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1.
Artigo em Inglês | MEDLINE | ID: mdl-33806725

RESUMO

BACKGROUND: Research, practice, and policy have focused on educating family caregivers to sustain care but failed to equip healthcare providers to effectively support family caregivers. Family physicians are well-positioned to care for family caregivers. METHODS: We adopted an interpretive description design to explore family physicians and primary care team members' perceptions of their current and recommended practices for supporting family caregivers. We conducted focus groups with family physicians and their primary care team members. RESULTS: Ten physicians and 42 team members participated. We identified three major themes. "Family physicians and primary care teams can be a valuable source of support for family caregivers" highlighted these primary care team members' broad recognition of the need to support family caregiver's health. "What stands in the way" spoke to the barriers in current practices that precluded supporting family caregivers. Primary care teams recommended, "A structured approach may be a way forward." CONCLUSION: A plethora of research and policy documents recommend proactive, consistent support for family caregivers, yet comprehensive caregiver support policy remains elusive. The continuity of care makes primary care an ideal setting to support family caregivers. Now policy-makers must develop consistent protocols to assess, and care for family caregivers in primary care.


Assuntos
Cuidadores , Médicos de Família , Grupos Focais , Pessoal de Saúde , Humanos , Atenção Primária à Saúde
2.
J Immunol ; 205(10): 2750-2762, 2020 11 15.
Artigo em Inglês | MEDLINE | ID: mdl-32998983

RESUMO

Mycobacterium tuberculosis, the causative agent of pulmonary tuberculosis (TB), is responsible for millions of infections and deaths annually. Decades of TB vaccine development have focused on adaptive T cell immunity, whereas the importance of innate immune contributions toward vaccine efficacy has only recently been recognized. Airway macrophages (AwM) are the predominant host cell during early pulmonary M. tuberculosis infection and, therefore, represent attractive targets for vaccine-mediated immunity. We have demonstrated that respiratory mucosal immunization with a viral-vectored vaccine imprints AwM, conferring enhanced protection against heterologous bacterial challenge. However, it is unknown if innate immune memory also protects against M. tuberculosis In this study, by using a murine model, we detail whether respiratory mucosal TB vaccination profoundly alters the airway innate immune landscape associated with AwM prior to M. tuberculosis exposure and whether such AwM play a critical role in host defense against M. tuberculosis infection. Our study reveals an important role of AwM in innate immune protection in early stages of M. tuberculosis infection in the lung.


Assuntos
Imunidade Inata , Macrófagos Alveolares/imunologia , Mycobacterium tuberculosis/imunologia , Vacinas contra a Tuberculose/administração & dosagem , Tuberculose Pulmonar/imunologia , Administração através da Mucosa , Animais , Líquido da Lavagem Broncoalveolar/citologia , Líquido da Lavagem Broncoalveolar/imunologia , Modelos Animais de Doenças , Feminino , Humanos , Camundongos , Vacinas contra a Tuberculose/imunologia , Tuberculose Pulmonar/diagnóstico , Tuberculose Pulmonar/microbiologia , Tuberculose Pulmonar/prevenção & controle , Vacinas Sintéticas/administração & dosagem , Vacinas Sintéticas/imunologia
3.
J Interprof Care ; 34(1): 87-96, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-31043099

RESUMO

Canadian pharmacists now have prescribing authority and little is documented about the physicians' perception, experience and relational dynamics evolving around the pharmacists' prescribing practice. The objective of this study was to explore Albertan family physicians' perceptions and experiences of pharmacists' prescribing practice. We used purposeful and maximum variation sampling method and semi-structured face to face or telephone interviews to collect data. From October 2014 to February 2016, we interviewed 12 family physicians in Alberta, having experience with pharmacist prescribing. Interviews were audio recorded and transcribed verbatim for analysis using an interpretive description method, guided by "Relational Coordination" theory. NVivo software was used to manage the data. Three key beliefs (i.e., renewal versus initiate new prescription, community versus team pharmacists, and "I am responsible") about pharmacist prescribing were identified. Trust and communication were prominent themes which shaped participants' collaboration with pharmacist prescribers. Participants were classified as either "collaborative" or "consultative". Participants had greater collaboration with the team pharmacist prescribers compared to community pharmacists due to a higher level of trust and ease of communication. Renewal prescribing by any pharmacist was well accepted but participants showed hesitancy in accepting pharmacist-initiated prescriptions. Our findings provide insight into interprofessional collaboration and communication between physician and pharmacist prescribers.


Assuntos
Atitude do Pessoal de Saúde , Prescrições de Medicamentos/normas , Farmacêuticos/organização & administração , Médicos de Família/psicologia , Papel Profissional/psicologia , Adulto , Idoso , Alberta , Conscientização , Comunicação , Comportamento Cooperativo , Feminino , Humanos , Relações Interprofissionais , Entrevistas como Assunto , Masculino , Pessoa de Meia-Idade , Pesquisa Qualitativa , Confiança
6.
Sci Rep ; 7(1): 9525, 2017 08 25.
Artigo em Inglês | MEDLINE | ID: mdl-28842633

RESUMO

Lung resident memory T cells (TRM) characterized by selective expression of mucosal integrins VLA-1 (α1ß1) and CD103 (αEß7) are generated following primary respiratory viral infections. Despite recent progress, the generation of lung TRM and the role of mucosal integrins following viral vector respiratory mucosal immunization still remains poorly understood. Here by using a replication-defective viral vector tuberculosis vaccine, we show that lung Ag-specific CD8 T cells express both VLA-1 and CD103 following respiratory mucosal immunization. However, VLA-1 and CD103 are acquired in differential tissue sites with the former acquired during T cell priming in the draining lymph nodes and the latter acquired after T cells entered the lung. Once in the lung, Ag-specific CD8 T cells continue to express VLA-1 at high levels through the effector/expansion, contraction, and memory phases of T cell responses. Using a functional VLA-1 blocking mAb, we show that VLA-1 is not required for trafficking of these cells to the lung, but it negatively regulates them in the contraction phase. Furthermore, VLA-1 plays a negligible role in the maintenance of these cells in the lung. Our study provides new information on vaccine-inducible lung TRM and shall help develop effective viral vector respiratory mucosal tuberculosis vaccination strategies.


Assuntos
Linfócitos T CD8-Positivos/imunologia , Expressão Gênica , Memória Imunológica , Integrina alfa1beta1/genética , Mucosa Respiratória/imunologia , Vacinas contra a Tuberculose/imunologia , Tuberculose/etiologia , Animais , Linfócitos T CD8-Positivos/metabolismo , Epitopos de Linfócito T/imunologia , Feminino , Vetores Genéticos/genética , Imunofenotipagem , Integrina alfa1beta1/metabolismo , Linfonodos/imunologia , Linfonodos/metabolismo , Camundongos , Mucosa Respiratória/metabolismo , Mucosa Respiratória/microbiologia , Tuberculose/metabolismo , Tuberculose/prevenção & controle
7.
J Immunol ; 199(7): 2555-2569, 2017 10 01.
Artigo em Inglês | MEDLINE | ID: mdl-28827285

RESUMO

Although most novel tuberculosis (TB) vaccines are designed for delivery via the muscle or skin for enhanced protection in the lung, it has remained poorly understood whether systemic vaccine-induced memory T cells can readily home to the lung mucosa prior to and shortly after pathogen exposure. We have investigated this issue by using a model of parenteral TB immunization and intravascular immunostaining. We find that systemically induced memory T cells are restricted to the blood vessels in the lung, unable to populate either the lung parenchymal tissue or the airway under homeostatic conditions. We further find that after pulmonary TB infection, it still takes many days before such T cells can enter the lung parenchymal tissue and airway. We have identified the acquisition of CXCR3 expression by circulating T cells to be critical for their entry to these lung mucosal compartments. Our findings offer new insights into mucosal T cell biology and have important implications in vaccine strategies against pulmonary TB and other intracellular infections in the lung.


Assuntos
Pulmão/imunologia , Mycobacterium tuberculosis/imunologia , Receptores CXCR3/metabolismo , Vacinas contra a Tuberculose/imunologia , Tuberculose Pulmonar/imunologia , Transferência Adotiva , Animais , Antígenos de Bactérias/imunologia , Linfócitos T CD8-Positivos/imunologia , Movimento Celular , Imunização , Memória Imunológica , Leucócitos/imunologia , Pulmão/citologia , Pulmão/microbiologia , Camundongos , Receptores CXCR3/genética , Receptores CXCR3/imunologia , Mucosa Respiratória/imunologia , Mucosa Respiratória/microbiologia , Transdução de Sinais , Vacinas contra a Tuberculose/administração & dosagem , Tuberculose Pulmonar/microbiologia
8.
J Immunol ; 195(6): 2900-7, 2015 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-26268652

RESUMO

Emerging evidence suggests a role of B cells in host defense against primary pulmonary tuberculosis (TB). However, the role of B cells in TB vaccine-induced protective T cell immunity still remains unknown. Using a viral-vectored model TB vaccine and a number of experimental approaches, we have investigated the role of B cells in respiratory mucosal vaccine-induced T cell responses and protection against pulmonary TB. We found that respiratory mucosal vaccination activated Ag-specific B cell responses. Whereas respiratory mucosal vaccination elicited Ag-specific T cell responses in the airway and lung interstitium of genetic B cell-deficient (Jh(-/-) knockout [KO]) mice, the levels of airway T cell responses were lower than in wild-type hosts, which were associated with suboptimal protection against pulmonary Mycobacterium tuberculosis challenge. However, mucosal vaccination induced T cell responses in the airway and lung interstitium and protection in B cell-depleted wild-type mice to a similar extent as in B cell-competent hosts. Furthermore, by using an adoptive cell transfer approach, reconstitution of B cells in vaccinated Jh(-/-) KO mice did not enhance anti-TB protection. Moreover, respiratory mucosal vaccine-activated T cells alone were able to enhance anti-TB protection in SCID mice, and the transfer of vaccine-primed B cells alongside T cells did not further enhance such protection. Alternatively, adoptively transferring vaccine-primed T cells from Jh(-/-) KO mice into SCID mice only provided suboptimal protection. These data together suggest that B cells play a minimal role, and highlight a central role by T cells, in respiratory mucosal vaccine-induced protective immunity against M. tuberculosis.


Assuntos
Aciltransferases/imunologia , Antígenos de Bactérias/imunologia , Linfócitos B/imunologia , Linfócitos T CD8-Positivos/imunologia , Vacinas contra a Tuberculose/imunologia , Tuberculose Pulmonar/imunologia , Transferência Adotiva , Animais , Linfócitos B/transplante , Feminino , Imunidade nas Mucosas/imunologia , Depleção Linfocítica , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Knockout , Camundongos SCID , Mycobacterium tuberculosis/imunologia , Mucosa Respiratória/imunologia , Mucosa Respiratória/microbiologia , Tuberculose Pulmonar/prevenção & controle , Vacinação
9.
PLoS One ; 10(6): e0131175, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26098423

RESUMO

Tuberculosis (TB) remains a global pandemic despite the use of Bacillus Calmette-Guérin (BCG) vaccine, partly because BCG fails to effectively control adult pulmonary TB. The introduction of novel boost vaccines such as the human Adenovirus 5-vectored AdHu5Ag85A could improve and prolong the protective immunity of BCG immunization. Age at which BCG immunization is implemented varies greatly worldwide, and research is ongoing to discover the optimal stage during childhood to administer the vaccine, as well as when to boost the immune response with potential novel vaccines. Using a murine model of subcutaneous BCG immunization followed by intranasal AdHu5Ag85A boosting, we investigated the impact of age at BCG immunization on protective efficacy of BCG prime and AdHu5Ag85A boost immunization-mediated protection. Our results showed that age at parenteral BCG priming has limited impact on the efficacy of BCG prime-AdHu5Ag85A respiratory mucosal boost immunization-enhanced protection. However, when BCG immunization was delayed until the maturity of the immune system, longer sustained memory T cells were generated and resulted in enhanced boosting effect on T cells of AdHu5Ag85A respiratory mucosal immunization. Our findings hold implications for the design of new TB immunization protocols for humans.


Assuntos
Vacina BCG/farmacologia , Mycobacterium tuberculosis/imunologia , Vacinas contra a Tuberculose/uso terapêutico , Tuberculose Pulmonar/prevenção & controle , Fatores Etários , Animais , Vacina BCG/imunologia , Modelos Animais de Doenças , Feminino , Citometria de Fluxo , Memória Imunológica , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Mucosa Respiratória/imunologia , Linfócitos T/imunologia , Vacinas contra a Tuberculose/imunologia , Tuberculose Pulmonar/imunologia
10.
Eur J Immunol ; 44(5): 1375-86, 2014 May.
Artigo em Inglês | MEDLINE | ID: mdl-24519467

RESUMO

The immune mechanisms underlying delayed induction of Th1-type immunity in the lungs following pulmonary mycobacterial infection remain poorly understood. We have herein investigated the underlying immune mechanisms for such delayed responses and whether a selected innate immune-modulating strategy can accelerate Th1-type responses. We have found that, in the early stage of pulmonary infection with attenuated Mycobacterium tuberculosis (M.tb H37Ra), the levels of infection in the lung continue to increase logarithmically until days 14 and 21 postinfection in C57BL/6 mice. The activation of innate immune responses, particularly DCs, in the lung is delayed. This results in a delay in the subsequent downstream immune responses including the migration of antigen-bearing DCs to the draining lymph node (dLN), the Th1-cell priming in dLN, and the recruitment of Th1 cells to the lung. However, single lung mucosal exposure to the TLR agonist FimH postinfection is able to accelerate protective Th1-type immunity via facilitating DC migration to the lung and draining lymph nodes, enhancing DC antigen presentation and Th1-cell priming. These findings hold implications for the development of immunotherapeutic and vaccination strategies and suggest that enhancement of early innate immune activation is a viable option for improving Th1-type immunity against pulmonary mycobacterial diseases.


Assuntos
Células Dendríticas/imunologia , Imunidade Inata , Pulmão/imunologia , Mycobacterium tuberculosis/imunologia , Células Th1/imunologia , Tuberculose Pulmonar/imunologia , Animais , Células Dendríticas/microbiologia , Células Dendríticas/patologia , Pulmão/microbiologia , Pulmão/patologia , Linfonodos/imunologia , Linfonodos/microbiologia , Linfonodos/patologia , Camundongos , Camundongos Transgênicos , Células Th1/patologia , Fatores de Tempo , Tuberculose Pulmonar/genética , Tuberculose Pulmonar/patologia
11.
Artigo em Inglês | MEDLINE | ID: mdl-26015944

RESUMO

Pneumococcal infections are the leading cause of community-acquired pneumonia. Although the type 1 interferon-α (IFN-α) is a well-known antiviral cytokine, the role of IFN-α in antipneumococcal host defense and its therapeutic potential remain poorly understood. We have investigated these issues by using a murine transgene expression model. We found that in control animals, Streptococcus pneumoniae infection caused severe weight loss and excessive lung inflammation, associated with rapid bacterial outgrowth. In contrast, the animals that received a single dose of an adenoviral vector expressing IFN-α prior to pneumococcal infection demonstrated rapid and effective control of bacterial replication and lung inflammation and improved clinical outcome. Enhanced protection by IFN-α was due to increased activation of neutrophils and macrophages with increased release of reactive oxygen and nitrogen species and bacterial killing. Furthermore, we found that raised levels of IFN-α in the lung remained immune protective even when the gene transfer vector was given at a time postpneumococcal infection. Our study thus shows that the classically antiviral type 1 IFN can be exploited for enhancing immunity against pneumococcal infection via its activating effects on innate immune cells. Our findings hold implications for the therapeutic use of IFN-α gene transfer strategies to combat pneumococcal infections.

12.
PLoS One ; 8(3): e59185, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23527127

RESUMO

Pulmonary tuberculosis (TB), caused by Mycobacterium tuberculosis, is the leading cause of death due to a bacterial pathogen. Emerging epidemiologic evidence suggests that the leading risk factor associated with TB mortality is cigarette smoke exposure. Despite this, it remains poorly understood what is the effect of cigarette smoke exposure on anti-TB immunity and whether its potential detrimental effect can be reversed by cigarette smoking cessation. In our current study, we have investigated the impact of both continuous and discontinuous cigarette smoke exposure on the development of anti-mycobacterial type 1 immunity in murine models. We find that while continuous cigarette smoke exposure severely impairs type 1 immunity in the lung, a short-term smoking cessation allows rapid restoration of anti-mycobacterial immunity. The ability of continuous cigarette smoke exposure to dampen type 1 protective immunity is attributed locally to its affects on innate immune cells in the lung. Continuous cigarette smoke exposure locally, by not systemically, impairs APC accumulation and their production of TNF, IL-12, and RANTES, blunts the recruitment of CD4+IFN-γ+ T cells to the lung, and weakens the formation of granuloma. On the other hand, smoking cessation was found to help restore type 1 immunity by rapidly improving the functionality of lung APCs, enhancing the recruitment of CD4+IFN-γ+ T cells to the lung, and promoting the formation of granuloma. Our study for the first time demonstrates that continuous, but not discontinuous, cigarette smoke exposure severely impedes the lung expression of anti-TB Th1 immunity via inhibiting innate immune activation and lung T cell recruitment. Our findings thus suggest cigarette smoking cessation to be beneficial to the control of pulmonary TB.


Assuntos
Células Apresentadoras de Antígenos/imunologia , Imunidade Celular/efeitos dos fármacos , Abandono do Hábito de Fumar , Fumar/efeitos adversos , Células Th1/efeitos dos fármacos , Tuberculose Pulmonar/imunologia , Animais , Linfócitos T CD4-Positivos/imunologia , Ensaio de Imunoadsorção Enzimática , Feminino , Pulmão/microbiologia , Pulmão/patologia , Camundongos , Camundongos Endogâmicos C57BL , Óxido Nítrico/metabolismo , Células Th1/imunologia
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