Fungi in chronic hyperplastic eosinophilic sinusitis - Reasonable doubt

被引:13
作者
Borish, Larry [1 ]
Rosenwasser, Lanny
Steinke, John W.
机构
[1] Univ Virginia Hlth Syst, Beirne Carter Ctr Immunol Res, Asthma & Allerg Dis Ctr, Charlottesville, VA 22903 USA
[2] Univ Missouri, Childrens Mercy Hosp & Clin, Dee Lyons Missouri Endowed Chair Pediat Immunol R, Kansas City, MO 64110 USA
关键词
chronic sinusitis; allergic inflammation; fungal colonization; bacterial superantigen; eosinophil;
D O I
10.1385/CRIAI:30:3:195
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Chronic hyperplastic eosinophilic sinusitis (CHES) is a T-helper (Th)2-like, lymphocyte-initiated, eosinophil-rich inflammatory disease. The complex immune interactions required to orchestrate these processes begin with the presentation of antigen by mature dendritic cells to Th lymphocytes that display the appropriate antigen-specific T-cell receptor. The objective of sinus research must be to identify and target that antigen; this will lead to the cure for this condition. This article reviews numerous models that may be responsible for the pathophysiology of this disorder, including putative roles for allergens, bacteria, and bacterial-derived superantigens, as well as recent interest in fungal-derived antigens. Additionally, we speculate that whatever the inciting cause of CHES may be, it is plausible that once initiated, cellular differentiation pathways may lead to the development of an antigen-independent permanent phase. More than one of these may be valid in different subjects and, furthermore, this list almost assuredly does not explain all cases of CHES. The concept that fungal antigens colonizing the sinuses are responsible for CHES represents an intriguing, but unproven, hypothesis. Presently, the case for the fungus remains circumstantial. The case for fungi will be proved only with definitive proof that T-cells within the sinuses are actively responding to fungal antigens present in the sinus and with the further demonstration that removal of those fungal antigens ameliorates the disease.
引用
收藏
页码:195 / 203
页数:9
相关论文
共 41 条
[1]   Does inhaled pollen enter the sinus cavities? [J].
Adkins, TN ;
Goodgold, HM ;
Hendershott, L ;
Slavin, RG .
ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY, 1998, 81 (02) :181-184
[2]   IL-5 synthesis is upregulated in human nasal polyp tissue [J].
Bachert, C ;
Wagenmann, M ;
Hauser, U ;
Rudack, C .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1997, 99 (06) :837-842
[3]   Total and specific IgE in nasal polyps is related to local eosinophilic inflammation [J].
Bachert, C ;
Gevaert, P ;
Holtappels, G ;
Johansson, SGO ;
van Cauwenberge, P .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2001, 107 (04) :607-614
[4]   Nasal allergen challenge leads to bilateral maxillary sinus eosinophil influx [J].
Baroody, FM ;
Saengpanich, S ;
Detineo, M ;
Haney, L ;
Votypka, V ;
Naclerio, RM .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2002, 109 (01) :S84-S84
[5]  
BORTS MR, 1989, J ALLERGY CLIN IMMUN, V83, P302
[6]   Nasal allergen provocation induces adhesion molecule expression and tissue eosinophilia in upper and lower airways [J].
Braunstahl, GJ ;
Overbeek, SE ;
KleinJan, A ;
Prins, JB ;
Hoogsteden, HC ;
Fokkens, WJ .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2001, 107 (03) :469-476
[7]   Pathogenesis of chronic rhinosinusitis: role of airborne fungi and bacteria [J].
Davis, LJB ;
Kita, H .
IMMUNOLOGY AND ALLERGY CLINICS OF NORTH AMERICA, 2004, 24 (01) :59-+
[8]   ASSESSMENT OF INFLAMMATION IN NONINFECTIOUS CHRONIC MAXILLARY SINUSITIS [J].
DEMOLY, P ;
CRAMPETTE, L ;
MONDAIN, M ;
CAMPBELL, AM ;
LEQUEUX, N ;
ENANDER, I ;
SCHWARTZ, LB ;
GUERRIER, B ;
MICHEL, FB ;
BOUSQUET, J .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1994, 94 (01) :95-108
[9]   Haemopoietic mechanisms in nasal polyposis and asthma [J].
Denburg, JA .
THORAX, 2000, 55 :S24-S25
[10]  
Denburg Judah A., 2000, Journal of Allergy and Clinical Immunology, V106, pS242