Bronchus-associated Lymphoid Tissue Research Articles

Bronchial Associated Lymphoid Tissue Lymphoma in Systemic Lupus Erythematosus Successfully Treated with Rituximab

We present, for the first time to our knowledge, a patient with Systemic Lupus Erythematosus (SLE) with pulmonary Bronchial-Associated Lymphoid Tissue (BALT) lymphoma, refractory to chemotherapy but after a single four-week course of rituximab experienced significant regression of pulmonary lesions and remained progressionfree six months post- treatment. This case report demonstrates the promising role for rituximab in refractory BALT lymphoma.

Differential Expression of IL-8 in The Parenchyma, Bronchi and Bronchus-associated Lymphoid Tissue (BALT) of Pigs Infected with Mycoplasma hyopneumoniae (MHYO)

Differential Expression of IL-8 in The Parenchyma, Bronchi and Bronchus-associated Lymphoid Tissue (BALT) of Pigs Infected with Mycoplasma hyopneumoniae (MHYO)

<i>Mycobacterium vaccae</i> Immunization to Pregnant BALB/c Mice Ameliorated Lung Histopathology and Bone Marrow Eosinophila in Ovalbumin Sensitized Offsprings

Context: One of the treatment strategies for atopic diseases is to skew immune response away from Th2 dominance by using Mycobacterial strains. Objective: We wanted to find out whether M. vaccae administration to pregnant mice had any preventive effect on the offsprings in the development of a murine asthma model. Materials and Methods: Pregnant BALB/c mice were divided into two groups; first group received heat-killed M. vaccae subcutaneously on 12th day of pregnancy and the latter group received PBS. After delivery, newborn mice of each group were further divided into two subgroups as M. vaccae/Ovalbumin (OVA), M. vaccae/control, PBS/OVA and PBS/ control. To establish experimental murine asthma model, mice were intraperitoneally sensitized and challenged intratracheally with Ovalbumin. We analysed airway histopathology, bone marrow eosinophil progenitors and splenic cell cytokine profiles of the offsprings. Results: Comparison of offsprings in M. vaccae/OVA group were not different than PBS controls with respect to thicknesses of airway epithelium, basement membrane, subepithelial smooth muscles and number of hyperplasic goblet cells as well as bronchial associated lymphoid tissue density and eosinophil progenitors in the bone marrow. Comparison of M. vaccae/OVA group to asthma model revealed significant differences and lower levels of OVA-induced IL-5. Conclusions: We propose that immunization of pregnant BALB/c with M. vaccae could prevent histopathological alterations in the airways related to the asthma model and down-regulates IL-5 secretion from splenocytes of offsprings.

Lymphoproliferative Lung Disorders: A Radiologic-Pathologic Overview. Part I: Reactive disorders

Lymphoid tissue is a normal component of the lung and manifests as intrapulmonary lymph nodes, bronchus-associated lymphoid tissue (BALT), peripheral lymphocytic aggregates, solitary lymphocytes, and phagocytic cells. Pulmonary lymphoid lesions are thought to develop as a consequence of anomalous stimulation and response of the bronchus-associated lymphoid tissue and manifests as a spectrum of lymphoproliferative disorders that may be reactive or neoplastic. Reactive disorders are polyclonal abnormalities and include nodular lymphoid hyperplasia, lymphocytic interstitial pneumonia, follicular bronchiolitis, angiofollicular hyperplasia, and enlarged intrapulmonary lymph nodes. Affected patients are often asymptomatic. Imaging findings include focal nodules, diffuse bilateral centrilobular nodules, and hilar or mediastinal masses.

Inducible Bronchus-Associated Lymphoid Tissue (iBALT) Synergizes with Local Lymph Nodes during Antiviral CD4+ T Cell Responses

Exposure of the lungs to an antigen or pathogen elicits the formation of lymphoid satellite islands termed inducible bronchus-associated lymphoid tissue (iBALT). However, little is known about how the presence of iBALT, induced by a stimulus unrelated to the subsequent challenge agent, influences systemic immunity in distal locations, whether it be independently, antagonistically, or synergistically. Here, we determined the kinetics of the influenza-specific responses in the iBALT, tracheobronchial lymph node (TBLN), and spleen of mice with and without pre-formed iBALT. Mice with VLP-induced iBALT or no pre-formed iBALT were challenged with influenza. We found that, as we have previously described, those mice whose lungs contained pre-formed iBALT were protected from morbidity, and furthermore, that these mice had increased dendritic cell, and alveolar macrophage accumulation in both the iBALT and TBLNs. This translated to similarly accelerated kinetics and intensified influenza-specific CD4(+), but not CD8(+) T cell responses in the iBALT, TBLN, and spleen. This expansion was then followed by a more rapid T cell contraction in all lymphoid tissues in the mice with pre-formed iBALT. Thus, iBALT itself may not be responsible for the accelerated primary immune response we observe in mice with pre-formed iBALT, but may contribute to an overall accelerated local and systemic primary CD4(+), but not CD8(+) T cell response. Furthermore, less damaging immune responses observed in mice with pre-formed iBALT may be due to a quicker contraction of CD4(+) T cell responses in both local and systemic secondary lymphoid tissue.

Lymphoproliferative lung disorders: clinicopathological aspects

Lymphoproliferative disorders are rarely observed as primary lesions in the lung, representing only 0.3% of all primary pulmonary malignancies, <1% of all the cases of non-Hodgkin lymphoma and 3–4% of all the extra nodal manifestations of non-Hodgkin lymphoma. The earliest comprehensive studies of pulmonary lymphomas were those of Saltzstein [1] and Papioannou and Watson [2], which were published in the 1960s. These investigators made important observations: low-grade neoplasms were more frequent than higher grade lymphomas (reticulum cell sarcomas) and both tumours had better clinical outcomes than their nodal-based counterparts. The authors also concluded that the majority of neoplasms with a low-grade cytological appearance should be considered as reactive proliferations, introducing the term “pseudo-lymphoma”. This hypothesis showed significant weak points and, approximately 20 years later, Addis et al. [3] concluded that “most if not all the cases of pseudo-lymphoma can be classified, when re-evaluated, as malignant lymphoma”. Knowledge of these entities expanded rapidly after the advent of new investigative tools such as immunohistochemistry and molecular biology techniques. The World Health Organization (WHO) classification of lymphoid neoplasm recently emphasised the importance of clinical features [4]. table 1 provides an overall classification of lymphoproliferative disorders, which are described as: reactive/non-neoplastic lymphoid lesions, malignant parenchymal lymphoproliferative lesions (primary or secondary) and post-transplant lymphoproliferative disorders. View this table: Table 1. Classification system for the pulmonary lymphoproliferative disorders ### Reactive pulmonary lymphoid diseases Three rare forms of benign hyperplasia of pulmonary lymphoid tissue, namely follicular bronchiolitis, pulmonary nodular lymphoid hyperplasia and lymphocytic interstitial pneumonia, are regarded as part of the spectrum of lymphoid hyperplasia of the bronchus-associated lymphoid tissue (table 1) [5, 6]. Follicular bronchiolitis is characterised by lymphoid follicular hyperplasia, often with reactive germinal centres, in the walls of bronchioles with narrowing of the lumen. Pulmonary nodular lymphoid hyperplasia (pulmonary pseudo-lymphoma) is a distinct form of reactive …

Intranasal Administration of Perillyl Alcohol Activates Peripheral and Bronchus-Associated Immune System In Vivo

Perillyl alcohol (POH) presents antitumoral activity but clinical application is hampered by adverse effects following oral administration. This work aimed to verify the cytotoxic effect of intranasal POH administration in the histology of lung, liver, brain; the cellularity and function of peripheral and bronchoalveolar-associated immune system. C57 adult mice received 1-min inhalation with POH, vehicle 70% ethanol or saline buffer, once (84μg/day) or twice (164μg/day) during five consecutive days, and were killed 72h after treatment. Spleen, cervical and mesenteric lymph nodes were removed for (3)H-thymidine proliferation assay, leukocyte cellularity and flow cytometry analysis. Peripheral blood and bronchoalveolar lavage cells were collected to assess cellularity and immunoglobulin (IgA, IgM) levels. Intranasal POH did not alter body weight or liver, brain and lung morphology, but increased splenocyte and cervical lymph node cell proliferation, and IgM production without altering peripheral lymphocyte subsets. Treatment also increased the percentage of alveolar macrophages (83%) and IgA-producing lymphocytes (15%), a pattern characteristic of activated bronchoalveolar innate immune system. Intranasal administration of POH activated peripheral immune system and innate immunity of bronchus-associated lymphoid tissue, thus suggesting a possible role for POH as a chemotherapeutic drug also in pathological processes affecting the lung.

Bronchus-associated Lymphoid Tissue in Pulmonary Hypertension Produces Pathologic Autoantibodies

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. 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. We used animal models, histology, and gene expression assays to evaluate the role of bronchus-associated lymphoid tissue in pulmonary hypertension. 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 CD3(+) T cells over a core of CD45RA(+) 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(+) 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. 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.

Immune stimulation following dermal exposure to unsintered indium tin oxide

In recent years, several types of pulmonary pathology, including alveolar proteinosis, fibrosis, and emphysema, have been reported in workers in the indium industry. To date, there remains no clear understanding of the underlying mechanism(s). Pulmonary toxicity studies in rats and mice have demonstrated the development of mediastinal lymph node hyperplasia and granulomas of mediastinal lymph nodes and bronchus-associated lymphoid tissues following exposure to indium tin oxide. Given the association between exposure to other metals and the development of immune-mediated diseases, these studies were undertaken to begin to investigate the immuno-modulatory potential of unsintered indium tin oxide (uITO) in a mouse model. Using modifications of the local lymph node assay, BALB/c mice (five animals/group) were exposed topically via intact or breached skin or injected intradermally at the base of the ear pinnae with either vehicle or increasing concentrations 2.5–10% uITO (90:10 indium oxide/tin oxide, particle size <50 nm). Dose-responsive increases in lymphocyte proliferation were observed with a calculated EC3 of 4.7% for the intact skin study. Phenotypic analysis of draining lymph node cells following intradermal injection with 5% uITO yielded a profile consistent with a T-cell-mediated response. These studies demonstrate the potential for uITO to induce sensitization and using lymphocyte proliferation as a biomarker of exposure, and demonstrate the potential for uITO to penetrate both intact and breached skin.

Sarcoidosis lymphoma syndrome - the value of PET-CT in the diagnosis

We report a 52-year-old patient who developed B-cell non-Hodgkin’s lymphoma subsequent to sarcoidosis. Sarcoidosis was diagnosed 16 years ago and remained asymptomatic for 14 years after steroid treatment. She presented with new symptoms of arthralgia, photosensitivity, butterfly erythema, autoimmune antibodies (ANA, chromatin positivity) associated with progression of the known left upper lobe lesion on the chest X-ray suggesting primary autoimmune disease (systemic lupus erythematosus). As steroid treatment was not effective, we started bolus cyclophosphamide therapy after which progression was seen on the chest X-ray. Computed tomography (CT)-guided needle biopsy confirmed malignancy of indefinable origin. Despite of the well-known fluorodeoxyglucose (FDG) avidity in active sarcoidosis, a FDG-positron emission tomography (PET) scan was performed to stage the primary tumour. Intensive FDG uptake was detected in the affected lung segment, with moderate uptake in mediastinal lymph nodes. The patient underwent left upper lobectomy. The histology showed pulmonary mucosa-associated lymphoma (bronchus-associated lymphoid tissue (BALT) lymphoma) in the lung tissue, while only sarcoidosis was present in the mediastinal lymph nodes. Bone marrow biopsy was negative.The association between sarcoidosis and lymphoma is known as sarcoidosis lymphoma syndrome, which is a rare disease. PET-CT was helpful in the differentiation of sarcoidosis and malignancy in this patient. It is important to be aware of the risk of lymphoma in sarcoidosis and FDG-PET, used for adequate purpose, can help the diagnosis.

Two tracheal BALT lymphoma patients successfully treated with chemotherapy including rituximab

Bronchus-associated lymphoid tissue (BALT) lymphoma of the trachea, an important differential diagnosis for tracheal tumors, is a rare disease with characteristic bronchoscopic findings. In this study, we reviewed 2 cases of patients who were symptomatic at the time of diagnosis, with tumors in the trachea and left main bronchus, putting them at high risk for asphyxia. Chemotherapies including rituximab were administered, and complete remission was confirmed in both cases. Because tracheal tumors often have a pernicious course, it might be beneficial to initiate a chemotherapeutic treatment regimen instead of adopting the "wait-and-see" approach in patients with symptomatic tracheal BALT lymphoma.

Imaging manifestations of autoimmune disease-associated lymphoproliferative disorders of the lung

Lymphoproliferative disorders (LPDs) may involve intrathoracic organs in patients with autoimmune disease, but little is known about the radiologic manifestations of autoimmune disease-associated LPDs (ALPDs) of the lungs. The purpose of our work was to identify the radiologic characteristics of pulmonary involvement in ALPDs. A comprehensive search for PubMed database was conducted with the combination of MeSH words. All articles which had original images or description on radiologic findings were included in this analysis. Also, CT images of eight patients with biopsy-proven lymphoproliferative disorder observed from our institution were added. Overall, 44 cases of ALPD were identified, and consisted of 24 cases of bronchus-associated lymphoid tissue lymphoma (BALToma), eight cases of non-Hodgkin's lymphoma (NHL), six cases of lymphoid interstitial pneumonia (LIP), two cases of nodular lymphoid hyperplasia, two cases of unclassified lymphoproliferative disorder, and one case each of lymphomatoid granulomatosis and hyperblastic BALT. Multiple nodules (n = 14, 32 %) and single mass (n = 8, 18 %) were the predominant radiologic manifestations. The imaging findings conformed to previously described findings of BALToma, NHL, or LIP. Data suggest that BALToma, NHL, and LIP are the predominant ALPDs of the lung, and ALPD generally shared common radiologic features with sporadic LPDs. Familiarity with ALPDs and their imaging findings may enable radiologists or clinicians to include the disease as a potential differential diagnosis and thus, to prompt early biopsy followed by appropriate treatment.

Inducible bronchus-associated lymphoid tissue reduces Th2-driven pathology by redistributing leukocytes within the lung (P6214)

Abstract Inducible bronchus-associated lymphoid tissue (iBALT) is an ectopic lymphoid tissue formed in the lung after pulmonary infection or inflammation. This local lymphoid tissue is structurally similar to conventional secondary lymphoid organs, with separated B and T cell areas, specialized stromal cells and lymphoid dendritic cells (DCs). Here, we tested whether the presence of iBALT affects pulmonary immune responses to allergens. We induced iBALT formation in neonatal mice by pulmonary administration of LPS, and when the mice were adults, challenged them intranasally with OVA. We found that although mice with iBALT had more lymphocytes in their lungs, they had fewer eosinophils, less goblet cells and had reduced Th2 cytokine production in bronchoalveolar (BAL) fluid and lung tissue after OVA challenge. Surprisingly, using IL-4 reporter and by transferring OVA-specific OT-II cells, we found that the presence of iBALT did not reduce the number of Th2 cells that accumulated in the lung. Despite similar numbers of Th2 effectors in the lungs of mice with and without iBALT, we found that Th2 cells were differentially distributed in these two groups of mice. Those in the lungs of mice without iBALT were more widely dispersed, whereas the cells in the lungs of mice with iBALT were predominantly concentrated in the lymphoid tissue. These results suggest that the reduction in Th2-driven pathology with iBALT is due to the redistribution of leukocytes within the lung after iBALT formation.

Pulmonary Nodular Lymphoid Hyperplasia (Pulmonary Pseudolymphoma)

On the basis of an initial case, we hypothesized that IgG4-positive plasma cells may be increased in pulmonary nodular lymphoid hyperplasia (PNLH) compared with other lymphoid proliferations of the lung. Six cases of PNLH, 9 cases of low-grade B-cell lymphoma of the bronchus-associated lymphoid tissue (BALT), 8 cases of intraparenchymal lymph nodes, 8 cases of either primary or secondary follicular bronchiolitis, and 4 cases of lymphocytic interstitial pneumonitis were stained by immunohistochemical analysis for IgG4 and IgG. The mean number of IgG4-positive and IgG-positive plasma cells and the IgG4/IgG ratio were determined from a manual count of images from 3 separate high-power fields (hpf) of areas showing the highest numbers of stained cells, respectively. The mean number of IgG4-positive plasma cells and the IgG4/IgG ratio were significantly increased in PNLH (IgG4=78/hpf, IgG4/IgG=0.35) compared to low-grade lymphoma of BALT (IgG4=4/hpf, P=0.02; IgG4/IgG=0.03, P=0.005), intraparenchymal lymph nodes (IgG4=7/hpf, P=0.03; IgG4/IgG=0.06, P=0.007), follicular bronchiolitis (IgG4=0/hpf, P=0.02; IgG4/IgG=0, P=0.004), and lymphocytic interstitial pneumonitis (IgG4=2/hpf, P=0.02; IgG4/IgG=0.06, P=0.007). These findings support our current understanding of PNLH as a distinct form of reactive lymphoid proliferation, potentially aid in its distinction from low-grade B-cell lymphoma of BALT, and raise the possibility that PNLH may belong within the family of IgG4-related sclerosing diseases.

Non-Hodgkin's Lymphoma Presenting as a Primary Endobronchial Tumor - A Case Report

Non-Hodgkin’s lymphoma (NHL) involving the endobronchial tree is uncommon, and the initial presentation of NHL as an endobronchial tumor is extremely rare. Several clinical reports have described bronchial-associated lymphoid tissue (BALT) lymphoma as an endobronchial lesion. A 77 year old male hospitalized in another hospital for acute breathlessness and mechanically ventilated. He was shifted to Delhi Heart And Lung Institute because of failed extubation after 3 days of mechanical ventilation and reintubated .Past History of intubation was present 1 month back and diagnosed as a case of acute bronchitis. On evaluation at another hospital, the patient was found to have normal chest radiograph. Chest examination revealed findings consistent assisted ventilatory breath sounds associated with bilateral ronchi. Blood investigations were within normal limit. Contrast enhanced computed tomography of the chest revealed endoluminal soft tissue mass lesion at carina significantly obliterating bilateral main bronchi.USG Whole Abdomen revealed mild hepatomegaly and left renal cortical cyst measuring 4×5 cm and grade l BPH.Fibreoptic bronchoscopy revealed a globular smooth mass causing near complete obstruction of left main bronchus. Histopathological examination of the endobronchial biopsy showed tumor cells have a round or oval nucleus that appears vesicular because of margination of chromatin at the nuclear membrane, but large multilobed or cleaved nuclei predominate in some cases . Immunohistochemical staining was positive for LCA, CD20, and CD79a and negative for CD3, CD5, CD30, NSE, CK, Ki67, Chromogranin and Synaptophysin. While in the hospital, the patient was managed with mechanical ventilation and symptomatic treatment. FOB and rigid Bronchoscope, debulking of tumour growths was done using electrocautery snare. Patient was continued on overnight mechanical ventilation and extubated after one day. Post extubation, patient remained alright without any respiratory distress and discharged in stable condition. Latter on patient followed in Rajiv Gandhi Cancer Hospital. He underwent PET scan of whole body, which revealed normal study. Patient was managed with chemotherapeutic agents and he is still alive after 3 years of management without any symptoms. NHL rarely presents as an endobronchial growth and only histopathology can differentiate it from other benign and malignant endobronchial masses. SAARC Journal of Tuberculosis, Lung Diseases &amp; HIV/AIDS; 2012; IX(2) 37-40 DOI: http://dx.doi.org/10.3126/saarctb.v9i2.7978

Dietary modulation of BALT on a rat mammary tumor model

Murine bronchus associated lymphoid tissue (BALT) is a mirror of systemic immunity since it varies greatly with immune status of the animal and plays a pivotal role in local immune responses at the lung surface. BALT enhanced histopathology (EH) is a semiquantitative screening tool to determine whether there is a potential effect on the immune system of rats under controlled conditions.168 Sprague Dawley virgin female rats with 42 days were randomly distributed for seven groups of 24 animals each. Besides group I, at 55 days the groups were induced for mammary cancer with 20mg of 1,12‐dimetilbenzantracene (DMBA). Dietary protocols were applied for 150 days as following. Group I: standard diet (SD), 300Kcal/100g; Group II: DMBA +SD; Group III: SD + beans 40g/Kg of SD, 341Kcal/100g; Group IV: SD + olive oil (50ml/Kg of SD); Group V: fiber supplement 4× the SD, 250Kcal/100g; Group VI: fiber supplement 4× the SD + beans 19,95gr + olive oil 25ml on 1Kg of SD; Group VII: SD + mediterranean lyophilized diet (41Kcal). The animals were ethically euthanized and the lungs were routinely fixed and stained with hematoxylin‐eosin. BALT was evaluated by EH.The BALT morphology of tumoral rats with mediterranean diet and caloric restrain was similar to the BALT of control group. The other tumoral groups had decreased BALT in size and lymphocyte number compared to control group.These results suggest that diet can interfere on BALT morphology.

Autoreactive T and B Cells Induce the Development of Bronchus-Associated Lymphoid Tissue in the Lung

Rheumatoid arthritis-related interstitial lung disease (RA-ILD) is associated with significant morbidity and mortality. Studies in humans have found that the incidence of bronchus-associated lymphoid tissue (BALT) correlates with the severity of lung injury. However, the mechanisms underlying the development of BALT during systemic autoimmunity remain unknown. We have determined whether systemic autoimmunity in a murine model of autoimmune arthritis can promote the development of BALT by generating a novel murine model derived from K/BxN mice. Transgenic mice with the KRN T-cell receptor specific for the autoantigen, glucose-6-phosphate isomerase (GPI), were crossed with GPI-specific immunoglobulin heavy and light chain knock-in mice, producing mice with a majority of T and B cells specific for the same autoantigen. We found that 67% of these mice demonstrated lymphocytic infiltration in the lungs, localized to either the perivascular or peribronchial regions. Fifty percent of the mice with lymphocytic infiltration manifested lymphoid-like lesions resembling BALT, with distinct T and B cell follicles. The lungs from mice with lymphoid infiltrates had increased numbers of cytokine-producing T cells, including IL-17A(+) T cells and increased major histocompatibility complex Class II expression on B cells. Interestingly, challenge with bleomycin failed to elicit a significant fibrotic response, compared with wild-type control mice. Our data suggest that systemic autoreactivity promotes ectopic lymphoid tissue development in the lung through the cooperation of autoreactive T and B cells. However, these BALT-like lesions may not be sufficient to promote fibrotic lung disease at steady state or after inflammatory challenge.

Autoreactive Bronchus-Associated Lymphoid Tissue in Interstitial Lung Disease: Friend or Foe?

Autoreactive Bronchus-Associated Lymphoid Tissue in Interstitial Lung Disease: Friend or Foe?

Recombinant Influenza Virus Carrying the Respiratory Syncytial Virus (RSV) F 85-93 CTL Epitope Reduces RSV Replication in Mice

Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infections in infants worldwide. Despite decades of research, there is still no registered vaccine available for this major pathogen. We investigated the protective efficacy of a recombinant influenza virus, PR8/NA-F(85-93), that carries the RSV CD8(+) T cell epitope F(85-93) in its neuraminidase stalk. F(85-93)-specific cytotoxic T lymphocytes (CTLs) were induced in mice after a single intranasal immunization with PR8/NA-F(85-93) virus, and these CTLs provided a significant reduction in the lung viral load upon a subsequent challenge with RSV. To avoid influenza-induced morbidity, we treated mice with matrix protein 2 (M2e)-specific monoclonal antibodies before PR8/NA-F(85-93) virus infection. Treatment with anti-M2e antibodies reduced the infiltration of immune cells in the lungs upon PR8/NA-F(85-93) infection, whereas the formation of inducible bronchus-associated lymphoid tissue was not affected. Moreover, this treatment prevented body weight loss yet still permitted the induction of RSV F-specific T cell responses and significantly reduced RSV replication upon challenge. These results demonstrate that it is possible to take advantage of the infection-permissive protection of M2e-specific antibodies against influenza A virus to induce heterologous CD8(+) T cell-mediated immunity by an influenza A virus vector expressing the RSV F(85-93) epitope.

Synchronous BALT Lymphoma and Squamous Cell Carcinoma of the Lung: Coincidence or Linkage?

A 72-year-old man presented with weight loss, fever, and malaise. Chest radiograph and CT revealed two large ill-defined masses in middle and left lower lobes. CT-guided biopsy of left lower lobe mass disclosed bronchus-associated lymphoid tissue (BALT) lymphoma. Middle lobe mass was considered second deposit in contralateral lung. The patient received chemotherapy for BALT. Followup CT disclosed regression of left lower lobe mass and stability of middle-lobe mass and of right paratracheal lymph nodes. CT-guided biopsy of middle-lobe mass revealed squamous cell lung carcinoma. Surgical biopsy of right paratracheal lymph nodes revealed malignancy. Disease was staged T3, N2, and M0. Combined chemotherapy for lung cancer and BALT lymphoma was initiated.