Fungi & Chronic Rhinosinusitis (CRS)

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Questions and Answers

Which statement most accurately reflects the current understanding of the fungal hypothesis in chronic rhinosinusitis (CRS)?

The presence of fungi in the nasal cavity, along with eosinophilic mucin, universally indicates an exaggerated inflammatory response, confirming the fungal etiology of CRS.
It is definitively proven that fungi, especially _Alternaria_, directly cause CRS through a universal hyper-responsiveness.
The original hypothesis suggesting fungi as the primary antigenic stimulus in CRS is well-supported by recent clinical trials and in vitro studies.
While not considered the primary cause of all CRS, fungi may act as disease modifiers or play a role in specific subtypes like allergic fungal rhinosinusitis (AFRS). (correct)

How might fungi contribute to the pathogenesis of chronic rhinosinusitis (CRS) beyond a direct antigenic response?

By directly triggering mast cell activation and histamine release in the nasal mucosa.
Through intrinsic protease activity exacerbating inflammation and the presence of chitin in fungal cell walls inciting eosinophilic responses. (correct)
By inducing a universal IgE-mediated hypersensitivity reaction, leading to immediate mucosal swelling.
Via the production of potent mycotoxins that directly damage the sinus epithelium, initiating a chronic inflammatory cycle.

A researcher is investigating the role of Alternaria in chronic rhinosinusitis (CRS). Which finding would most strongly contradict the original fungal hypothesis of CRS?

A separate study fails to replicate the fungal-induced cytokine responses from peripheral blood mononuclear cells in CRS patients. (correct)
Peripheral blood mononuclear cells from CRS patients exhibit a consistent cytokine response when exposed to supraphysiologic levels of _Alternaria_ in vitro.
A multicenter randomized controlled trial shows significant anti-inflammatory effects of intranasal amphotericin B lavages in CRS patients.
Nasal mucus from CRS patients consistently triggers eosinophil migration in vitro.

What clinical characteristic is most indicative of allergic fungal rhinosinusitis (AFRS) as a distinct subset of chronic rhinosinusitis (CRS)?

<p>Type 1 hypersensitivity response to fungi, type 2 cytokine expression, nasal polyps, and eosinophilic mucin. (D)</p> Signup and view all the answers

In the context of paranasal sinus fungal balls, which statement best describes their relationship to chronic rhinosinusitis (CRS)?

<p>Fungal balls may cause symptoms indistinguishable from CRS in immunocompetent individuals, and symptoms resolve with removal of the lesion, though the precise pathophysiologic link remains unclear. (B)</p> Signup and view all the answers

Flashcards

Fungal Hypothesis of CRS

An exaggerated inflammatory reaction to common airborne fungi, like Alternaria, once thought to be the main cause of both CRSsNP and CRSwNP.

Allergic Fungal Rhinosinusitis (AFRS)

A subset of CRS marked by a type 1 hypersensitivity to fungi, type 2 cytokine expression, nasal polyps, and eosinophilic mucin.

Fungal Protease Activity

Enzymes that can worsen inflammation in CRS by interacting with upregulated protease-activated receptors (PARs) in nasal epithelial cells.

Chitin

A polysaccharide in fungal cell walls suggested as a potential cause of eosinophilic responses in some studies.

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Paranasal Sinus Fungal Balls

Tangled hyphae of various fungal species in the paranasal sinuses that may cause symptoms similar to CRS or be asymptomatic.

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Study Notes

Fungi's role in Chronic Rhinosinusitis (CRS) etiology remains debated.

Detection of Fungi in Nasal Cavity

Fungi are detectable in the nasal cavity of all patients, including those with and without CRS.
There isn't a definitive increase in fungal biomass in CRS patients.
The presence of fungi and eosinophilic mucin in all CRS patients initially supported the fungal hypothesis of CRS.

Fungal Hypothesis of CRS

The theory suggests an exaggerated inflammatory reaction to the airborne fungus Alternaria as the cause of CRSsNP and CRSwNP.
These are considered forms of the same disease differing in intensity.
In vitro studies showed that high Alternaria levels triggered a cytokine response from CRS patients' blood mononuclear cells, but not from controls.
Nasal mucus or tissue from CRS patients induced eosinophil migration.
A 60-kDa component of Alternaria was found to trigger eosinophil degranulation in vitro.
Alternaria proteins presented to sensitized T cells induce a cytokine response, attracting and activating eosinophils.
Alternaria serves as a target of eosinophils, triggering degranulation and mucosal damage.
Attempts to replicate fungal-induced cytokine responses failed, indicating no universal hyperresponsiveness to fungal antigens in CRS patients.
A multicenter randomized controlled trial using intranasal amphotericin B lavages showed no significant anti-inflammatory effect in CRS.
Literature doesn't support routine use of topical antifungals for CRS.
Support for the original fungal hypothesis is limited.

Alternative Views on Fungi Role in CRS

Fungi may play a role in allergic fungal rhinosinusitis (AFRS), a CRS subset characterized by type 1 hypersensitivity to fungi, type 2 cytokine expression, nasal polyps, and eosinophilic mucin.
It is unclear whether fungus initiates the inflammatory response even in AFRS.
Fungi have intrinsic protease activity.
Upregulation of protease-activated receptors (PARs) in nasal epithelial cells (ECs) of CRS patients, combined with fungi protease activity, may exacerbate inflammatory processes in CRS.
Fungal cell walls contain chitin, which has been proposed as an etiologic driver of eosinophilic responses.
The clinical significance of chitin remains uncertain.
Paranasal sinus fungal balls can cause symptoms similar to CRS or be asymptomatic and discovered incidentally.
Pathology reveals tangled hyphae of fungal species.
Symptoms resolve with lesion removal, although the pathophysiologic relationship to AFS or typical CRS is unclear

Conclusion

There is a lack of consistent in vitro or in vivo evidence that fungal antigens are the primary targets of mucosal immune responses in CRS, except possibly in AFRS.
Fungi can incite epithelial immune responses, suggesting a potential secondary role as disease modifiers in some CRS subtypes.

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Description

An overview of fungi's debated role in Chronic Rhinosinusitis (CRS) etiology. Detection of fungi in the nasal cavity, fungal biomass, and the fungal hypothesis of CRS are discussed. Studies show Alternaria triggers cytokine response.