Upper Airway Infections

Author(s):  
Michael J. Rutter
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ji In Park ◽  
Tae-Yoon Kim ◽  
Bumjo Oh ◽  
Hyunjeong Cho ◽  
Ji Eun Kim ◽  
...  

Abstract Immunoglobulin A nephropathy (IgAN) involves repeated events of gross haematuria with concurrent upper airway infections. The mucosal immune system, especially the tonsil, is considered the initial site of inflammation, although the role of the tonsillar microbiota has not been established in IgAN. In this study, we compared the tonsillar microbiota of patients with IgAN (n = 21) and other glomerular diseases (n = 36) as well as, healthy controls (n = 23) from three medical centres in Korea. The microbiota was analysed from tonsil swabs using the Illumina MiSeq system based on 16S rRNA gene. Tonsillar bacterial diversity was higher in IgAN than in other glomerular diseases, although it did not differ from that of healthy controls. Principal coordinates analysis revealed differences between the tonsillar microbiota of IgAN and both healthy and disease controls. The proportions of Rahnella, Ruminococcus_g2, and Clostridium_g21 were significantly higher in patients with IgAN than in healthy controls (corrected p < 0.05). The relative abundances of several taxa were correlated with the estimated glomerular filtration rate, blood urea nitrogen, haemoglobin, and serum albumin levels. Based on our findings, tonsillar microbiota may be associated with clinical features and possible immunologic pathogenesis of IgAN.


2020 ◽  
Vol 96 ◽  
pp. 111-119
Author(s):  
Santiago Alfayate Miguélez ◽  
Luis Garcia‐Marcos

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e19020-e19020 ◽  
Author(s):  
Caroline Chaul Barbosa ◽  
Lisa Marie DeAngelis ◽  
Christian Grommes

e19020 Background: Ibrutinib (IBRU) is a Bruton tyrosine kinase (BTK) inhibitor that has been FDA approved for chronic lymphocytic leukemia (CLL), mantle cell lymphoma (MCL) and Waldenstrom's Macroglobulinemia (WM). BTK inhibition may contribute to immunosuppression through B- and T-cell inhibition, resulting in an increase in infections. We therefore characterized IBRU-related infections retrospectively. Methods: The study was an IRB approved retrospective review. Patients (pts) treated with IBRU between 4/2014-11/2016 who developed any infection were identified using ICD10 codes in a clinical database. Study population was defined using descriptive statistics. Results: 200 pts were identified: 78 pts had CLL (39%), 30 diffuse large B-cell lymphoma (15%), 28 MCL (14%), 19 WM (9.5%), 15 (7.5%) marginal zone lymphoma, 14 (7%) follicular lymphoma, 7 (3.5%) multiple myeloma, 7 (3.5%) T-cell lymphoma and 2 (1%) primary central nervous system lymphoma (PCNSL). Median age was 68 (range 28-96), 34% were men and median ECOG was 1. The majority of pts received IBRU as second line treatment (172, 86%) with a median of 2 prior lines of treatment; 23 pts (11.5%) were post transplant. Median IBRU dose was 420mg daily (range 140-840mg), administered a median of 316 days (range 3-1780). Single agent IBRU was used in 162 pts (81%). 105 pts (52%) developed an infection, with pneumonia (30%), upper airway infection (26%); skin infection (18%); and sinusitis (13%) being the most common. 10 (9.5%) had neutropenic fever and 1 (1%) cryptococcal pneumonia. Seven (7%) developed fungal infections, with invasive aspergillosis in 5 (5%). 34 (32%) developed ≥3 infections. 46 pts (44%) were hospitalized, 10 (9.5%) interrupted IBRU and 3 pts (2.9%) died due to infections (2 pneumonia; 1 neutropenic fever). The median time to infection after starting IBRU was 70 days (range 2-1261). The highest infection rate was seen in pts with PCNSL (100%, 2/2), MZL (67%, 10/14), followed by CLL (64%, 50/78). Conclusions: We identified infections in half of the pts treated with IBRU. Pts treated with IBRU should be monitored closely for the development of infections, particularly airway infections.


2000 ◽  
Vol 109 (5) ◽  
pp. 488-496 ◽  
Author(s):  
Katarina Olofsson ◽  
Sten Hellström ◽  
Marie-Louise Hammarström

Upper airway infections often lead to macroscopic changes in the architecture of the uvula. Using immunomorphometric analysis, we investigated the frequency and distribution of immune cells and of cytokine-producing cells in uvular samples. Tissue macrophages, αß T cells, γδ T cells, and B cells were, in declining order, the main cell populations. γδ T cells and B cells exhibited reciprocal localization, with almost all γδ T cells residing in the vicinity of the epithelium, and all B cells in the glandular area. The presence of cells expressing the suppressor phenotype CD8+CD28− αβ T cells is suggested. Fifteen to twenty-five percent of the immune cells expressed the down-regulatory cytokine tumor growth factor ß. Most macrophages were located subepithelially, in the vicinity of the basal lamina. The composition and cytokine profile of leukocytes in the tissue suggest that the uvula may be a site, additional to the jejunal mucosa, for induction of mucosal tolerance to inhaled and ingested antigens. Concomitantly, the uvula appears to be protected from invasion of microbial pathogens by a subepithelial barrier of macrophages and γδ T cells.


2013 ◽  
Vol 81 (8) ◽  
pp. 2714-2723 ◽  
Author(s):  
Keunwook Lee ◽  
Kelli L. Boyd ◽  
Diptiben V. Parekh ◽  
Thomas E. Kehl-Fie ◽  
H. Scott Baldwin ◽  
...  

ABSTRACTThe small Rho GTPase Cdc42 regulates key signaling pathways required for multiple cell functions, including maintenance of shape, polarity, proliferation, invasion, migration, differentiation, and morphogenesis. As the role of Cdc42-dependent signaling in fibroblastsin vivois unknown, we attempted to specifically delete it in these cells by crossing the Cdc42fl/flmouse with an fibroblast-specific protein 1 (FSP1)-Cre mouse, which is thought to mediate recombination exclusively in fibroblasts. Surprisingly, the FSP1-Cre;Cdc42fl/flmice died at 3 weeks of age due to overwhelming suppurative upper airway infections that were associated with neutrophilia and lymphopenia. Even though major aberrations in lymphoid tissue development were present in the mice, the principal cause of death was severe migration and killing abnormalities of the neutrophil population resulting in an inability to control infection. We also show that in addition to fibroblasts, FSP1-Cre deleted Cdc42 very efficiently in all leukocytes. Thus, by using this nonspecific Cre mouse, we inadvertently demonstrated the importance of Cdc42 in host protection from lethal infections and suggest a critical role for this small GTPase in innate immunity.


2018 ◽  
Vol 53 (2) ◽  
pp. 71-77 ◽  
Author(s):  
Gholamreza Bayazian ◽  
◽  
Shirin Sayyahfar ◽  
Mahdi Safdarian ◽  
Farbood Kalantari ◽  
...  

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