Immunologic Reactions of Bronchial Tissues in Asthma

Callerame, Mary Lou; Condemi, John J.; Bohrod, Milton G.; Vaughan, John H.

doi:10.1056/nejm197103042840902

Cited by 72 publications

(19 citation statements)

References 11 publications

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“…However, concerning LTC, production, enhancing and suppressive effects were observed for TNF-a and NGF-P, respectively (17). The experiments, in which the kinetics of IL-3 or IL-5 priming was examined, also showed that the optimal preincubation time was 10 for ECP release and LTC, production, respectively (this study, 14). These results indicate that degranulation and LTC, generation are clearly separately regulated.…”

Section: Discussionmentioning

confidence: 57%

“…However, it has been reported that some asthmatic patients developed reduced hemolytic-component activity or C4 in arterial or venous blood after allergen provocation (9). Complement deposition has been found in the bronchial mucosa of asthmatic patients (10). Some in vitro studies have demonstrated that the complement system can be activated by allergens via the classical pathway (ll), the alternative pathway (12), or both pathways (13) in normal human serum and in the sera of asthmatic patients.…”

Section: Effects Of Interleukin (Il)mentioning

confidence: 99%

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Effects of interleukin (IL)‐3 and IL‐5 on human eosinophil degranulation induced by complement components C3a and C5a*

Takafuji

Tadokoro

Itō

1996

Allergy

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It is suggested that eosinophils (Eos) play an important role in the pathogenesis of bronchial asthma by releasing cytotoxic cationic eosinophil granule proteins and damaging bronchial epithelial cells. However, the exact nature of the actual inducer of eosinophil degranulation in vivo is unclear. We examined eosinophil cationic protein (ECP) release from human Eos in response to soluble agonists such as C5a, C3a, platelet‐activating factor, and FMLP with or without interleukin (IL)‐3 or IL‐5 priming. Eosinophil degranulation induced by these soluble agonists required the pretreatment of Eos by cytochalasin B even in IL‐3 priming. Among four agonists, C5a was the most effective stimulus of ECP release either with or without IL‐5 priming. IL‐3 and IL‐5 remarkably enhanced ECP release in Eos triggered by C3a and C5a. The enhancement of ECP release by IL‐3 and IL‐5 occurred at 0.1–0.3 ng/ml and became maximal at 10–30 ng/ml, concentration‐dependently. The enhancement of ECP release by cytokines became optimal at an interval of 10 min. Our data support the importance of complement components and cytokines in eosinophil degranulation in vivo.

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Section: Discussionmentioning

confidence: 57%

Section: Effects Of Interleukin (Il)mentioning

confidence: 99%

Effects of interleukin (IL)‐3 and IL‐5 on human eosinophil degranulation induced by complement components C3a and C5a*

Takafuji

Tadokoro

Itō

1996

Allergy

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“…O ur findin gs a re simila r to th ose rep orted in severa l hist ol ogic [3,5,6], immun o logic [4,II] and electron m icroscopi c [I I ] stud ies o f hu ma n pati en ts with as th ma . Hist ol og ically, an acid ophi lic, hom ogen o us thi cken ed me mbr an e, va ry ing in widt h, wa s seen beneath th e ciliated pseudostratified co lumnar ep ithelium o f th e tr ach ea .…”

Section: Discussionmentioning

confidence: 86%

“…T hese results a re diffe ren t fro m th ose re po rted in ma n by GERBER et al [9], who fo un d li near a nti-IgA sta ining and a bse nce of BIC in th e ba se-ment membrane a nd mucosal ep ithelium of small bro nchi. CA LLERA ME et al [4] felt that the localization of immun oglo bulins below the basement membrane was very cha racteristic of asthma in man. MCCARTER a nd VA ZQUEZ [II] stated that mem bran e formation with localizat io n of immunoglobu lins was not specific fo r asthma and may rep resent a ma nifestat ion of a n 'exudati ve process' .…”

Section: Discussionmentioning

confidence: 99%

“…Thicken in g of th e trach eal basem ent membran e occ ur s in a va riety o f human d iseases such as asth ma , chro nic b ron chit is, Loeffler's sy nd ro me a nd p ulmo nary allergic gra nu lo ma tosis [2][3][4]6,II ,14]. In these d iseases it s pa thoge nes is a nd importan ce a re un kn own , but it may be a resp on se o f the tra chea to chro nic mu co sal injury.…”

mentioning

confidence: 99%

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Tracheal Basement Membrane Thickening in Rhesus Monkeys

Splitter¹,

Butcher²,

Stevens³

1974

Vet Pathol

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Abs tract. T hicke ned hyalin e tr ache al membra ne simila r to that which occurs with severa l respira to ry co nditions in man was seen in Rhe su s mo nkeys. Th e memb ran e was cosinophili c a nd up to 50.4 urn thic k. Freq uentl y eosino phils a nd ma st ce lls were seen in the trach ea l mucosa a nd submucos a. Us ing fluore scent microscop y, IgG, B 1C, B1A a nd a lbumin were identifi ed in the membran e. Electro n microscop y sho wed tha t the membra ne was co mposed of I8.8-nm co llage n-like fibr ils wit h occasional peri odicity. T he ca use of the thicke ned hyalin e tr acheal mem bran e could not be determ ined . T he cha nges pr oba bly represent a response to mild repe a ted or co nti nuou s trac hea l inj ury ow ing to a variety of causes. De linea tion of the ca use of this pr oce ss in non hu ma n primat es may hclp in the understan d ing of respirato ry diseases in man.Thicken in g of th e trach eal basem ent membran e occ ur s in a va riety o f human d iseases such as asth ma , chro nic b ron chit is, Loeffler's sy nd ro me a nd p ulmo nary allergic gra nu lo ma tosis [2-4, 6, II , 14]. In these d iseases it s pa thoge nes is a nd importan ce a re un kn own , but it may be a resp on se o f the tra chea to chro nic mu co sal injury. The th ickened membran e is co m posed o f hyal ine mat eri al a nd is ind uce d by a hype rsen siti vit y sta te [3]. Immunoglobul ins have been identifi ed in thi ck en ed br onchi al ba sem ent membranes [4, I I].Other ca uses o f trach eal ba sement membran e thi ck enin g a re endopa rasites, whi ch a re rep orted to produce hyper sen siti vity [7,13]. Vermin ou s pn eumonia in sea lion s [7] often is acco mp a n ied by a n eosi no philic hyalin e materi al adj acent to th e ba sement membran e o f th e trach ea a nd large br on chi . lnfrequentl y, hum an asthma has been a tt ributed to inh al ati on o f hou se mit es in du st , w h ich th en act a s a so urce o f allergen as d o non-li vin g materi al s [8].Snee zing a nd co ug hi ng a re associated with acariasis in O ld W orld prim at es[10] ; but no a lle rgic sy nd ro me o r tr ach eal basem ent thi ck en ing was rep o rt ed .Thi s paper describes t hicke ned tr ach eal basem ent membra nes in 90 Rh esu s monkeys.

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Clinical Profiles of Bronchial Asthma

Mathison¹

1973

JAMA

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Immunologic Reactions of Bronchial Tissues in Asthma

Cited by 72 publications

References 11 publications

Effects of interleukin (IL)‐3 and IL‐5 on human eosinophil degranulation induced by complement components C3a and C5a*

Effects of interleukin (IL)‐3 and IL‐5 on human eosinophil degranulation induced by complement components C3a and C5a*

Tracheal Basement Membrane Thickening in Rhesus Monkeys

Clinical Profiles of Bronchial Asthma

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