Allergic fungal rhinosinusitis

Luong, Amber U.; Marple, Bradley F.

doi:10.1007/s11882-004-0013-5

Cited by 31 publications

(18 citation statements)

References 34 publications

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“…Fungal elements are one of the causative agents of CRS, possibly by an allergic mechanism (2107-2110), but controversy has accumulated concerning the prevalence of fungal CRS (2111,2112) and benefits of topical amphotericin B therapy are inconsistent (2113,2114).…”

Section: Rhinosinusitismentioning

confidence: 99%

Allergic Rhinitis and its Impact on Asthma (ARIA) 2008*

Bousquet¹,

Khaltaev²,

Cruz³

et al. 2008

Allergy

3,861

1,761

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Section: Rhinosinusitismentioning

confidence: 99%

Allergic Rhinitis and its Impact on Asthma (ARIA) 2008*

Bousquet¹,

Khaltaev²,

Cruz³

et al. 2008

Allergy

3,861

1,761

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“…Curvularia species has been found to cause allergic fungal sinusitis mainly due to the growth of fungus in the area of abnormal tissue drainage (Luong and Marple, 2004;Bush et al, 2006). Among the various toxins produced by different Fusarium species vomiting and nausea have been reported to be caused by deoxynivalenol while Fumonisin B1 has been found with the ability to cause oesophagus cancer in humans (Bucci et al, 1996;Rotter et al, 1996;Bennett and Klich, 2003).…”

Section: Gram Negative Bacteriamentioning

confidence: 99%

Identification and Characterization of Size-Segregated Bioaerosols at Different Sites in Delhi

Lal

Ghosh

Srivastava

et al. 2017

Aerosol Air Qual. Res.

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Ambient levels of culturable bioaerosol were measured at four different sites of Delhi, India in six size ranges (> 7.0 µm, 7.0-4.7 µm, 4.7-3.3 µm, 3.3-2.1 µm, 2.1-1.1 µm, < 1.1 µm). The study also accounted the seasonal variation (monsoon, post monsoon, winter and pre-monsoon) of the air microbes. The sampling was carried out for three different fractions of bioaerosols viz. fungi, gram positive and negative bacteria during August 2010 to April 2011 using a six-stage viable cascade impactor sampler. Unlike gram positive and negative bacteria, the concentration of fungal bioaerosol found in different stages at each site seems to follow a typical pattern in all four season. The typical pattern of concentration depicts that majority of the fungal species found in the diameter range of 3.3-2.1 µm, which coincides with the penetration range in the secondary bronchi of the lungs in the human body. This reveals that majority of the immunotoxic and allergic fungi found at this stage are mostly prone to affect the secondary bronchi in human lungs when inhaled. At all four sites maximum fungal concentration (1740.5-3224.7 CFU m -3 ), gram-positive bacterial concentration (2790.6-9428.3 CFU m -3 ) and gram-negative bacterial concentration (1990.3-7609 CFU m -3 ) were found in post monsoon season. In the majority of the sites, minimum concentrations were found in monsoon period which probably may be due to rain wash during the sampling. For all the three bioaerosol fractions no particular relationship pattern was found to exist between their respective concentrations with temperature and relative humidity (RH). However, higher range of variation was observed at higher concentration levels and lower range of variation at low concentration levels for all the three bioaerosol fractions. Most of the fungal bioaerosol identified such as Penicillium sp., Alternaria sp. and Aspergillus sp. are associated with immunotoxic and allergic diseases.

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“…In addition to asymptomatic colonization of the upper and lower respiratory tracts, fungi are strongly linked to noninvasive disease processes in which organism growth is confined to the airway epithelial surface in association with allergic fungal rhinosinusitis (AFRS) (33), allergic bronchopulmonary aspergillosis (ABPA) (48), and aspergillomas (fungus balls). Additional syndromes in which fungi become locally invasive in the airway epithelium and submucosa, such as chronic necrotizing aspergillosis and advanced ABPA, are more clearly linked to the fungal infection itself (59).…”

mentioning

confidence: 99%

“…Fungi can spread hematogenously from the lung to any organ, but the brain is especially susceptible to disease and, when involved, portends an exceptionally poor outcome (5). A diagnosis of ABPA or AFRS further carries a very strong risk of having concomitant allergic asthma, and antifungal antibiotics have recently been shown to have significant utility in the treatment of both asthma and ABPA with fungal sensitization (15,16,33,41,48). Thus, fungal mucosal infection potentially underlies a spectrum of airway disorders ranging from the rare to the exceptionally common, with important implications for the medical management of these conditions.…”

mentioning

confidence: 99%

Necessary and Sufficient Role for T Helper Cells To Prevent Fungal Dissemination in Allergic Lung Disease

et al. 2011

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Mucosal immune responses to fungal infection range from T helper type 2 (Th2) cell-directed allergic inflammation to Th1-predominant neutrophilic inflammation, but the mechanisms directing these divergent mucosal immune outcomes and the role of T cells in host defense against mucosal fungal infections are not known. Here we examined the mouse mucosal immune responses to 12 filamentous environmental fungal species over a broad range of exposure doses and determined the requirement of T cells for host defense. For all tested fungi, low-grade conidium exposures induced Th2-and eosinophil-predominant allergic lung disease, whereas higher exposures led to rapid conversion to neutrophil-and Th1 cell-predominant inflammation, a phenomenon we term immune phenotype switching. All fungal exposure doses were further linked to the secretion of interleukin-17A (IL-17A). Fungal infections with Curvularia lunata and Aspergillus fumigatus were typically confined to the airway during allergic inflammation but became locally invasive and disseminated to the brain at higher conidium challenge doses, in association with predominant Th1 responses. Fungal dissemination occurred at relatively low challenge doses with the conidia of Aspergillus fumigatus administered to recombinase activating gene 1 (Rag-1)-deficient mice, which lack B and T cells, but B cell-deficient MT mice and T helper cell-reconstituted Rag-1-deficient mice were comparable to wild-type mice in preventing fungal dissemination. Our findings demonstrate that Th2 cell-predominant allergic responses followed by immune phenotype switching and fungal dissemination are highly predictable outcomes with progressive fungal infectious burdens and that T helper cell responses are protective against lethal fungal dissemination.

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Allergic fungal rhinosinusitis

Cited by 31 publications

References 34 publications

Allergic Rhinitis and its Impact on Asthma (ARIA) 2008*

Allergic Rhinitis and its Impact on Asthma (ARIA) 2008*

Identification and Characterization of Size-Segregated Bioaerosols at Different Sites in Delhi

Necessary and Sufficient Role for T Helper Cells To Prevent Fungal Dissemination in Allergic Lung Disease

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