Development of Bronchus-Associated Lymphoid Tissue Hyperplasia Following Lipopolysaccharide-Induced Lung Inflammation in Rats

Bánfi, Andrea; Tiszlavicz, László; Székely, E; Peták, Ferenc; Tóth‐Szűki, Valéria; Baráti, Levente; Bari, Ferenc; Novàk, Zoltán

doi:10.1080/01902140802495862

Cited by 15 publications

(11 citation statements)

References 39 publications

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“…The field of lymphoid organ development has progressed significantly since the discovery that Lta À/À mice do not develop LNs or Peyer's patches (Banks et al, 1995;de Togni et al, 1994). The critical signal for lymphoid organ development comes through the LTbR on mesenchymal cells, which leads to the production of homeostatic chemokines, such as CCL19, CCL21, and CXCL13, that in turn recruit lymphocytes and promote lymphoid organ development (Mebius, 2003;Randall et al, 2008).…”

Section: Role Of Homeostatic Chemokines and Ltmentioning

confidence: 99%

Bronchus-Associated Lymphoid Tissue (BALT)

Randall

2010

Advances in Immunology

214

194

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Bronchus-associated lymphoid tissue (BALT) is a constitutive mucosal lymphoid tissue adjacent to major airways in some mammalian species, including rats and rabbits, but not humans or mice. A related tissue, inducible BALT (iBALT), is an ectopic lymphoid tissue that is formed upon inflammation or infection in both mice and humans and can be found throughout the lung. Both BALT and iBALT acquire antigens from the airways and initiate local immune responses and maintain memory cells in the lungs. Here, we discuss the development and function of BALT and iBALT in the context of pulmonary immunity to infectious agents, tumors, and allergens as well as autoimmunity and inflammatory diseases of the lung.

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Section: Role Of Homeostatic Chemokines and Ltmentioning

confidence: 99%

Bronchus-Associated Lymphoid Tissue (BALT)

Randall

2010

Advances in Immunology

214

194

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“…The presence of iBALT is associated with various lung inflammatory conditions, including severe asthma, COPD (18) and lung complications of rheumatoid arthritis (21). iBALT has been detected in the lungs of mice infected with virus (20), mycobacteria (22) or exposed neonatally to the bacterial product lipopolysaccharide (LPS) (23), although the precise pathways by which each of these conditions result in iBALT might not be identical (24). In any case, the function of OSM in iBALT formation and B cell responses during respiratory infection remains to be understood.…”

Section: Introductionmentioning

confidence: 99%

Pulmonary Expression of Oncostatin M (OSM) Promotes Inducible BALT Formation Independently of IL-6, Despite a Role for IL-6 in OSM-Driven Pulmonary Inflammation

Botelho

Rangel-Moreno

Fritz

et al. 2013

The Journal of Immunology

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Inducible Bronchus-Associated Lymphoid Tissue (iBALT) is associated with immune responses to respiratory infections as well as with local pathology derived from chronic inflammatory lung diseases. Here we assessed the role of Oncostatin M (OSM) in B cell activation and iBALT formation in mouse lungs. We found that C57Bl/6 mice responded to an endotracheally-administered adenovirus vector expressing mouse OSM (Ad-mOSM), with marked iBALT formation, increased cytokine (IL-4, IL-5, IL-6, IL-10, TNFα and IL-12) and chemokine (CXCL13, CCL20, CCL21, Eotaxin-2, KC and MCP-1) production as well as inflammatory cell accumulation in the airways. B cells, T cells and dendritic cells were also recruited to the lung, where many displayed an activated phenotype. Mice treated with control adenovirus vector (Addl70) were not affected. Interestingly, IL-6 was required for inflammatory responses in the airways and for the expression of most cytokines and chemokines. However, iBALT formation and lymphocyte recruitment to the lung tissue occurred independently of IL-6 and STAT6 as assessed in gene-deficient mice. Collectively, these results support the ability of OSM to induce B cell activation and iBALT formation independently of IL-6 and highlight a role for IL-6 downstream of OSM in the induction of pulmonary inflammation.

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“…In the rat, BALTs are sparsely present compared with rats with lung inflammation and/or infection (16). We reasoned that differences between rat BALTs from control animals and from PH would offer clues as to the development of BALT in humans.…”

Section: Balt Numbers Increase In Phmentioning

confidence: 99%

Bronchus-associated Lymphoid Tissue in Pulmonary Hypertension Produces Pathologic Autoantibodies

Colvin¹,

Cripe²,

Ivy³

et al. 2013

Am J Respir Crit Care Med

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Rationale: Autoimmunity has long been associated with pulmonary hypertension. Bronchus-associated lymphoid tissue plays important roles in antigen sampling and self-tolerance during infection and inflammation. Objectives: We reasoned that activated bronchus-associated lymphoid tissue would be evident in rats with pulmonary hypertension, and that loss of self-tolerance would result in production of pathologic autoantibodies that drive vascular remodeling. Methods: We used animal models, histology, and gene expression assays to evaluate the role of bronchus-associated lymphoid tissue in pulmonary hypertension. Measurements and Main Results: Bronchus-associated lymphoid tissue was more numerous, larger, and more active in pulmonary hypertension compared with control animals. We found dendritic cells in and around lymphoid tissue, which were composed of CD31 T cells over a core of CD45RA 1 B cells. Antirat IgG and plasma from rats with pulmonary hypertension decorated B cells in lymphoid tissue, resistance vessels, and adventitia of large vessels. Lymphoid tissue in diseased rats was vascularized by aquaporin-1 1 high endothelial venules and vascular cell adhesion molecule-positive vessels. Autoantibodies are produced in bronchus-associated lymphoid tissue and, when bound to pulmonary adventitial fibroblasts, change their phenotype to one that may promote inflammation. Passive transfer of autoantibodies into rats caused pulmonary vascular remodeling and pulmonary hypertension. Diminution of lymphoid tissue reversed pulmonary hypertension, whereas immunologic blockade of CCR7 worsened pulmonary hypertension and hastened its onset. Conclusions: Bronchus-associated lymphoid tissue expands in pulmonary hypertension and is autoimmunologically active. Loss of self-tolerance contributes to pulmonary vascular remodeling and pulmonary hypertension. Lymphoid tissue-directed therapies may be beneficial in treating pulmonary hypertension.Keywords: hypertension; pulmonary; lymphoid tissue; inflammation; autoimmunity Pulmonary hypertension (PH) is characterized by progressive increases in pulmonary artery pressure and pulmonary vascular resistance resulting in right ventricular failure (1). The primary histopathologic finding in PH is vascular remodeling, in which the pulmonary vasculature becomes stiff, occluded, and fibrotic (2). Vascular remodeling seems to require lung infiltration of inflammatory cells, and continual influx likely sustains a cycle of perpetual inflammation and remodeling by poorly defined mechanisms (3).The bronchovascular space is a structure that marries sterile (vasculature) and nonsterile (airway) components. Bronchusassociated lymphoid tissues (BALTs) are tertiary lymphoid organs that provide an elegant immune surveillance apparatus ensuring airway and vessel homeostatic patency. They are histologically similar to lymph nodes containing afferent lymphatic connection, B cells, T cells, antigen-presenting cells, stroma, and a vascular supply (4). The chief antigen-presenting cells in BALT are dendritic ce...

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Development of Bronchus-Associated Lymphoid Tissue Hyperplasia Following Lipopolysaccharide-Induced Lung Inflammation in Rats

Cited by 15 publications

References 39 publications

Bronchus-Associated Lymphoid Tissue (BALT)

Bronchus-Associated Lymphoid Tissue (BALT)

Pulmonary Expression of Oncostatin M (OSM) Promotes Inducible BALT Formation Independently of IL-6, Despite a Role for IL-6 in OSM-Driven Pulmonary Inflammation

Bronchus-associated Lymphoid Tissue in Pulmonary Hypertension Produces Pathologic Autoantibodies

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