fibroblasts/metabolism ; Humans ; Inflammation ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Peritoneum/immunology ; Peritoneum/pathology ; Reticulin/metabolism ; Sepsis/metabolism ; Signal Transduction ; Toll-Like Receptor 9/metabolism
Chemical Substances	Chemokine CXCL13 ; Chemokines ; Cxcl13 protein, mouse ; Cytokines ; Reticulin ; TLR9 protein, human ; Tlr9 protein, mouse ; Toll-Like Receptor 9
Language	English
Publishing date	2019-08-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI127542
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Article ; Online: Interleukin-33 contributes to ILC2 activation and early inflammation-associated lung injury during abdominal sepsis.

Xu, Hui / Xu, Jing / Xu, Li / Jin, Shuqing / Turnquist, Heth R / Hoffman, Rosemary / Loughran, Patricia / Billiar, Timothy R / Deng, Meihong

Immunology and cell biology

2018 Volume 96, Issue 9, Page(s) 935–947

Abstract: Sepsis is defined as infection with organ dysfunction due to a dysregulated immune response. The lung is one of the most vulnerable organs at the onset of sepsis. Interleukin (IL)-33 can be released by injured epithelial and endothelial cells in the lung ...

Abstract	Sepsis is defined as infection with organ dysfunction due to a dysregulated immune response. The lung is one of the most vulnerable organs at the onset of sepsis. Interleukin (IL)-33 can be released by injured epithelial and endothelial cells in the lung and regulate immune activation and infiltration. Therefore, we postulated that IL-33 would contribute to the immune response in the lung during sepsis. Using the cecal ligation and puncture (CLP) sepsis model, we show here that IL-33 contributes significantly to both sepsis-induced inflammation in the lung and systemic inflammatory response in the early phase of sepsis. Despite the higher intra-peritoneal bacterial burden, the absence of IL-33 resulted in less infiltration of neutrophils and monocytes into the lungs in association with lower circulating, lung and liver cytokine levels as well as reduced lung injury at 6 h after sepsis. IL-33 was required for the upregulation of IL-5 in type 2 Innate Lymphoid Cells (ILC2), while IL-5 neutralization suppressed neutrophil and monocyte infiltration in the lungs during CLP sepsis. This reduction in leukocyte infiltration in IL-33-deficient mice was reversed by administration of recombinant IL-5. These results indicate that IL-33 plays a major role in the local inflammatory changes in the lung, in part, by regulating IL-5 and this axis contributes to lung injury early after the onset of sepsis.
MeSH term(s)	Animals ; Disease Models, Animal ; Immunity, Innate ; Interleukin-33/immunology ; Interleukin-5/immunology ; Lung/immunology ; Lymphocytes/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Neutrophil Infiltration ; Pneumonia/immunology ; Sepsis/immunology
Chemical Substances	Il33 protein, mouse ; Interleukin-33 ; Interleukin-5
Language	English
Publishing date	2018-05-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	284057-1
ISSN	1440-1711 ; 0818-9641
ISSN (online)	1440-1711
ISSN	0818-9641
DOI	10.1111/imcb.12159
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Uc I Zs.175: Show issues

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Article ; Online: NK1.1

Chen, Shuhua / Hoffman, Rosemary A / Scott, Melanie / Manson, Joanna / Loughran, Patricia / Ramadan, Mostafa / Demetris, Anthony J / Billiar, Timothy R

Journal of leukocyte biology

2017 Volume 102, Issue 1, Page(s) 127–134

Abstract: Various cell populations expressing NK1.1 contribute to innate host defense and systemic inflammatory responses, but their role in hemorrhagic shock and trauma remains uncertain. NK1 ... ...

Abstract	Various cell populations expressing NK1.1 contribute to innate host defense and systemic inflammatory responses, but their role in hemorrhagic shock and trauma remains uncertain. NK1.1
MeSH term(s)	Alanine Transaminase/blood ; Alanine Transaminase/immunology ; Animals ; Antigens, Ly/blood ; Antigens, Ly/immunology ; Aspartate Aminotransferases/blood ; Aspartate Aminotransferases/immunology ; Cytokines/blood ; Cytokines/immunology ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Mice ; NK Cell Lectin-Like Receptor Subfamily B/blood ; NK Cell Lectin-Like Receptor Subfamily B/immunology ; Shock, Hemorrhagic/blood ; Shock, Hemorrhagic/immunology ; Shock, Hemorrhagic/pathology ; Wounds and Injuries/blood ; Wounds and Injuries/immunology ; Wounds and Injuries/pathology
Chemical Substances	Antigens, Ly ; Cytokines ; Klrb1c protein, mouse ; NK Cell Lectin-Like Receptor Subfamily B ; Aspartate Aminotransferases (EC 2.6.1.1) ; Alanine Transaminase (EC 2.6.1.2)
Language	English
Publishing date	2017-05-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1189/jlb.3A0716-333R
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Article ; Online: Companion Animals.

Hoffman, Rosemary G

Journal of gerontological social work

1992 Volume 18, Issue 1-2, Page(s) 195–205

Abstract: No abstract available for this article. ...

Abstract	No abstract available for this article.
Language	English
Publishing date	1992-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	779365-0
ISSN	1540-4048 ; 0163-4372
ISSN (online)	1540-4048
ISSN	0163-4372
DOI	10.1300/J083V18N03_14
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Article ; Online: Platelet HMGB1 is required for efficient bacterial clearance in intra-abdominal bacterial sepsis in mice.

Zhou, Hui / Deng, Meihong / Liu, Yingjie / Yang, Chenxuan / Hoffman, Rosemary / Zhou, Jingjiao / Loughran, Patricia A / Scott, Melanie J / Neal, Matthew D / Billiar, Timothy R

Blood advances

2018 Volume 2, Issue 6, Page(s) 638–648

Abstract: Thrombocytopenia impairs host defense and hemostasis in sepsis. However, the mechanisms of how platelets regulate host defense are not fully understood. High-mobility group box 1 (HMGB1), a danger-associated molecular pattern protein, is released during ... ...

Abstract	Thrombocytopenia impairs host defense and hemostasis in sepsis. However, the mechanisms of how platelets regulate host defense are not fully understood. High-mobility group box 1 (HMGB1), a danger-associated molecular pattern protein, is released during infection and contributes to the pathogenesis of sepsis. Platelets express HMGB1, which is released on activation and has been shown to play a critical role in thrombosis, monocyte recruitment, and neutrophil extracellular trap (NET) production. However, the contribution of platelet HMGB1 to host defense is unknown. To determine the role of platelet HMGB1 in polymicrobial sepsis, platelet-specific HMGB1 knockout (HMGB1 platelet factor 4 [PF4]) mice were generated and were subjected to cecal ligation and puncture (CLP), a clinically relevant intra-abdominal sepsis model. Compared with HMGB1 Flox mice and wild-type (WT) mice, HMGB1 PF4 mice showed significantly higher bacterial loads in the peritoneum and blood, an exaggerated systemic inflammation response, and significantly greater mortality after CLP. Deletion of HMGB1 in platelets was associated with lower platelet-derived chemokines (PF4 and RANTES) in the peritoneal cavity, and a decrease of platelet-neutrophil interaction in the lung after CLP. In vitro, neutrophils cocultured with activated HMGB1 knockout platelets showed fewer platelet-neutrophil aggregates, reduced reactive oxygen species (ROS) burst as compared with control. Taken together, these data reveal an unrecognized role of platelet HMGB1 in the regulation of neutrophil recruitment and activation via modulation of platelet activation during sepsis.
MeSH term(s)	Abdominal Cavity/microbiology ; Adoptive Transfer ; Animals ; Bacterial Load ; Blood Platelets/metabolism ; Cell Communication ; Disease Models, Animal ; Extracellular Traps/immunology ; Extracellular Traps/metabolism ; HMGB1 Protein/genetics ; Male ; Mice ; Mice, Transgenic ; Neutrophil Activation/immunology ; Neutrophils/immunology ; Neutrophils/metabolism ; Neutrophils/microbiology ; Platelet Activation ; Reactive Oxygen Species/metabolism ; Sepsis/genetics ; Sepsis/metabolism ; Sepsis/microbiology ; Sepsis/mortality
Chemical Substances	HMGB1 Protein ; Reactive Oxygen Species
Language	English
Publishing date	2018-03-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2876449-3
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2017011817
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Article ; Online: Deep vein thrombosis in mice is regulated by platelet HMGB1 through release of neutrophil-extracellular traps and DNA.

Dyer, Mitchell R / Chen, Qiwei / Haldeman, Shannon / Yazdani, Hamza / Hoffman, Rosemary / Loughran, Patricia / Tsung, Allan / Zuckerbraun, Brian S / Simmons, Richard L / Neal, Matthew D

Scientific reports

2018 Volume 8, Issue 1, Page(s) 2068

Abstract: Venous thromboembolic (VTE) disease, consisting of deep venous thrombosis (DVT) and pulmonary embolism (PE) is a leading cause of morbidity and mortality. Current prophylactic measures are insufficient to prevent all occurrence in part due to an ... ...

Abstract	Venous thromboembolic (VTE) disease, consisting of deep venous thrombosis (DVT) and pulmonary embolism (PE) is a leading cause of morbidity and mortality. Current prophylactic measures are insufficient to prevent all occurrence in part due to an incomplete understanding of the underlying pathophysiology. Mounting evidence describes interplay between activation of the innate immune system and thrombus development. Recent work has demonstrated that platelet release of HMGB1 leads to increased microvascular complications following injury. Additionally, platelet HMGB1 was found to enhance DVT and increase the formation of neutrophil extracellular traps (NETs), although the role of HMGB1 induced NET release in thrombosis remains unexplored. Utilizing a transgenic mouse lacking HMGB1 specifically from platelets and megakaryocytes we now demonstrate the specific role of platelet-derived HMGB1 in acute and subacute/chronic venous thrombosis. Platelets account for the majority of circulating HMGB1 and HMGB1 deposition within the developing clot. The pro-thrombotic effect of platelet-derived HMGB1 is mediated through enhanced neutrophil recruitment, NET formation and specifically release of extracellular DNA during NET formation. Taken together, these data suggest that platelet HMGB1 mediated NET release is a primary regulator of DVT formation in mice.
MeSH term(s)	Animals ; Blood Platelets/metabolism ; Cells, Cultured ; DNA/metabolism ; Extracellular Traps/metabolism ; HMGB1 Protein/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Neutrophils/metabolism ; Venous Thrombosis/metabolism ; Venous Thrombosis/pathology
Chemical Substances	HMGB1 Protein ; HMGB1 protein, mouse ; DNA (9007-49-2)
Language	English
Publishing date	2018-02-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-20479-x
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